ArticleFrontiers in oncology2026
Mechanism of N6-methyladenosine (m6A)-mediated upregulation of LINC00958 in the growth of cervical cancer.
Article in Frontiers in oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Objective: Cervical cancer (CC) remains a prominent contributor to cancer mortality amongst women. Long non-coding RNAs (LncRNAs) participate in CC progression. This study probed into the potential mechanism of LINC00958 in CC growth. Materials and methods: LINC00958 expression in CC tissues and cells was determined. The correlation between LINC00958 expression and CC prognosis was analyzed. LINC00958 expression was interfered in CC cells, followed by assessment of CC cell proliferation and apoptosis. An xenograft tumor model was established in nude mice. METTL3, c-MYC, and BAG3 expression was determined. m6A level was quantitatively analyzed, and the level of m6A-modified LINC00958 was detected. The binding of LINC00958 to c-MYC, as well as the binding of c-MYC to BAG3 were confirmed. Functional rescue experiments were designed to verify the effect of METTL3/BAG3 on CC growth. Results: LINC00958 expression was elevated in CC and correlated with the prognosis and clinicopathological features of CC patients. LINC00958 silencing suppressed CC cell proliferation and facilitated apoptosis Conclusion: METTL3-mediated m6A modification elevated LINC00958 expression. LINC00958 enhanced CC cell proliferation but depressed apoptosis via the c-MYC/BAG3 axis.
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