He-da Zhang1, Da-Wei Sun2, Ling Mao3, Jun Zhang4, Lin-Hong Jiang5, Jian Li6, Ying Wu7, Hao Ji8, Wei Chen8, Jing Wang7, Rong Ma9, Hai-Xia Cao9, Jian-Zhong Wu9, Jin-Hai Tang10. 1. Department of General Surgery, Xuzhou Medical College, Xuzhou, Jiangsu, China; Department of General Surgery, Nanjing Medical University Affiliated Cancer Hospital, Cancer Institute of Jiangsu Province, Nanjing, Jiangsu, China. Electronic address: zhanghedazhd@163.com. 2. Department of General Surgery, Nanjing Medical University Affiliated Cancer Hospital, Cancer Institute of Jiangsu Province, Nanjing, Jiangsu, China; Nanjing University of Chinese Medicine, Nanjing, Jiangsu, China. 3. Department of General Surgery, Huai an Second People's Hospital, Xuzhou Medical College, Huai'an, Jiangsu, China. 4. Anhui University of Chinese Medicine, Anhui, China. 5. Xuzhou Infectious Disease Hospital, Xuzhou, Jiangsu, China. 6. Department of General Surgery, Nanjing Medical University Affiliated Cancer Hospital, Cancer Institute of Jiangsu Province, Nanjing, Jiangsu, China. 7. Nanjing Medical University, Nanjing, Jiangsu, China. 8. Department of General Surgery, Xuzhou Medical College, Xuzhou, Jiangsu, China. 9. Research Center of Clinical Oncology, The Affiliated Jiangsu Cancer Hospital, Nanjing Medical University, Nanjing, Jiangsu, China. 10. Department of General Surgery, Nanjing Medical University Affiliated Cancer Hospital, Cancer Institute of Jiangsu Province, Nanjing, Jiangsu, China. Electronic address: jinhaitang1@hotmail.com.
Abstract
OBJECTIVES: MiRNA-139 is located at 11q13.4 and it has anti-oncogenic and antimetastatic activity in humans. However, its role in controlling apoptosis, invasion and metastasis and the development of chemosensitivity to docetaxel in breast cancer cells are not fully understood. The aim of this study was to research the biological function of miR-139-5p and the efficacy of chemosensitivity to docetaxel. METHODS: MiR-139-5p expression in MCF-7, MCF-7/Doc cells and in selected breast cancer tissue samples was confirmed by real-time PCR; cell viability was analyzed by Cell Counting Kit-8 assay; apoptosis and cell cycle were analyzed by flow cytometry; control of metastasis and invasion of breast cancer cells was measured by transwell assay; expression of Notch1 was measured by western blot; a luciferase reporter vector was constructed to identify the miR-139-5p target gene. RESULTS: MiR-139-5p was significantly down-regulated in breast cancer cells. MiR-139-5p inhibits the viability of breast cancer cells. MiR-139-5p induces apoptosis, causes cell cycle arrest in S phase, inhibits migration and invasion in breast cancer cells, however, MiR-139-5p play the opposite role in docetaxel-induced breast cancer cells. CONCLUSIONS: MiR-139-5p not only attenuated the development of breast cancer cells but also mediated drug-resistance by regulating the expression of the downstream target gene Notch1.
OBJECTIVES: MiRNA-139 is located at 11q13.4 and it has anti-oncogenic and antimetastatic activity in humans. However, its role in controlling apoptosis, invasion and metastasis and the development of chemosensitivity to docetaxel in breast cancer cells are not fully understood. The aim of this study was to research the biological function of miR-139-5p and the efficacy of chemosensitivity to docetaxel. METHODS:MiR-139-5p expression in MCF-7, MCF-7/Doc cells and in selected breast cancer tissue samples was confirmed by real-time PCR; cell viability was analyzed by Cell Counting Kit-8 assay; apoptosis and cell cycle were analyzed by flow cytometry; control of metastasis and invasion of breast cancer cells was measured by transwell assay; expression of Notch1 was measured by western blot; a luciferase reporter vector was constructed to identify the miR-139-5p target gene. RESULTS:MiR-139-5p was significantly down-regulated in breast cancer cells. MiR-139-5p inhibits the viability of breast cancer cells. MiR-139-5p induces apoptosis, causes cell cycle arrest in S phase, inhibits migration and invasion in breast cancer cells, however, MiR-139-5p play the opposite role in docetaxel-induced breast cancer cells. CONCLUSIONS:MiR-139-5p not only attenuated the development of breast cancer cells but also mediated drug-resistance by regulating the expression of the downstream target gene Notch1.
Authors: Marta Geretto; Alessandra Pulliero; Camillo Rosano; Dinara Zhabayeva; Rakhmet Bersimbaev; Alberto Izzotti Journal: Am J Cancer Res Date: 2017-06-01 Impact factor: 6.166