The study team, led by researchers at Zhejiang University and The Third Affiliated Hospital of Guangzhou Medical University, analyzed ten human cervical tissue samples spanning the full pathological continuum. Single-cell RNA sequencing allowed them to profile thousands of individual cells, resolving not only which cell types were present at each disease stage but also how their gene-expression programs shifted as lesions progressed. Whole-genome bisulfite sequencing added a crucial layer of epigenetic information, revealing how DNA methylation patterns change across cell types during carcinogenesis, while spatial transcriptomic data from a public cohort confirmed that the cellular relationships observed in dissociated single-cell data hold true within intact tissue architecture.

One of the most striking findings is that disease progression is accompanied by a marked increase in NK/T cell infiltration. As normal tissue advances through LSIL and HSIL toward invasive carcinoma, immune cells of the NK and T lineages crowd increasingly into the lesion environment. This might, at first glance, seem encouraging, since cytotoxic lymphocytes are the very cells capable of destroying tumor cells. Yet the infiltration coincides with upregulation of galectin-9, an immune checkpoint ligand encoded by the LGALS9 gene. Galectin-9 is known to bind Tim-3 on T cells, a interaction that dampens antitumor immunity and drives T-cell exhaustion. In other words, the tumor microenvironment appears to respond to escalating immune pressure by deploying an immunosuppressive ligand, a classic example of adaptive immune resistance.

The epigenetic data revealed something particularly interesting about how this deployment unfolds over time. The LGALS9 promoter underwent progressive demethylation beginning at the low-grade squamous intraepithelial lesion stage, indicating that the gene was being epigenetically primed for expression long before invasive cancer appeared. However, robust transcriptional induction of LGALS9 only became prominent at the high-grade lesion stage, coinciding with activation of interferon-gamma response programs. This temporal separation between demethylation and transcriptional activation suggests a two-step mechanism: early epigenetic poising followed by inflammatory triggering. The researchers found a remarkably tight correlation between interferon-gamma activity and LGALS9 expression at the sample level, with a Pearson correlation coefficient of 0.95, indicating that the very immune cells infiltrating the lesion may be inducing the ligand that ultimately silences them.

Beyond galectin-9, trajectory analysis of the single-cell data delineated the evolution of CD8-positive T cells across disease stages and identified TFCP2 as a transcriptional regulator whose activity is associated with patient prognosis. The study also documented enrichment of LAMP3-positive mature dendritic cells in tumor tissues compared with normal controls. These dendritic cells, which emerge along a maturation trajectory from conventional cDC1 and cDC2 subsets, carried a mixture of costimulatory molecules such as CD40 and CD80 and inhibitory checkpoint molecules including CD274, IDO1, and LGALS9 itself, suggesting that even the antigen-presenting arm of the immune response becomes entangled in the checkpoint machinery as cancer develops.

Multiplex immunohistochemistry provided protein-level confirmation of the story told by the sequencing data. Staining for exhausted CD8-positive T cells, marked by the co-expression of CD3, CD8, and Tim-3, alongside staining for the epithelial marker pan-cytokeratin and galectin-9, showed that galectin-9-positive epithelial cells increase in abundance as tissue progresses from normal cervix through LSIL and HSIL to cancer. The physical co-localization of Tim-3-expressing exhausted T cells with galectin-9-expressing epithelium within the same tissue sections strengthens the argument that this ligand-receptor pair represents a functional axis of immune evasion operating during precancerous progression, not merely a correlate of advanced disease.

Perhaps the most translational portion of the work came from animal experiments. The researchers established an ectopic subcutaneous syngeneic cervical cancer model in immunocompetent mice, an experimental system in which the immune system is fully intact and therefore capable of mounting genuine antitumor responses. Blocking galectin-9 in this model reduced tumor burden, demonstrating that the protein is not simply a passive biomarker but an active contributor to tumor growth. More strikingly, combining galectin-9 blockade with an agonist antibody against GITR, a costimulatory receptor on T cells, significantly enhanced the clonal expansion and cytotoxic activity of CD8-positive T cells. This combination strategy suggests that releasing one brake on the immune system while simultaneously pressing the accelerator may produce therapeutic effects greater than either intervention alone.

The findings arrive at a moment when immune checkpoint blockade has transformed the treatment of many cancers but has delivered comparatively modest results in cervical cancer. Understanding which checkpoint pathways are active at which stages of disease could allow clinicians to intervene earlier and more precisely. The observation that LGALS9 epigenetic poising begins at the LSIL stage is particularly provocative, since low-grade lesions are common, usually regress spontaneously, and are typically managed conservatively. If reliable markers of galectin-9 activation could be incorporated into screening algorithms, they might help distinguish the minority of low-grade lesions destined for progression from those that will resolve, sparing unnecessary procedures while directing attention to lesions that truly warrant close surveillance.

The study also illustrates the growing power of integrated multi-omics approaches in cancer biology. No single technology used here could have revealed the full sequence of events. Single-cell transcriptomics exposed the cellular composition and signaling programs of each lesion stage, but only DNA methylation profiling revealed that LGALS9 had been epigenetically prepared in advance of its expression, and only spatial transcriptomics could verify that the relevant cell populations occupy adjacent territories within intact tissue. Copy number variation inference, pseudotime trajectory modeling, and regulon analysis with tools such as pySCENIC and Monocle2 added further resolution, while methylation-based deconvolution using EpiSCORE extended the key NK/T cell infiltration trend across a larger cohort of twenty-one bulk tissue samples.

Caveats remain, as they do in any early-stage translational study. The human cohort comprised ten deeply profiled samples, and the syngeneic mouse model, while immunocompetent, does not fully recapitulate HPV-driven human cervical carcinogenesis. Clinical testing of galectin-9 blockade in cervical cancer patients would need to demonstrate safety and efficacy in the neoadjuvant, recurrent, or metastatic settings where immunotherapy is currently deployed. Nevertheless, by pinpointing a checkpoint ligand whose activation is detectable during precancerous progression and whose blockade shows antitumor efficacy in vivo, the study provides both a mechanistic framework for understanding immune evasion in cervical carcinogenesis and a concrete, testable therapeutic hypothesis. For a disease that remains a leading cause of cancer death among women globally, that combination of mechanistic insight and actionable target represents a meaningful step forward.

Subject of Research: Multi-omics analysis of immune evasion during cervical carcinogenesis and galectin-9 as a candidate immunotherapeutic target

Article Title: Multi-omics analysis of cervical carcinogenesis reveals galectin-9 driven immune evasion as a candidate immunotherapeutic target

Article References: Multi-omics analysis of cervical carcinogenesis reveals galectin-9 driven immune evasion as a candidate immunotherapeutic target. (n.d.). https://doi.org/10.1186/s12935-026-04458-1

Image Credits: AI Generated

DOI: 10.1186/s12935-026-04458-1

Keywords: cervical cancer, galectin-9, LGALS9, single-cell RNA sequencing, spatial transcriptomics, DNA methylation, CD8-positive T cells, immune evasion, immunotherapy, tumor microenvironment, interferon-gamma, cervical carcinogenesis

Hypoxia, defined as a deficiency in oxygen supply within the tumor microenvironment, is widely recognized as a pivotal factor contributing to tumor malignancy, metastasis, and treatment resistance. Cervical cancer tissues characteristically experience hypoxic stress due to aberrant vasculature and rapid cell proliferation. Despite its known clinical significance, the exact molecular interplay linking hypoxia to cervical cancer progression has remained elusive. The current study spearheaded by Zhang et al. systematically dissects this relationship with a focus on ATXN3 and its interaction with key signaling proteins within cancer cells.

ATXN3 is traditionally known for its involvement in neurodegenerative disorders like Machado-Joseph disease; however, its function in cancer biology has emerged only recently. By meticulously examining cervical cancer cell lines and patient-derived tumor samples under varying oxygen conditions, the researchers demonstrated that ATXN3 expression is markedly upregulated in hypoxic environments. This increased expression was found to modulate distinct downstream signaling cascades contingent on cellular context and oxygen availability, highlighting the multifaceted role of ATXN3 in tumor physiology.

One of the pivotal findings is the observation that ATXN3 enhances the stability of P53—a canonical tumor suppressor protein notorious for its regulation of cell cycle arrest, apoptosis, and DNA repair. Under hypoxic stress, ATXN3 deubiquitinates P53, thereby preventing its proteasomal degradation and leading to its accumulation within cancer cells. Contradictory to traditional views where increased P53 stabilizes and inhibits tumor growth, this study demonstrates a nuanced role whereby hypoxia-associated P53 stabilization driven by ATXN3 paradoxically promotes tumor cell survival, potentially due to altered downstream transcriptional programs induced under low oxygen tension.

Concomitantly, the research sheds light on an alternative pathway wherein ATXN3 modulates the phosphorylation status of STAT5, a transcription factor implicated in cell proliferation and immune evasion. The study found that under hypoxia, ATXN3 enhances STAT5 phosphorylation, activating pro-survival and proliferative gene expression profiles. This hyperactivation of STAT5 signaling contributes directly to the increased invasiveness and metastatic potential observed in cervical cancer models, delineating a dual signaling axis controlled by ATXN3.

Methodologically, the investigators employed a comprehensive suite of biochemical assays, including immunoprecipitation, ubiquitination assays, and phospho-protein analysis, alongside advanced genetic manipulation techniques such as CRISPR-mediated knockout and overexpression systems. These approaches allowed for precise interrogation of the ATXN3-P53 and ATXN3-STAT5 interactions, convincingly establishing a mechanistic framework that underpins hypoxia-driven cervical cancer progression.

Importantly, in vivo studies utilizing xenograft mouse models recapitulated the in vitro findings, corroborating that silencing ATXN3 resulted in significant tumor growth retardation and diminished metastatic spread. These findings provide compelling evidence for the therapeutic potential of targeting ATXN3, or its downstream effectors P53 and STAT5 phosphorylation, in hypoxia-associated cervical malignancies.

The implications of these discoveries extend beyond cervical cancer, as hypoxia and aberrant P53 or STAT5 signaling pathways are ubiquitous features across multiple solid tumors. By decoding the relationship between hypoxia and ATXN3 function, this research paves the way for novel therapeutic interventions designed to exploit this vulnerability. Targeting ATXN3 could disrupt the hypoxia-adaptive responses that facilitate tumor cell survival and aggressiveness, thus potentially enhancing the efficacy of existing therapies.

Moreover, the study raises provocative questions about the intricate dual roles of P53 in cancer biology under stress conditions such as hypoxia. The classical tumor-suppressive role of P53 appears context-dependent, with modifications induced by ATXN3 altering its downstream effects. This mechanistic insight demands further exploration to fully apprehend how the hypoxic microenvironment reprograms tumor suppressor functions to favor oncogenesis.

The research also underscores the importance of post-translational modifications in regulating signaling networks within cancer cells. The enzymatic activity of ATXN3 reverses ubiquitination on key regulatory proteins, revealing a layer of control that is both dynamic and highly influential on cancer cell fate. Future therapeutic strategies might center around modulating such post-translational modifications to restore normal regulatory mechanisms disrupted in cancer.

Clinically, the identification of ATXN3 as a hypoxia-responsive factor with dual roles in stabilizing P53 and activating STAT5 heralds an opportunity for biomarker development. Measuring ATXN3 levels or its enzymatic activity could serve as an indicator of hypoxia-driven tumor aggressiveness, guiding personalized treatment approaches. Additionally, selective inhibitors of ATXN3’s deubiquitinase activity could be developed, offering precision therapeutics aimed at mitigating tumor progression.

Beyond therapeutic utility, these findings contribute fundamentally to the broader understanding of tumor biology, emphasizing the complexity of hypoxia responses and the interconnectedness of signaling pathways. Given the prevalence of hypoxia in solid tumors and its role in treatment resistance, interventions disrupting the hypoxia-ATXN3 axis could synergize with immunotherapy or conventional chemotherapy, overcoming current therapeutic limitations.

The translational potential of this study is vast, but it also highlights the need for continued research into the regulation of ATXN3 expression and activity in diverse cancer contexts. Understanding how tumor cells upregulate ATXN3 in response to hypoxia and identifying potential co-factors or inhibitors will be crucial next steps in advancing from bench to bedside.

In conclusion, the work by Zhang and colleagues represents a significant leap forward in elucidating the molecular underpinnings of hypoxia-driven cervical cancer progression. By delineating the role of ATXN3 in modulating P53 stability and STAT5 phosphorylation, this study not only identifies novel targets for therapeutic intervention but also exposes the dynamic adaptability of cancer cells to hostile microenvironments. As the battle against cancer continues, insights like these will be indispensable in crafting innovative strategies that outmaneuver tumor plasticity and improve patient outcomes.

Subject of Research: Hypoxia-mediated molecular mechanisms driving cervical cancer progression through ATXN3 modulation of P53 stability and STAT5 phosphorylation.

Article Title: Hypoxia promotes progression of cervical cancer by modulating the ATXN3-enhanced P53 stability or STAT5 phosphorylation.

Article References:
Zhang, R., Chai, S., Zhang, F. et al. Hypoxia promotes progression of cervical cancer by modulating the ATXN3-enhanced P53 stability or STAT5 phosphorylation. Cell Death Discov. 12, 4 (2026). https://doi.org/10.1038/s41420-025-02822-0

Image Credits: AI Generated

DOI: 08 January 2026

The investigators meticulously searched six prominent electronic databases to collect relevant original research articles that explored the role of SNHG expression in cervical cancer. Each study was evaluated rigorously using the Newcastle–Ottawa Scale (NOS) to ensure high research quality. Key data points extracted included SNHG expression levels, patient survival outcomes, and clinical pathological features such as tumor-node-metastasis (TNM) stage, tumor size, and lymph node metastasis. These parameters were statistically synthesized through hazard ratios (HRs) and odds ratios (ORs) with corresponding 95% confidence intervals (CIs) to ascertain the association between SNHG expression and clinical outcome measures.

A striking finding from the pooled data was that higher SNHG expression nearly doubled the risk of poor overall survival (OS) in cervical cancer patients, as indicated by a combined HR of 2.046 with a robust 95% confidence interval ranging from 1.402 to 2.691. This statistically significant association firmly positions SNHGs as promising prognostic biomarkers. Given the intricate biology of lncRNAs and SNHGs, their upregulation might underpin mechanisms that favor aggressive tumor behavior, contribute to immune evasion, or foster resistance to standard therapies.

Notably, the meta-analysis further demonstrated that elevated SNHG expression correlates strongly with more advanced disease states. Specifically, higher SNHG levels were associated with advanced TNM stages (OR: 1.476), increased likelihood of lymph node metastasis (OR: 1.614), and larger tumor sizes (OR: 1.299). These findings highlight the role of SNHGs not just as a passive marker but potentially as an active participant in tumor progression pathways. The association with lymph node metastasis is particularly consequential, as this feature frequently signals poorer clinical outcomes and challenges in treatment management.

Interestingly, the study did not find significant associations between SNHG expression and other clinical characteristics such as histological grade, distant metastasis (DM), depth of invasion, or patient age. This suggests a more nuanced role for SNHGs that may be context-dependent or modulated by specific tumor microenvironment factors. The lack of significant correlation with distant metastasis despite the link to lymph node spread hints at potentially distinct molecular mechanisms regulating local versus systemic dissemination in cervical cancer.

One of the key strengths of this investigation lies in its robust methodological approach. The researchers conducted sensitivity analyses to confirm the reliability and stability of their overall survival findings. Additionally, Begg’s test was applied to evaluate publication bias, with results suggesting the absence of significant bias among the included studies. These quality control measures enhance the credibility of the conclusions and underscore the potential translational relevance of SNHGs in clinical oncology.

The molecular underpinnings driving the upregulation of SNHGs in cervical cancer remain an active area of research. Emerging evidence indicates that SNHGs can modulate gene expression and signaling pathways critical to cell proliferation, apoptosis, epithelial-mesenchymal transition (EMT), and angiogenesis. Their involvement in chromatin remodeling and interaction with microRNAs further underscores their multifaceted roles in malignancy. As non-coding RNAs, SNHGs do not code for proteins but influence cellular behavior through diverse mechanisms including RNA scaffolding and molecular sponging.

From a clinical perspective, the identification of SNHGs as prognostic biomarkers offers promising avenues for personalized medicine. In the era of precision oncology, molecular markers that enhance risk stratification can inform treatment decisions and follow-up strategies. For instance, patients exhibiting high SNHG expression might benefit from more aggressive therapeutic regimens or enrollment in clinical trials exploring SNHG-targeted interventions. Moreover, SNHGs themselves might constitute viable therapeutic targets. Antisense oligonucleotides or small molecule inhibitors designed to suppress SNHG expression or function could disrupt malignant processes and improve outcomes.

The translational potential of these findings extends to diagnostic development as well. SNHG levels could be measured from tumor biopsies or potentially from circulating tumor cells or extracellular vesicles in blood, enabling minimally invasive prognostic assessments. Advances in liquid biopsy technologies might therefore facilitate dynamic monitoring of SNHGs during disease progression or treatment response.

Cervical cancer’s burden remains disproportionately high in low- and middle-income countries where access to advanced screening and treatment options is limited. Thus, understanding molecular biomarkers such as SNHGs could contribute to global cancer control strategies. Biomarker-driven risk stratification might optimize resource allocation and tailor interventions in underserved populations, ultimately improving survival rates.

Despite these compelling insights, the authors acknowledge several limitations inherent to meta-analyses. Variability among included studies in terms of patient populations, SNHG expression detection methods, and follow-up durations could influence pooled estimates. Standardization of SNHG measurement techniques and prospective validation in large, multi-center cohorts are essential next steps to translate these findings into clinical practice reliably.

Furthermore, mechanistic studies are warranted to dissect the specific biological pathways through which SNHGs contribute to cervical tumor initiation and progression. Such research could reveal novel nodes for therapeutic intervention and deepen our understanding of cervical carcinogenesis. Integration with other molecular markers and clinical parameters may also yield composite prognostic models with superior predictive power.

In conclusion, this exhaustive meta-analysis shines a spotlight on the pivotal role of small nucleolar RNA host genes in cervical cancer prognosis. By linking elevated SNHG expression to poorer overall survival and more aggressive disease characteristics, it establishes SNHGs as both valuable prognostic markers and potential therapeutic targets. As the molecular landscape of cervical cancer continues to unfold, SNHG-focused research promises to enhance prognostication, guide individualized therapies, and ultimately improve patient outcomes on a global scale.

Continued research efforts marrying molecular biology, bioinformatics, and clinical oncology are critical to unlocking the full potential of SNHGs in the fight against cervical cancer. This evolving narrative adds a vital chapter in our understanding of long non-coding RNAs and their emerging importance in human malignancies, signaling a future where SNHGs may become central to cervical cancer management and therapy.

Subject of Research: The prognostic significance and clinical correlations of small nucleolar RNA host genes (SNHGs) expression in cervical cancer.

Article Title: High SNHG expression may contribute to poor cervical cancer prognosis, based on systematic reviews and meta-analyses.

Article References:
Zhang, Z., Wu, H., Huang, Y. et al. High SNHG expression may contribute to poor cervical cancer prognosis, based on systematic reviews and meta-analyses. BMC Cancer 25, 1350 (2025). https://doi.org/10.1186/s12885-025-14497-y

Image Credits: Scienmag.com

DOI: https://doi.org/10.1186/s12885-025-14497-y

Cervical cancer remains a leading cause of mortality among women globally, particularly in China, where incidence and death rates from this malignancy eclipse those of other female reproductive tract cancers. Despite advances in screening and vaccination, cervical cancer continues to present daunting challenges, partly due to its molecular heterogeneity and capacity for aggressive progression. Against this backdrop, the identification of novel molecular regulators such as SNHG15 and miR-200a-3p is of profound clinical importance.

The investigators began their research by evaluating expression patterns of SNHG15 in various cell lines, including human cervical immortalized squamous cells (Ect1/E6E7) and multiple cervical cancer cell lines such as SiHa, HeLa, Caski, and C-33 A. Using quantitative reverse transcription PCR (qRT-PCR), they observed that SNHG15 expression was markedly elevated in the cancerous lines compared to the immortalized normal control cells. Among these, HeLa and SiHa cells exhibited the most significant overexpression, making them prime models for subsequent functional experiments.

By manipulating SNHG15 expression levels in HeLa and SiHa cells, the researchers observed compelling changes in cellular behavior. Silencing SNHG15 via short hairpin RNA (shRNA) led to a reduction in proliferation, migration, and invasion capabilities, while overexpressing SNHG15 had the opposite effect, enhancing these malignant phenotypes. These findings strongly suggest that SNHG15 acts as an oncogenic driver within cervical cancer cells.

Given the emerging role of microRNAs (miRNAs) as critical post-transcriptional regulators in cancer, the research team investigated whether SNHG15 interacts with miRNAs to exert its effects. miR-200a-3p, a miRNA previously implicated in tumor suppression and modulation of epithelial-to-mesenchymal transition, was found to be inversely correlated with SNHG15 expression in cervical cancer cells. Dual luciferase reporter assays demonstrated direct binding between SNHG15 and miR-200a-3p, identifying a regulatory axis where SNHG15 acts as a competing endogenous RNA (ceRNA), sequestering miR-200a-3p and thereby modulating its downstream targets.

This SNHG15-miR-200a-3p interaction has significant implications for cervical cancer biology. By sponging miR-200a-3p, SNHG15 effectively releases the brakes on pathways that foster tumor cell proliferation and metastatic potential. Conversely, downregulation of miR-200a-3p directly enhanced malignant traits similar to those triggered by SNHG15 overexpression, confirming the axis as a pivotal modulator of tumor aggressiveness.

Cellular assays including the CCK8 proliferation test, as well as migration and invasion assays, corroborated these molecular findings with functional evidence. Cells with high SNHG15 and low miR-200a-3p levels exhibited robust growth and invasiveness, key features that contribute to cervical cancer progression and poor clinical outcomes. These in vitro results provide a compelling rationale to explore this RNA axis as a therapeutic target.

At the mechanistic level, the study adds to the growing body of literature positioning long non-coding RNAs as master regulators in cancer through their ability to modulate microRNA activity. SNHG15 appears to fit this paradigm, serving not only as a molecular sponge but potentially influencing epigenetic and signaling networks that drive oncogenesis. The intricate balance between oncogenic lncRNAs and tumor suppressive miRNAs thus emerges as a crucial battlefield in cancer biology.

The demonstrated capacity of SNHG15 to influence apoptosis was also touched upon in the research, though detailed mechanistic pathways remain to be fully elucidated. The modulation of apoptotic pathways by non-coding RNAs often involves cross-talk with key signaling hubs like p53, Bcl-2 family members, and caspases, and future studies will be pivotal in mapping these interactions in the context of SNHG15 and miR-200a-3p.

This study’s retrospective trial registration underscores the clinical relevance and timely nature of the research. The findings pave the way for translational approaches that could harness SNHG15 or miR-200a-3p modulation to impair cervical cancer growth and dissemination, offering hope for improved patient outcomes.

Indeed, targeting lncRNAs therapeutically has emerged as a promising frontier, albeit one with significant delivery and specificity challenges. The identification of SNHG15 as a nodal player opens potential strategies, including antisense oligonucleotides or small molecules designed to disrupt its interaction with miR-200a-3p or associated protein complexes.

Moreover, miR-200a-3p restoration represents an alternative therapeutic axis. Given its tumor suppressor role, strategies to elevate its expression or mimic its activity could counteract the oncogenic effects of SNHG15 overexpression. Such microRNA-based therapies have shown promise in preclinical models and some clinical trials across diverse cancer types.

The implications of this study extend beyond cervical cancer, as SNHG15 and miR-200a-3p have been implicated in other malignancies. The elucidation of their interplay may thus have broader relevance, potentially informing pan-cancer molecular targeting strategies.

In conclusion, this research not only highlights the pivotal role of the SNHG15-miR-200a-3p axis in cervical cancer cell malignancy but also contributes to the expanding understanding of non-coding RNA regulatory networks in cancer. As precision medicine advances, such molecular insights are essential for developing next-generation diagnostics and therapeutics tailored to disrupt cancer’s complex molecular circuitry.

Future work is needed to delineate the downstream gene targets modulated by the SNHG15-miR-200a-3p axis, to uncover the full spectrum of signaling pathways implicated. Additionally, in vivo studies and clinical validations will be critical to confirm the translational potential of these findings.

The evolving landscape of cervical cancer research thus welcomes SNHG15 as a novel and influential player. It reinforces the concept that targeting RNA molecules—once considered “junk”—is a powerful approach to alter cancer trajectories and improve survival outcomes.

As the field moves forward, integrating such molecular insights with existing treatment paradigms, including immunotherapy and chemotherapy, may offer synergistic benefits and personalized therapeutic options for patients battling cervical cancer worldwide.

Subject of Research: Molecular mechanisms underlying cervical cancer progression focusing on LncRNA SNHG15 and microRNA miR-200a-3p interaction.

Article Title: LncRNA SNHG15 targets miR-200a-3p affects the proliferation, apoptosis, migration, and invasion of cervical cancer cells.

Article References:
Han, S., Qin, Y., He, Y. et al. LncRNA SNHG15 targets miR-200a-3p affects the proliferation, apoptosis, migration, and invasion of cervical cancer cells. BMC Cancer 25, 1279 (2025). https://doi.org/10.1186/s12885-025-14600-3

Image Credits: Scienmag.com

DOI: https://doi.org/10.1186/s12885-025-14600-3