Nestin expression involves invasiveness of esophageal carcinoma and its downregulation enhances paclitaxel sensitivity to esophageal carcinoma cell apoptosis
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Jinghang Zhang1,*, Jiateng Zhong1,*, Jian Yu1, Jinsong Li1, Wenyu Di1, Ping Lu1, Xiaoyu Yang1, Weixing Zhao1, Xianwei Wang2 and Wei Su1
1Department of Pathology, The First Affiliated Hospital of Xinxiang Medical University, Xinxiang 453003, P.R. China
2Henan Key Laboratory of Medical Tissue Regeneration, Xinxiang Medical University, Xinxiang 453003, P.R. China
*These authors have contributed equally to this work
Xianwei Wang, email: firstname.lastname@example.org
Wei Su, email: email@example.com
Keywords: nestin, paclitaxel, apoptosis, metastasis, esophageal carcinoma
Received: December 12, 2016 Accepted: April 25, 2017 Published: May 10, 2017
Paclitaxel has been generally used to treat primary and metastatic esophageal carcinoma. It has been shown that nestin is highly expressed in esophageal carcinoma and that there is a strong association of nestin expression with poor prognosis in esophageal carcinoma patients. In this study, using immunohistochemistry, in situ hybridization and Western blotting we demonstrated that nestin was overexpressed in the invasive esophageal carcinoma. To further elucidate whether nestin inhibition could enhance paclitaxel sensitivity to esophageal carcinoma cells, we applied nestin siRNA in esophageal squamous cell carcinoma Eca-109 cells. Flow cytometry and TUNEL staining both showed that combination of paclitaxel treatment and nestin knockdown resulted in greater induction of apoptosis of esophageal carcinoma cells as compared with the cells transfected with control siRNA (also treated with paclitaxel). This study indicates that nestin knockdown enhances chemotherapeutic sensitivity of paclitaxel to esophageal carcinoma, and suggests that silencing of nestin could be a valuble therapeutic approach for enhancing drug sensitivity and thereby improving the treatment outcome of esophageal carcinoma patients.
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