Current and potential roles of RNA modification-mediated autophagy dysregulation in cancer.

Autophagy, a cellular lysosomal degradation and survival pathway, supports nutrient recycling and adaptation to metabolic stress and participates in various stages of tumor development, including tumorigenesis, metastasis, and malignant state maintenance. Among the various factors contributing to the dysregulation of autophagy in cancer, RNA modification can regulate autophagy by directly affecting the expression of core autophagy proteins. We propose that autophagy disorder mediated by RNA modification is an important mechanism for cancer development.

L3MBTL2-mediated CGA transcriptional suppression promotes pancreatic cancer progression through modulating autophagy.

L3MBTL2 is a crucial component of ncPRC1.6 and has been implicated in transcriptional repression and chromatin compaction. However, the repression mechanism of L3MBTL2 and its biological functions are largely undefined.

TSPAN1-elevated FAM110A promotes pancreatic cancer progression by transcriptionally regulating HIST1H2BK.

FAM110A belongs to the FAM110 family, which mainly functions in biological processes associated with the cell cycle. However, the biological functions in which FAM110A participates are largely undefined. In particular, its potential role in cancer remains unknown.

WBSCR22 and TRMT112 synergistically suppress cell proliferation, invasion and tumorigenesis in pancreatic cancer via transcriptional regulation of ISG15.

Pancreatic cancer (PC) is one of the most aggressive and devastating types of cancer owing to its poor prognosis and deadly characteristics. It is well established that aberrations in the expression of key regulatory genes, namely tumor suppressors and oncogenes, predispose patients to progression and metastasis of PC. Upregulation of Williams‑Beuren syndrome chromosomal region 22 (WBSCR22) expression, a ribosomal biogenesis factor, has been reported in multiple types of human cancer.

Ribosome 18S mA methyltransferase METTL5 promotes pancreatic cancer progression by modulating c‑Myc translation.

Methyltransferase N6‑adenosine (METTL5) is a methyltransferase that specifically catalyzes 18S rRNA N6 methylation at adenosine 1832 (mA), which is located in a critical position in the decoding center, therefore suggesting its potential importance in the regulation of translation. However, the underlying mechanism of METTL5‑mediated translation regulation of specific genes and its biological functions are largely undefined. To the best of our knowledge, the present study demonstrated for the first time that METTL5 was an oncogene that promoted cell proliferation, migration, invasion and tumorigenesis in pancreatic cancer.

tRNA modifications and their potential roles in pancreatic cancer.

Since the breakthrough discovery of N6-methyladenosine (mA), the field of RNA epitranscriptomics has attracted increasing interest in the biological sciences. Transfer RNAs (tRNAs) are extensively modified, and various modifications play a crucial role in the formation and stability of tRNA, which is universally required for accurate and efficient functioning of tRNA. Abnormal tRNA modification can lead to tRNA degradation or specific cleavage of tRNA into fragmented derivatives, thus affecting the translation process and frequently accompanying a variety of human diseases.