J Cancer 2016; 7(12):1694-1700. doi:10.7150/jca.15086 This issue

Research Paper

Lentivirus-mediated Knockdown of HDAC1 Uncovers Its Role in Esophageal Cancer Metastasis and Chemosensitivity

Min Song1,3, Gang He1, Yan Wang1, Xueli Pang2, Bo Zhang1✉

1. Department of Medical Genetics, Third Military Medical University
2. Department of oncology, Southwest Hospital, Third Military Medical University
3. Department of neurology, the second Affiliated Hospital of Chongqing Medical University

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Song M, He G, Wang Y, Pang X, Zhang B. Lentivirus-mediated Knockdown of HDAC1 Uncovers Its Role in Esophageal Cancer Metastasis and Chemosensitivity. J Cancer 2016; 7(12):1694-1700. doi:10.7150/jca.15086. Available from https://www.jcancer.org/v07p1694.htm

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Histone deacetylationase 1 (HDAC1) is ubiquitously expressed in various cell lines and tissues and play an important role of regulation gene expression. Overexpression of HDAC1 has been observed in various types of cancers, which indicated that it might be a target for cancer therapy. To test HDAC1 inhibition for cancer treatment, the gene expression of HDAC1 was knockdown mediated by a lentivirus system. Our data showed the gene expression of HDAC1 could be efficiently knockdown by RNAi mediated by lentivirus in esophageal carcinoma EC109 cells. Knockdown of HDAC1 led to significant decrease of cell growth and altered cell cycle distribution. The result of transwell assay showed that the numbers of cells travelled through the micropore membrane was significantly decreased as HDAC1 expression was knockdown. Moreover, HDAC1 knockdown inhibited the migration of EC109 cells as determining by scratch test. Additionally, enhancement of cisplatin-stimulated apoptosis was detected by HDAC1 knockdown. Our data suggested inhibition of HDAC1 expression by lentivirus mediated shRNA might be further applied for esophageal cancer chemotherapy.

Keywords: histone deacetylationase, lentivirus, chemosensitivity, EC109 cells