Expression patterns of mA RNA methylation regulators under apoptotic conditions in various human cancer cell lines.

BACKGROUND/AIM: Cancer is a complex disease that involves both genetic and epigenetic factors. While emerging evidence clearly suggests that changes in epitranscriptomics play a crucial role in cancer pathogenesis, a comprehensive understanding of the writers, erasers, and readers of epitranscriptomic processes, particularly under apoptotic conditions remains lacking. The aim of this study was to uncover the changes in the expression of mA RNA modifiers under apoptotic conditions across various cancer cell lines.

MATERIALS AND METHODS

Initially, we quantified the abundance of mA RNA modifiers in cervical (HeLa and ME180), breast (MCF7 and MDA-MB-231), lung (A549 and H1299), and colon (Caco-2 and HCT116) cancer cell lines using qPCR. Subsequently, we induced apoptosis using cisplatin and tumor necrosis factor-alpha (TNF-α) to activate intrinsic and extrinsic pathways, respectively, and assessed apoptosis rates via flow cytometry. Further, we examined the transcript abundance of mA RNA modifiers under apoptotic conditions in cervical, breast, and lung cancer cell lines using qPCR.

RESULTS

Overall, treatment with cisplatin increased the abundance of mA modifiers, whereas TNF-α treatment decreased their expression in cervical, breast, and lung cancer cell lines. Specifically, cisplatin-induced apoptosis, but not TNF-α-mediated apoptosis, resulted in decreased abundance of METTL14 and FTO transcripts. Additionally, cisplatin treatment drastically reduced the abundance of IGF2BP2 and IGF2BP3 readers.

CONCLUSION

These results suggest that the differential response of cancer cells to apoptotic inducers may be partially attributed to the expression of mA RNA modifiers.