Overexpression of CHI3L1 is associated with chemoresistance and poor outcome of epithelial ovarian carcinoma
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Ying-Cheng Chiang1,2, Han-Wei Lin3, Chi-Fang Chang1, Ming-Cheng Chang1, Chi-Feng Fu4, Tsung-Ching Chen1, Shu-Feng Hsieh1, Chi-An Chen1, Wen-Fang Cheng1,2,3
1Department of Obstetrics and Gynecology, College of Medicine, National Taiwan University, Taipei, Taiwan
2Graduate Institute of Clinical Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan
3Graduate Institute of Oncology, College of Medicine, National Taiwan University, Taipei, Taiwan
4Department of Obstetrics and Gynecology, E-da Hospital, Kaohsiung, Taiwan
Chi-An Chen, e-mail: email@example.com
Wen-Fang Cheng, e-mail: firstname.lastname@example.org
Keywords: CHI3L1, apoptosis, epithelial ovarian carcinoma, chemoresistance
Received: April 12, 2015 Accepted: September 25, 2015 Published: October 05, 2015
We propose CHI3L1 as a prognostic biomarker for patients with epithelial ovarian carcinoma (EOC) and also suggest possible biological functions of CHI3L1. We measured CHI3L1 expression with quantitative real time-polymerase chain reaction (qRT-PCR) in 180 women with EOC and evaluated correlations between CHI3L1 expression, clinicopathological characteristics, and the outcomes of the patients. The expression of CHI3L1 was higher in cancerous tissues than in normal tissues. The expression of CHI3L1 was also higher in patients with a serous histological type, advanced stage, and chemoresistance. Patients with high CHI3L1 expression had a shorter progression-free survival (p < 0.001)and overall survival (p < 0.001). Patients with high CHI3L1 expression also had a high risk of recurrence (p < 0.001)and death (p < 0.001). In vitro studies showed that CHI3L1 up-regulated the expression of anti-apoptotic Mcl-1 protein and hampered paclitaxel-induced apoptosis of ovarian cancer cells. These results suggest that CHI3L1 shows potential as a prognostic biomarker for EOC. CHI3L1 may promote chemoresistance via inhibition of drug-induced apoptosis by up-regulating Mcl-1.
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