Overexpression of Cathepsin L is associated with chemoresistance and invasion of epithelial ovarian cancer
Metrics: PDF 1482 views | HTML 1817 views | ?
Hongying Sui1, Caixia Shi1, Zhipeng Yan1, Mei Wu1
1Department of Gynecological Oncology, Hunan cancer hospital, The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Hunan, China
Hongying Sui, email: email@example.com
Keywords: ovarian cancer, CTSL, chemoresistance, SKOV3/TAX cells, proliferation
Received: March 08, 2016 Accepted: June 03, 2016 Published: June 24, 2016
Paclitaxel is recommended as a first-line chemotherapeutic agent against, ovarian cancer, however, the development of chemoresistance is a major obstacle in patients with aggressive ovarian cancer and results in recurrence after conventional therapy. The key molecule or mechanism associated with paclitaxel resistance in ovarian cancer still remains unclear. Cathepsin L (CTSL) is overexpressed in various cancers, however, the association between CTSL expression and paclitaxel resistance remains unclear. In the present study, we investigated the role of CTSL in paclitaxel-resistant SKOV3/TAX cells by CTSL silencing. Expression of CTSL was examined by immunohistochemistry and qRT-PCR in 58 clinical samples, and in SKOV3 cells and SKOV3/TAX cells. Effects of CTSL knockdown on ovarian cancer cell proliferation, apoptosis, migration, and invasion were also studied. The IHC and real-time PCR results showed that the difference of CTSL expression between ovarian cancer and the adjacent non-tumourous ovarian tissues was statistically significant. Western blot analysis showed that the CTSL was overexpressed in SKOV3/TAX cells and weakly detectable in paclitaxel-sensitive SKOV3 cells. Knocking-down of CTSL in ovarian cancer cells could decrease cell proliferation, migration, and invasion, and potentiate apoptosis induced by paclitaxel, suggesting CTSL may contribute to Paclitaxel resistance in ovarian cancer.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.