NCAPH promotes glucose metabolism reprogramming and cell stemness in ovarian cancer cells through the MEK/ERK/PD-L1 pathway

Abstract Backgrounds: Ovarian cancer is a prevalent malignant tumors affecting the female reproductive organs with the characteristic of high heterogeneity. Non-structural maintenance of chromosomes condensin I complex subunit H (NCAPH) has been implicated in a variety of cancers. Methods The expression of NCAPH before or after transfection was detected using RT-qPCR and western blot. Cell stemness was assessed with spheroid formation assay. The extracellular acidification rate (ECAR) of ovarian cancer cells was appraised utilizing Seahorse Glycolysis Stress Test Assay while oxygen consumption rate (OCR) was estimated with Seahorse Mito Stress Test Assay. Lactate production and glucose consumption were evaluated with corresponding assay kits. Western blot was adopted to evaluate the contents of stem cell markers, glycolysis- and MEK/ERK/PD-L1 signaling pathway-related proteins. In vivo, the tumor size and weight were measured and KI67 expression in tumor tissues of nude mice was appraised utilizing immunohistochemical staining. Results It was found that NCAPH expression was upregulated in ovarian cancer cells. After silencing NCAPH expression, the stemness and glucose metabolism reprogramming were repressed. The MEK/ERK/PD-L1 signaling pathway was inhibited by NCAPH knockdown both in vitro and in vivo. NCAPH depletion was also discovered to suppress tumor growth in mice. Conclusion Collectively, NCAPH silence impeded the malignant progression of OC through the MEK/ERK/PD-L1 pathway.