TMEM132A promotes cervical cancer progression via HOMER3-mediated activation of FAK/PI3K/AKT signaling pathway.

TMEM132A is aberrantly expressed in multiple solid tumors, yet its role and mechanism in cervical cancer (CC) remain unclear. TMEM132A expression was analyzed using TCGA and GEO datasets and validated in CC cell lines and paired clinical tissues via qRT-PCR and Western blotting. Functional assays were systematically performed to evaluate the oncogenic roles of TMEM132A. Downstream pathways were explored through GSEA and co-expression analysis, with mechanistic interactions confirmed via TMEM132A/HOMER3 gain- and loss-of-function rescue experiments. TMEM132A was significantly upregulated in CC tissues and cell lines, correlating with aggressive tumor phenotypes. TMEM132A overexpression enhanced cell proliferation, migration, invasion, and S-phase progression, whereas its knockdown exerted opposite effects. Mechanistically, TMEM132A activated the FAK/PI3K/AKT pathway by positively regulating HOMER3. Silencing HOMER3 effectively abrogated TMEM132A-induced pathway activation and malignant behaviors. This study is the first to demonstrate that TMEM132A promotes CC progression through HOMER3-dependent stimulation of the FAK/PI3K/AKT axis. These findings position TMEM132A as a candidate molecular marker for future clinical evaluation and a potential node for subsequent therapeutic exploration in CC.