The crosstalk between cellular survival pressures and N6-methyladenosine modification in hepatocellular carcinoma.

Background: Within the tumor microenvironment, survival pressures are prevalent with potent drivers of tumor progression, angiogenesis, and therapeutic resistance. N6-methyladenosine (mA) methylation has been recognized as a critical post-transcriptional mechanism regulating various aspects of mRNA metabolism. Understanding the intricate interplay between survival pressures and mA modification provides new insights into the molecular mechanisms underlying hepatocellular carcinoma (HCC) progression and highlights the potential for targeting the survival pressures-mA axis in HCC diagnosis and treatment.

Data Sources: A literature search was conducted in PubMed, MEDLINE, and Web of Science for relevant articles published up to April 2024. The keywords used for the search included hepatocellular carcinoma, cellular survival, survival pressure, N6-methyladenosine, tumor microenvironment, stress response, and hypoxia.

Results: This review delves into the multifaceted roles of survival pressures and mA RNA methylation in HCC, highlighting how survival pressures modulate the mA landscape, the impact of mA modification on survival pressure-responsive gene expression, and the consequent effects on HCC cell survival, proliferation, metastasis, and resistance to treatment. Furthermore, we explored the therapeutic potential of targeting this crosstalk, proposing strategies that leverage the understanding of survival pressures and mA RNA methylation mechanisms to develop novel, and more effective treatments for HCC.

Conclusions: The interplay between survival pressures and mA RNA methylation emerges as a complex regulatory network that influences HCC pathogenesis and progression.