J Cancer 2018; 9(7):1318-1328. doi:10.7150/jca.20150
Downregulation of BANCR Promotes Aggressiveness in Papillary Thyroid Cancer via the MAPK and PI3K Pathways
1. Department of Thyroid and Breast Surgery, Tongji Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, Hubei 430030, P.R. China
2. Department of Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, P.R. China
Recent evidence indicates that long non-coding RNAs play important roles in tumorigenesis and cancer progression. BRAF-activated non-protein coding RNA (BANCR) is a novel and potential regulator of cancer cell proliferation and migration. However, little is known regarding the role of BANCR in papillary thyroid cancer (PTC). The current study used quantitative PCR to demonstrate that BANCR was significantly downregulated in 60 paired PTC tissues compared with normal tissues. In addition, BANCR was significantly correlated with lymph node metastasis (p = 0.02). Furthermore, Cell Counting Kits and Transwell assays were used to demonstrate that knocking down BANCR with short hairpin RNA (shRNA) transfection significantly promoted the proliferation and invasion of PTC cell lines. The flow cytometric analysis of apoptosis and the cell cycle revealed that the overexpression of BANCR inhibited cancer cell proliferation and invasion, which was associated with the induction of cell-cycle G2/M phase arrest and increased apoptosis. Moreover, western blotting was used to show that the MAPK and PI3K-Akt pathways were aberrantly activated during BANCR-mediated PTC cell proliferation and migration. These findings revealed that BANCR functions as a tumor suppressor during thyroid carcinogenesis.
Keywords: papillary thyroid cancer, BRAF-activated non-protein coding RNA, MAPK signaling pathway, PI3K-Akt signaling pathway, cell cycle, apoptosis
Zhang J, Du Y, Zhang X, Li M, Li X. Downregulation of BANCR Promotes Aggressiveness in Papillary Thyroid Cancer via the MAPK and PI3K Pathways. J Cancer 2018; 9(7):1318-1328. doi:10.7150/jca.20150. Available from http://www.jcancer.org/v09p1318.htm