ArticleMolecular and cellular biochemistry2026
The METTL3/LOXL2 axis participates in aberrant epithelial-fibroblast crosstalk and induces oral submucous fibrosis in rats.
Article in Molecular and cellular biochemistry, 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
Oral submucous fibrosis (OSF) is an oral potentially malignant disorder strongly associated with the areca nut alkaloids. Although lysyl oxidase-like 2 (LOXL2) is implicated in pathological collagen accumulation and fibrosis, its regulatory role in OSF progression remains unclear. Hematoxylin-eosin, Masson and immunofluorescent staining were performed on rat oral mucosal tissues to assess fibrotic and senescent phenotypes. Senescence of human oral keratinocytes (HOKs) was assessed by senescence-associated β-galactosidase staining, flow cytometry and western blotting. LOXL2 N6-methyladenosine (m6A) methylation levels in tissues and cells were then detected, and methyltransferase-like 3 (METTL3)-LOXL2 interactions were validated using RNA immunoprecipitation and photoactivatable ribonucleoside-enhanced cross-linking and immunoprecipitation assays. LOXL2 mRNA stability was further assessed after actinomycin D treatment. In addition, lactate levels were measured to explore epithelial-fibroblast crosstalk between HOKs and human oral mucosal fibroblasts. Arecoline-treated rats exhibited progressive epithelial thinning and collagen deposition in oral mucosal tissues, accompanied by upregulated expression of fibronectin, collagen type I, α-smooth muscle actin, p21, and p16. Arecoline exposure elevated reactive oxygen species levels and promoted co-localization of the senescence markers p16/p21 with the epithelial marker cytokeratin. LOXL2 was upregulated in arecoline-induced senescence models, and LOXL2 silencing suppressed fibroblast activation by inhibiting HOKs senescence. Mechanistically, METTL3 stabilized LOXL2 mRNA through m6A-dependent interactions. Downregulation of the METTL3/LOXL2 axis reduced lactate secretion from senescent HOKs, thereby attenuating fibroblast activation. Similar findings were observed in OSF rats. The METTL3/LOXL2 axis may mediate lactate secretion from senescent epithelial cells and regulate epithelial-fibroblast crosstalk during OSF pathogenesis. This study reveals a potential mechanism and candidate targets for further evaluation in OSF.
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