A small RNA fragment called tRF-Gln-CTG-7 is elevated in patients with acute myeloid leukemia (AML), and high levels of it are linked to shorter overall survival, according to a study published in Clinical and Experimental Medicine. The work, conducted by researchers including Liyun Yang and Guifang Ouyang, suggests that this molecule helps leukemia cells grow and survive by suppressing a gene known as AGGF1, and points to it as a possible prognostic marker and therapeutic target.
Acute myeloid leukemia is the most common acute leukemia in adults and is marked by substantial biological heterogeneity and an unfavorable prognosis. The study focused on tRNA-derived small RNAs, or tsRNAs, short fragments produced from transfer RNA molecules that have been implicated in tumor progression but remain poorly understood in AML. To identify candidates, the team used a tsRNA microarray to screen for differential expression between AML patients and healthy controls, and tRF-Gln-CTG-7 emerged for further investigation.
The researchers found that tRF-Gln-CTG-7 was consistently elevated in AML patients compared with healthy controls. Statistical analysis showed that high expression of the fragment was closely associated with shorter overall survival, supporting its potential value as a prognostic biomarker for the disease.
To test what the fragment does functionally, the team inhibited tRF-Gln-CTG-7 in two AML cell lines, OCI-AML2 and MOLM-13. Using a CCK-8 assay to measure cell growth and Western blotting to track protein changes, they observed that suppressing the fragment slowed AML cell growth and induced apoptosis, the programmed cell death process that cancer cells often evade.
The molecular mechanism was then explored with RNA sequencing, luciferase reporter assays and rescue experiments. These analyses indicated that tRF-Gln-CTG-7 inhibition increased both AGGF1 mRNA and protein levels, and that the fragment acts through an AGO2-associated mechanism targeting the 3′ untranslated region of the AGGF1 transcript, effectively suppressing the gene’s expression.
The rescue experiments provided the strongest functional link: when the researchers knocked down AGGF1, this reversed the growth arrest and apoptosis that tRF-Gln-CTG-7 inhibition had caused. In other words, AGGF1 appears to be the key mediator through which the RNA fragment promotes leukemia cell survival, since removing AGGF1’s protection restored the malignant cells’ growth even without the fragment.
The authors conclude that tRF-Gln-CTG-7 promotes AML cell growth by suppressing AGGF1, and that the fragment may represent a potential prognostic biomarker and therapeutic target for AML. Because the findings come from patient expression comparisons and cell-line experiments, they establish an association and a mechanistic model rather than demonstrating clinical benefit; validating the fragment’s utility in patients would require further studies.
The article was published open access on 17 October 2026 and is currently shared as an early, peer-reviewed accepted version carrying a permanent DOI, subject to further edits before the final version of record. Within the study’s scope, the results add tRNA-derived fragments to the growing list of small regulatory RNAs under investigation in leukemia biology and offer a concrete molecular axis, tRF-Gln-CTG-7 acting through AGO2 on AGGF1, that could guide future work on AML prognosis and treatment development.
Subject of Research: A tRNA-derived small RNA fragment, tRF-Gln-CTG-7, promotes acute myeloid leukemia cell growth and survival by suppressing AGGF1 and is associated with poor prognosis.
Article Title: tRF-Gln-CTG-7 promotes AML cell growth and survival through AGGF1 and is associated with poor prognosis
Article References: Yang, L., Shui, H., He, X., Yong, L., Wang, T., Chen, Y., Zou, D., Shi, C., Li, T., Mu, Q., & Ouyang, G. (2026). tRF-Gln-CTG-7 promotes AML cell growth and survival through AGGF1 and is associated with poor prognosis. Clinical and Experimental Medicine. https://doi.org/10.1007/s10238-026-02357-3
Image Credits: AI Generated
DOI: 10.1007/s10238-026-02357-3
Keywords: acute myeloid leukemia, tRF-Gln-CTG-7, tsRNAs, AGGF1, AGO2, apoptosis, prognosis, biomarker, RNA biology, cell growth, promotes, cell
Cite Scienmag News
Nathaniel Bowman. (October 29, 2026). tRF Fragment Drives AML Cell Growth by Suppressing AGGF1, Study Finds. Scienmag. https://scienmag.com/trf-fragment-drives-aml-cell-growth-by-suppressing-aggf1-study-finds/
Nathaniel Bowman. "tRF Fragment Drives AML Cell Growth by Suppressing AGGF1, Study Finds." Scienmag, 29 October 2026, https://scienmag.com/trf-fragment-drives-aml-cell-growth-by-suppressing-aggf1-study-finds/. Accessed 30 October 2026.
Nathaniel Bowman. "tRF Fragment Drives AML Cell Growth by Suppressing AGGF1, Study Finds." Scienmag. October 29, 2026. https://scienmag.com/trf-fragment-drives-aml-cell-growth-by-suppressing-aggf1-study-finds/








