TL;DR
The findings suggest that the effects of MIR100HG on oncogenic signaling are highly dependent on the cellular oxygenation context and that hypoxia reshapes the downstream signaling consequences of MIR100HG expression in HCC cells.
The molecular mechanism by which FAM117B promotes HCC progression via forming a bidirectional regulatory loop with NAT10 and activating the JAK-STAT3 signaling pathway through acetylation modification is revealed, providing a novel potential target and theoretical basis for targeted therapy of HCC.
A comprehensive pan-cancer transcriptomic analysis together with functional assays reveal that miR-210-3p not only mediates classical hypoxic responses but also amplifies mitotic gene expression through activation of FOXM1, positioning miR-210-3p as a molecular integrator linking pseudohypoxia to mitotic dysregulation.
The dual intracellular and extracellular functions of miR-142-3p in cancer are summarized and its contribution to treatment sensitivity and TME interactions is highlighted.
The long noncoding RNA H19 has been widely attested as a promoter of breast cancer by favoring proliferation, migration, invasion, and tumor growth. In this study, we attempted to decipher molecular mechanisms underlying oncogenic activities of H19. Transcriptomic analyses revealed that H19 overexpression correlates wi...
Hepatocellular carcinoma (HCC) remains one of the most prevalent and lethal malignancies worldwide, characterized by limited treatment options and a poor prognosis. Emerging evidence underscores the central role of metabolic reprogramming in HCC development, with microRNAs (miRNAs) recognized as key modulators. However...
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