The research, conducted by scientists from the China Academy of Chinese Medical Sciences and Fujian University of Traditional Chinese Medicine, addresses a major challenge in liver cancer treatment. Hepatocellular carcinoma often develops in the context of chronic liver disease and can be difficult to control once it has progressed. Although surgery, ablation, immunotherapy, targeted drugs, and chemotherapy can benefit selected patients, treatment resistance and disease recurrence remain widespread. Artesunate is already widely used against malaria, giving it an established pharmacological history and a well-characterized clinical profile. However, the molecular basis of its activity against cancer has remained incompletely understood.

The investigators first examined how artesunate affected the survival and growth of two human hepatocellular carcinoma cell lines, HepG2 and MHCC-97H. Using the CCK8 assay, which measures cellular metabolic activity as an indicator of viability and proliferation, they found that artesunate inhibited both cell lines in a concentration-dependent manner. HepG2 cells were more sensitive than MHCC-97H cells, suggesting that differences in metabolic state or drug-response pathways may influence the treatment’s effectiveness. Additional experiments showed that artesunate reduced cancer-cell proliferation and increased the proportion of cells undergoing apoptosis, a tightly regulated form of cell death that is frequently disabled in tumors.

The study also examined artesunate in an orthotopic mouse model, in which HepG2 cells were injected into the liver to reproduce a more realistic tumor environment than conventional subcutaneous models. Animals receiving low, middle, or high doses of artesunate showed evidence of increased tumor-cell apoptosis. TUNEL staining, which detects fragmented DNA associated with programmed cell death, and Hoechst staining, which reveals changes in nuclear structure, both supported the conclusion that artesunate promoted apoptosis in the tumors. The effects were compared with control animals and with a group receiving 5-fluorouracil, a commonly used anticancer drug. These experiments provided in vivo support for the cellular findings, although additional animal and clinical studies will be necessary to determine whether the effect can be translated into a useful treatment.

The researchers connected artesunate’s activity to sphingolipid metabolism, a biochemical network that produces and regulates lipids involved in membrane structure, cell signaling, inflammation, and cell death. GBA normally helps break down glucosylceramide, a glycosphingolipid, into downstream metabolic products. When GBA was inhibited by artesunate, glucosylceramide-related metabolites accumulated and the balance of cellular sphingolipids was disturbed. Such metabolic changes can place stress on organelles and alter signaling pathways that control survival. In the treated liver cancer cells, this disruption was associated with mitochondrial dysfunction, a critical event because mitochondria regulate the intrinsic pathway of apoptosis.

The study describes a signaling sequence linking altered lipid metabolism to mitochondrial apoptosis: GBA, ceramide, cathepsin D, alpha-synuclein, BID, and BAX. In this proposed GBA–ceramide–CTSD–α-syn–BID–BAX axis, artesunate first suppresses GBA activity, altering ceramide metabolism. The resulting biochemical imbalance interferes with the maturation or function of cathepsin D, a lysosomal protease. It also promotes the accumulation of alpha-synuclein, a protein better known for its association with neurodegenerative disease but increasingly recognized as a regulator of cellular stress and organelle communication. These changes facilitate cleavage of BID and increase the activity or abundance of BAX, two important components of the mitochondrial death pathway. BAX can promote mitochondrial membrane permeabilization, allowing apoptotic factors to escape and activate downstream caspases, the enzymes that dismantle the cell.

Rescue experiments strengthened the proposed mechanism. When researchers supplemented cells with ceramide, they were able to influence the apoptotic response, supporting the idea that sphingolipid imbalance lies between GBA inhibition and mitochondrial damage. Conversely, suppressing alpha-synuclein reduced key effects of artesunate, indicating that alpha-synuclein accumulation is not simply a passive consequence of treatment but contributes to the death signal. The researchers also tested LTI-291, described in the study as a GBA enzyme activator, in combination with high-dose artesunate. The combined treatment helped probe whether restoring GBA-related activity could counteract artesunate’s effects. Together, these interventions provided functional evidence that the pathway is central to the drug’s anticancer action rather than being an incidental molecular signature.

A particularly significant part of the work focused on the physical interaction between artesunate and GBA. Through computational modeling and biochemical analyses, the researchers identified three amino-acid residues—tyrosine 313, glutamate 340, and asparagine 396—as important potential contact points within the enzyme’s active site. Site-directed mutagenesis was then used to replace selected residues and test their importance experimentally. Mutations affecting E340 and N396 substantially weakened artesunate binding and reduced GBA enzymatic activity. The altered enzyme also lost much of its ability to transmit the downstream apoptotic response induced by artesunate. These results support a direct target-engagement model in which the drug’s chemical structure fits into a functional region of GBA and changes the enzyme’s behavior.

The findings are notable because they move beyond the observation that artesunate can kill cancer cells and begin to explain why. Drug repurposing often starts with a promising biological effect, but successful development requires knowledge of the target, the binding site, the responsive cancer subtypes, and the mechanisms that may produce resistance. By defining GBA as a direct molecular target and connecting it to a lipid-regulated apoptotic pathway, the study offers several possible directions for future research. GBA expression or sphingolipid profiles might eventually help identify tumors most likely to respond, while combinations involving ceramide metabolism, lysosomal function, or mitochondrial apoptosis could potentially improve treatment activity.

At the same time, the results should not be interpreted as evidence that artesunate is already an established liver cancer therapy. The experiments were performed mainly in cultured cell lines and mouse models, systems that cannot fully reproduce the genetic diversity, immune environment, drug metabolism, and treatment history of human tumors. The greater sensitivity of HepG2 cells compared with MHCC-97H cells also highlights the possibility that response depends on tumor-specific biology. Future work will need to test the mechanism in patient-derived organoids, genetically diverse xenograft models, and carefully designed pharmacological studies. Long-term safety, optimal dosing, interactions with current liver cancer treatments, and the effects of artesunate on healthy liver tissue will also require detailed evaluation.

Published in Genes & Diseases, the study presents artesunate as more than an antimalarial compound with broad anticancer activity. It identifies a defined enzyme target, maps critical binding residues, and traces a mechanistic route from altered sphingolipid metabolism to mitochondrial apoptosis in hepatocellular carcinoma. If the findings are confirmed in clinically relevant models and human studies, GBA-targeted strategies could expand the therapeutic possibilities for a cancer that continues to demand more effective and durable treatments. For now, the work provides a compelling molecular blueprint for investigating how an established medicine might be redesigned or repurposed to exploit metabolic weaknesses in liver cancer.

Subject of Research: Artesunate-induced apoptosis and GBA-targeted mechanisms in hepatocellular carcinoma

Article Title: Artesunate directly targets glucosylceramidase to suppress hepatocellular carcinoma proliferation and trigger apoptosis

Web References: https://doi.org/10.1016/j.gendis.2026.102045; https://www.sciencedirect.com/journal/genes-and-diseases

References: Genes & Diseases, DOI: 10.1016/j.gendis.2026.102045

Image Credits: Xia Mao, Xiangying Yan, Yawen Chen, Bingbing Cai, Wenjia Chen, Ya Lin, Na Lin, Yanqiong Zhang

Keywords

Artesunate, hepatocellular carcinoma, liver cancer, glucosylceramidase, GBA, sphingolipid metabolism, ceramide, mitochondrial apoptosis, cathepsin D, alpha-synuclein, BID, BAX, drug repurposing

Lamin A, a crucial nuclear envelope protein, provides structural support to the nucleus and plays essential roles in gene expression regulation, DNA replication, and cellular signaling. The ubiquitination of Lamin A has emerged as a pivotal post-translational modification that can influence its stability and function. However, the specific consequences of K144 ubiquitination in the context of HCC were poorly understood until this study. The research highlights UBC9 as a vital enzyme that mediates this modification, emphasizing its potential impact on the development of liver tumors.

The team conducted a series of experiments to determine the role of UBC9 in the ubiquitination process of Lamin A. Utilizing both in vitro and in vivo models, they assessed the expression levels of UBC9 alongside the K144 ubiquitination status of Lamin A. The results demonstrated a significant correlation; elevated UBC9 expression led to increased K144 ubiquitination, suggesting a direct regulatory mechanism. This finding is critical, as it establishes a link between UBC9 activity and the pathological modifications of Lamin A in HCC.

Furthermore, the implications of altered Lamin A ubiquitination are profound. The study posits that K144 ubiquitination may affect key biological processes, such as cell cycle regulation, apoptosis, and DNA repair mechanisms. Given that these processes are often dysregulated in cancer, particularly HCC, understanding the role of UBC9-mediated ubiquitination of Lamin A could highlight essential pathways leading to tumorigenesis. The researchers suggest that targeting UBC9 may provide a novel therapeutic intervention point for patients with hepatocellular carcinoma.

The methodology employed by Wang et al. included advanced imaging techniques and quantitative assays, allowing for precise assessment of ubiquitination levels and effective evaluation of cellular responses to various treatments. This rigorous approach strengthens the credibility of their findings, demonstrating a clear mechanistic view of how UBC9 influences Lamin A modifications. Moreover, the integration of computational modeling offers predictive insights into how manipulating UBC9 expression might alter cancer progression dynamics.

While the study yields crucial insights, the authors also acknowledge the complexity of ubiquitin signaling networks. The involvement of additional ubiquitin-conjugating enzymes and ligases presents a challenge for delineating specific pathways. Future research is required to map these interactions comprehensively and to validate the functional consequences of UBC9-mediated K144 ubiquitination in a broader context. The findings laid the groundwork for subsequent investigations into the therapeutic exploitation of these pathways.

In addition to its mechanistic contributions, the study highlights the potential for developing biomarkers based on UBC9 and K144 ubiquitination status. Such biomarkers could enhance diagnostic accuracy and predictive models regarding therapeutic responses in HCC patients. The prospect of personalized treatment strategies based on the molecular profile of tumors signals a paradigm shift in the management of liver cancer.

As hepatocellular carcinoma remains one of the leading causes of cancer-related mortality worldwide, understanding its molecular underpinnings is paramount. The results from this research provide a stepping stone toward identifying new targets for drug development, as well as strategies for early detection and intervention. This work underscores the importance of continued exploration into the molecular machinery governing cancer biology.

The broader implications of this research extend beyond hepatocellular carcinoma. The mechanism of ubiquitination is conserved across various cell types and diseases, suggesting that the findings may resonate within the fields of neurodegeneration, cardiovascular diseases, and other malignancies. Thus, the insights gained from this study may serve as a valuable resource for future investigations into the modulation of ubiquitination pathways across multiple domains of health and disease.

Scientific discourse thrives on the collaborative efforts of researchers who contribute to a more nuanced understanding of complex biological processes. This study is a testament to the power of interdisciplinary research, combining molecular biology, genetics, and bioinformatics to unravel the intricacies of cancer pathology. The implications for patients suffering from liver cancer are profound; novel strategies derived from these findings could transform the landscape of treatment and significantly impact patient outcomes.

In conclusion, the study by Wang, Liao, and Zhang represents a significant leap forward in cancer research, particularly concerning hepatocellular carcinoma. By elucidating the role of UBC9 in the regulation of K144 ubiquitination of Lamin A, these researchers have not only expanded the existing body of knowledge but have also set the stage for future innovations in diagnostic and therapeutic approaches. The intricate dance of cellular processes continues to fascinate scientists, driven by the promise of translating foundational discoveries into tangible benefits for patients worldwide.

The path from basic research to clinical application is often fraught with challenges, yet studies like this one pave the way for promising new strategies. By expounding on the relationship between UBC9, Lamin A, and liver cancer, researchers are forging a new path toward improved patient care, underscoring the necessity for ongoing investment in cancer research and therapeutic development. The journey may be complex, but the potential benefits for patients are indeed worth the pursuit.

In a world where hepatocellular carcinoma poses a significant health risk, the insights gained from this research are essential for steering the future of oncological treatment and enhancing the quality of life for those affected by such devastating diseases. The scientific community eagerly anticipates further developments stemming from this work, with hopes that it will lead to breakthroughs that substantially improve early detection, treatment efficacy, and ultimately, patient survival rates.

With the publication of their findings, the authors encourage further exploration and dialogue among researchers to build on this critical knowledge. As the field evolves, the collaboration and sharing of results will be vital in advancing our understanding and combating the challenges posed by liver cancer effectively. The future of hepatocellular carcinoma research is bright, illuminated by the promising discoveries highlighted in this transformative study.

Subject of Research: UBC9-mediated regulation of K144 ubiquitination of Lamin A and its implications for hepatocellular carcinoma.

Article Title: UBC9-mediated regulation of K144 ubiquitination of Lamin A and its implications for hepatocellular carcinoma.

Article References:

Wang, Q., Liao, Z., Zhang, H. et al. UBC9-mediated regulation of K144 ubiquitination of Lamin A and its implications for hepatocellular carcinoma.
J Transl Med (2026). https://doi.org/10.1186/s12967-026-07722-0

Image Credits: AI Generated

DOI: 10.1186/s12967-026-07722-0

Keywords: Hepatocellular carcinoma, Lamin A, UBC9, ubiquitination, cancer research, molecular pathways.

Hepatocellular carcinoma remains among the deadliest cancers globally, exacerbated by lifestyle factors such as excessive alcohol consumption and environmental carcinogens that induce molecular aberrations in hepatic cells. Traditional therapeutic avenues have often fallen short, primarily due to tumor heterogeneity and adaptive resistance mechanisms. This study by Ranjan, Sunita, and Pattanayak embarks on addressing these hurdles by utilizing MFER-Mc, a compound meticulously identified and characterized through LC-MS techniques, thus ensuring accuracy in molecular composition and purity which are critical for reproducibility and pharmacokinetic clarity.

The investigation begins with detailed in-silico analyses employing advanced computational simulations to predict the binding affinity and interaction dynamics of MFER-Mc with nuclear receptors LXR-α and LXR-β. These receptors are integral to cholesterol homeostasis and lipid metabolism in hepatocytes and have become attractive targets for anti-cancer drug development. The computational studies revealed that MFER-Mc exhibits strong and stable binding with these receptors, suggesting its capability to modulate downstream genetic pathways that govern cell proliferation and apoptosis in hepatic cancer cells.

Subsequent in-vitro experiments utilized cultured hepatocyte models exposed to alcohol and NDEA, replicating the carcinogenic environment seen in HCC patients. Treatment with MFER-Mc led to significant inhibition of cell proliferation and induced apoptosis, as evidenced by key markers such as caspase activation and DNA fragmentation. Moreover, dose-dependent suppression of HMG-CoA reductase, a rate-limiting enzyme in cholesterol biosynthesis implicated in tumor cell survival, corroborated the hypothesis that MFER-Mc exerts its anti-cancer effects through multifaceted metabolic interference.

Transitioning from cellular models to in-vivo systems, the research team employed rodent models with alcohol and NDEA-induced HCC to simulate the pathological milieu accurately. MFER-Mc administration demonstrated notable therapeutic responses, including tumor size reduction and improved liver histopathology. These effects were accompanied by modulation of LXR expression levels and downstream targets, validating the mechanistic pathways predicted in the in-silico phase. Importantly, the compound exhibited a favorable safety profile with minimal systemic toxicity, an essential consideration for clinical translation.

The study’s integrative approach underscores the potential of targeting nuclear receptors such as LXR-α and LXR-β, alongside the HMG-CoA pathway, constituting a dual-pronged attack against HCC. Their regulation is crucial not only in lipid metabolism but also in mediating inflammatory responses and cellular energy status, all of which contribute to tumorigenesis. By harnessing MFER-Mc to appropriately harness these pathways, the research suggests a paradigm where metabolic modulation becomes a cornerstone in cancer therapy, transcending the conventional cytotoxic strategies.

Another pivotal aspect of the research pertains to the utilization of high-precision LC-MS characterization, conferring an unmatched level of detail regarding the chemical nature and stability of MFER-Mc. This analytical rigor facilitates reproducible synthesis and aids in understanding the pharmacodynamics and pharmacokinetics critical for drug development. Such precision is indispensable in discerning subtle structural variations that may dictate bioavailability and receptor affinity, ultimately influencing therapeutic outcomes.

Equally compelling is the study’s exploration of the hepatoprotective attributes of MFER-Mc. Given that liver tissue is constantly challenged by oxidative stress and inflammatory insults induced by alcohol and NDEA, compounds that can also mitigate these insults hold substantial promise. Data from the in-vivo trials indicate reduced markers of oxidative damage and inflammatory cytokines, suggesting that MFER-Mc not only suppresses tumor growth but also preserves hepatic function, a dual advantage for patients suffering from HCC.

This research contributes profoundly to the expanding field of systems pharmacology, where drug actions are viewed within the broader network of cellular pathways and metabolic circuits. By intertwining computational insights with experimental validation, the study exemplifies how integrated methodologies can accelerate the discovery of potent therapeutics capable of targeting complex diseases like cancer more effectively. The synergy between LXR modulation and HMG-CoA pathway inhibition presents a novel combinatorial mechanism that could inspire future drug design endeavors beyond hepatic oncology.

The implications of these findings transcend laboratory settings, holding the potential to impact clinical management strategies for patients at high risk of HCC due to alcohol abuse and environmental carcinogen exposure. The prospect of introducing a compound like MFER-Mc into therapeutic regimens could enhance survival outcomes while reducing side effects associated with current chemotherapeutic agents. The research paves the way for subsequent clinical trials, which are crucial to confirm efficacy and optimize dosing protocols in human subjects.

Furthermore, this study enriches scientific understanding of the molecular underpinnings of HCC progression. By delineating the roles of LXRs and HMG-CoA enzyme activity in hepatocarcinogenesis, it opens avenues for biomarker development that can predict disease progression or therapeutic response. Such markers are invaluable for personalized medicine approaches, enabling clinicians to tailor interventions based on individual metabolic and genetic profiles, thereby maximizing treatment efficacy.

In addition to its therapeutic promise, the multidisciplinary approach of this investigation highlights the synergy between advanced analytical chemistry, molecular biology, pharmacology, and computational modeling, setting a precedent for future cancer research endeavors. The successful correlation among in-silico predictions, in-vitro functional assays, and in-vivo pathophysiological outcomes illustrates the strength of comprehensive, multi-level analysis in overcoming the complexities associated with cancer therapeutics.

The research team’s dedication to elucidating the mechanistic depth of MFER-Mc’s anticancer activity underscores the evolving nature of drug discovery where therapeutic candidates are scrutinized beyond mere efficacy metrics. Understanding how a compound interacts within intricate biological networks informs not only safety and toxicity assessments but also guides combinatorial therapy designs, resilience against resistance, and long-term management of cancer remission.

This study invites a broader reconsideration of metabolic pathways as targets in oncology, emphasizing that diseases like HCC are intricately linked to systemic metabolic dysregulations. The integration of LXR and HMG-CoA pathways within therapeutic strategies reflects an emerging consensus that effective cancer treatment must reconcile the metabolic demands of tumors with host physiology. MFER-Mc’s ability to navigate these pathways represents a novel therapeutic avenue that may establish a new standard in hepatic cancer treatment.

Ultimately, the promise of MFER-Mc extends into public health realms as well, offering hope for populations severely affected by hepatic carcinogens associated with lifestyle and environmental factors. If translated successfully into clinical therapies, this compound could mark a milestone in reducing the burden of liver cancer globally, aligning with broader efforts to mitigate risks associated with alcohol abuse and chemical carcinogen exposure. More broadly, it exemplifies the potential of rational drug design coupled with cutting-edge molecular profiling to generate next-generation oncological treatments.

Subject of Research: Therapeutic potential of LC-MS characterized MFER-Mc against alcohol and NDEA-induced hepatocellular carcinoma via LXR-α, LXR-β, and HMG-CoA pathways.

Article Title: A therapeutic approach of LC-MS characterised MFER-Mc against alcohol and NDEA induced hepatocellular carcinoma activity through LXR-α, LXR-β and HMG-CoA pathway: an in-silico, in-vitro and in-vivo study.

Article References:
Ranjan, S., Sunita, P. & Pattanayak, S.P. A therapeutic approach of LC-MS characterised MFER-Mc against alcohol and NDEA induced hepatocellular carcinoma activity through LXR-α, LXR-β and HMG-CoA pathway: an in-silico, in-vitro and in-vivo study. Med Oncol 43, 101 (2026). https://doi.org/10.1007/s12032-025-03175-5

Image Credits: AI Generated

DOI: https://doi.org/10.1007/s12032-025-03175-5

Hepatocellular carcinoma has emerged as a leading cause of cancer-related mortality worldwide, particularly in regions with high rates of hepatitis B and C virus infections. As the disease advances, understanding the molecular intricacies becomes imperative for developing effective treatment modalities. The CK1 family of serine/threonine kinases plays critical roles in several cellular processes, including cell cycle regulation, signaling pathways, and gene expression. Among its members, CSNK1E has shown promise as a potential key player in cancer biology.

The researchers, led by Zhou et al., conducted a series of experiments to explore the function of CSNK1E in HCC cell lines and patient-derived xenografts. Their approach involved a meticulous examination of the kinase’s expression levels in hepatic tissues, revealing that CSNK1E is often upregulated in HCC compared to normal liver tissue. These findings align with previous studies that suggest aberrant kinase activity may contribute to oncogenesis. Intriguingly, when CSNK1E expression was inhibited, a marked reduction in cell proliferation and migratory capabilities was observed, underscoring the kinase’s role in facilitating tumor growth and invasion.

To dissect the underlying mechanisms through which CSNK1E exerts its effects, the team focused on downstream signaling pathways involved in tumor biology. They discovered that CSNK1E modulates several key pathways, including the Wnt/β-catenin signaling cascade, which is frequently implicated in liver cancer. By phosphorylating specific substrates involved in this pathway, CSNK1E appears to enhance β-catenin stabilization and translocation to the nucleus, a critical step for promoting the expression of target genes that drive proliferation and metastasis in HCC.

Moreover, the researchers employed various assays to assess the functional implications of CSNK1E regulation on cellular behavior. They performed colony formation assays and wound healing assays, both of which quantitatively demonstrated that silencing CSNK1E led to a significant reduction in both anchorage-independent growth and motility of HCC cells. These results collectively suggest that targeting CSNK1E may offer a novel therapeutic strategy to inhibit HCC progression by simultaneously disrupting multiple oncogenic processes.

In addition to its role in promoting proliferation and migration, CSNK1E was also found to influence the expression of several proto-oncogenes and tumor suppressor genes. The identification of these transcriptional targets reveals a more complex regulatory network orchestrated by CSNK1E, with possible implications for the development of chemoresistance. Understanding this relationship is crucial, as it may help inform the design of combination therapies that could effectively counteract resistance mechanisms that often thwart current treatment strategies.

The implications of this study extend beyond basic science; they invite translational applications that resonate within clinical oncology. By identifying CSNK1E as a potential therapeutic target, the research provides a foundation for developing small molecule inhibitors or biological agents. These agents could specifically inhibit CSNK1E activity, offering a targeted approach to mitigate the aggressive nature of HCC. This strategy aligns with the growing trend of personalized medicine, where therapies are tailored to the molecular makeup of an individual’s tumor.

Furthermore, the study raises intriguing questions about the potential role of CSNK1E in other cancers. Given the pervasive nature of CK1 family kinases in various malignancies, further exploration into the role of CSNK1E in different tumor contexts could yield significant insights. This broader perspective may lead to the identification of universal biomarkers that enhance prognostic capabilities across cancer types, potentially transforming clinical approaches to diagnosis and treatment.

The study’s findings hold particular significance as hepatocellular carcinoma continues to frustrate oncologists with its late diagnosis and poor prognostic outcomes. By targeting CSNK1E, there’s a real potential not just for improving patient survival rates but also for enhancing the quality of life for individuals battling this formidable disease. Ongoing clinical trials focused on CK1 family members will be essential in validating these findings and determining their applicability in clinical settings.

In conclusion, the work by Zhou, Wang, and Li stands at the forefront of hepatocellular carcinoma research, providing a new perspective on the molecular underpinnings of this deadly cancer. The intricate interplay between CSNK1E and various signaling pathways highlights the complexity of tumor biology and reinforces the importance of novel therapeutic strategies. As further investigations unfold, the hope is that this research will contribute to a future where precision oncology can offer targeted, effective treatments for patients suffering from hepatocellular carcinoma and other malignancies influenced by CK1 activity.

This comprehensive exploration of CSNK1E’s role in hepatocellular carcinoma illustrates the intertwining relationship between basic research and clinical application, paving the way for innovative approaches to fighting cancer. With ongoing support and interest in the cancer research community, the insights from this study have the potential to catalyze significant advancements in our overall understanding of liver cancer treatment.

Subject of Research: The role of casein kinase 1 family member CSNK1E in proliferation and migration in hepatocellular carcinoma.

Article Title: Casein kinase 1 family member CSNK1E can regulate proliferation and migration in hepatocellular carcinoma.

Article References:

Zhou, J., Wang, YH., Li, YL. et al. Casein kinase 1 family member CSNK1E can regulate proliferation and migration in hepatocellular carcinoma.
J Cancer Res Clin Oncol 151, 269 (2025). https://doi.org/10.1007/s00432-025-06321-8

Image Credits: AI Generated

DOI:

Keywords: HCC, CSNK1E, casein kinase 1, proliferation, migration, liver cancer, signaling pathways.