<p>SPOCD1 accelerates ovarian cancer progression and inhibits cell apoptosis via the PI3K/AKT pathway</p>

Abstract

Background: Ovarian cancer (OC) is the most common type of gynecological malignant tumors with poor prognosis. The spen paralogue and orthologue C-terminal domain containing 1 (SPOCD1) is a newly identified molecule that has been indicated to discriminate progressive in human solid tumors. However, the role of SPOCD1 in OC remains unknown. Methods: The expression of SPOCD1 in OC and non-cancerous tissue was detected by Realtime polymerase chain reaction and immunohistochemical staining. The expression of SPOCD1 in OC cells (SKOV3 and CAOV3) was also detected by immunohistochemical staining. The effect of SPOCD1 on cell proliferation was analyzed by Cell Counting Kit 8 and colony formation assay, and cell migration was analyzed by transwell assay. Apoptosis was analyzed by flow cytometry. The protein expression of SPOCD1, PTEN, PI3K, p-AKT, and mTOR in OC cells was measured by Western blot. Results: SPOCD1 expression was significantly upregulated in OC tissues compared with non-cancerous tissues ( P < 0.01), and was positively correlated to FIGO stage and tumor grade of OC. Also, SPOCD1 was significantly expressed in nucleus and cytoplasm of SKOV3 and CAOV3 cells. Kaplan–Meier analysis indicated that patients with high SPOCD1 expression had shorter overall survival (HR =1.512, 95%CI: 1.321– 2.793, P =0.031) and progression-free survival (HR =1.875, 95%CI: 1.435– 3.157, P =0.028). SPOCD1 was upregulated in OC SKOV3 and CAOV3 cells. Further investigation revealed that downregulation of SPOCD1 inhibited the SKOV3 and CAOV3 cells proliferation and migration. In addition, the deficit of SPOCD1 increased the apoptosis in SKOV3 and CAOV3 cells. PI3K/AKT pathway was inhibited by knockdown of SPOCD1 in SKOV3 and CAOV3 cells. Conclusions: Our data suggest that SPOCD1 may act as a carcinogenesis factor by activating the PI3K/AKT pathway to restrained cell apoptosis in OC. Keywords: ovarian cancer, SPOCD1, proliferation, AKT