MAP7 Mediates Tumorigenicity in Human Ovarian Cancer Cells: A Prospective Laboratory Evaluation of Malignant Tissues

Background: Ovarian cancer (OC) is among the most common types of cancer affecting the female reproductive system, second only to cervical cancer in incidence. Recent studies have identified Microtubule associated protein 7 (MAP7) as a key factor influencing the malignant characteristics of various tumor cell types. However, the expression levels and functional roles of MAP7 in OC remain insufficiently characterized. This study aims to explore the expression profile of MAP7 and its functional implications in OC, with the goal of clarifying its potential contribution to tumor development and the underlying molecular mechanism. Methods: The MAP7 expression in OC was assessed using data from The Cancer Genome Atlas (TCGA), Genotype-Tissue Expression (GTEx), and The Human Protein Atlas (HPA) databases. A tissue microarray assay (TMA) was constructed to evaluate protein expression. Study gene function was investigated through MAP7 silencing and overexpression experiments in A2780 and SKOV3 OC cell lines. Cell proliferation and invasion/migration assays were conducted to assess cellular proliferation and mobility, respectively. Western blotting was performed to analyze related signaling pathways, while tumor formation in nude mice assessed in vivo tumorigenicity. Results: Data from TCGA and GTEx databases showed MAP7 overexpression in OC tissues, consistent with the findings from our local dataset. MAP7 mediated cell invasion, migration, and promoted cell proliferation in OC cells via the Protein Kinase B/mammalian Target of Rapamycin (Akt/mTOR) signaling pathway (p < 0.05). MAP7 knockdown significantly inhibited the tumorigenicity of OC cells in nude mice (p < 0.05). Conclusions: Our results highlight the role of MAP7 in the progression of OC. Given its involvement in Akt/mTOR signaling and tumorigenicity in preclinical models, MAP7 represents a novel potential therapeutic target for OC that warrants further investigation.