NCAPD2 facilitates ovarian cancer progression via MYC-mediated unfolded protein response.

Abstract

This study focused on defining the function and mechanism of non-SMC condensin I complex subunit D2 (NCAPD2) in ovarian cancer progression. NCAPD2 expression in ovarian cancer was analyzed using single-cell data and bioinformatic analysis. With the aim of uncovering the mechanistic role of NCAPD2 in ovarian cancer, we performed gene set enrichment analysis pathway enrichment analysis. To investigate NCAPD2 in ovarian cancer, we quantified its expression in cell lines and clinical specimens using western blot, reverse transcription quantitative polymerase chain reaction, and immunohistochemistry. The functional roles of NCAPD2 were evaluated through cell counting kit-8 assay, 5-ethynyl-2'-deoxyuridine assay staining, wound healing assay and Transwell assay. Western blot analysis was conducted for protein detection. In vivo tumor growth was examined using a mouse xenograft model. Ovarian cancer specimens exhibited elevated NCAPD2 expression. In vitro, NCAPD2 knockdown suppressed proliferation, migration, invasion, and expression of MYC, GRP78, IRE1α, and XBP1s; conversely, its overexpression elicited opposite effects. Furthermore, the suppressive effects of NCAPD2 knockdown on cell proliferation, cell invasion, and expression of GRP78, IRE1α, and XBP1s were partially reversed upon MYC upregulation. In vivo, NCAPD2 knockdown attenuated tumorigenicity. NCAPD2 facilitates ovarian cancer progression, which may be partially involved in MYC-mediated unfolded protein response.