Backgrounds: Recent studies have proven the oncogenic role of kinesin family member 20A () in several cancers. Tumor-associated macrophages (TAMs) were reported to participate in tumor initiation and metastasis. In this study, we aimed to explore the detailed mechanism underlying in regulating the progression of ovarian cancer and its involvement with TAMs.

Methods: and phosphatase and tensin homolog () levels were assessed using reverse-transcription quantitative polymerase chain reaction (RT-qPCR) and western blot. Cell Counting Kit-8 (CCK-8) assay, 5-Ethynyl-2'-deoxyuridine (EdU) staining assay, colony formation assay, flow cytometry, and western blot were employed to evaluate cell proliferation, apoptosis, and epithelial-mesenchymal transition (EMT). The relationship between and was validated using a dual-luciferase assay. M2 macrophage polarization was verified by detecting their markers using RT-qPCR. THP-1 cells were co-cultured with ovarian cancer cells to format TAMs.

Results: Ovarian cancer tissues and cells exhibited upregulated and downregulated levels ( < 0.05). Irradiation significantly decreased levels ( < 0.05) and blunted the progression of ovarian cancer by reducing cell proliferation and EMT ( < 0.05) and inducing apoptosis ( < 0.05). These effects were augmented by depletion ( < 0.05). depletion also suppressed ovarian cancer cell progression ( < 0.05). Our findings illustrated that negatively regulated PTEN expression in ovarian cancer cells. Moreover, the inhibitory effects of depletion on ovarian cancer development in irradiated ovarian cancer cells were obviously impeded by knockdown ( < 0.05). Additionally, we observed the increased expression in M2-like TAMs and its ability to induce M2 macrophage polarization ( < 0.05).

Conclusion: was found to induce M2 macrophage polarization in ovarian cancer, and depletion regulated to increase radiosensitivity and inhibit ovarian cancer development.

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http://dx.doi.org/10.24976/Discov.Med.202436191.224DOI Listing

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