Research Paper Volume 10, Issue 8 pp 2062—2078
LncRNA BANCR promotes tumorigenesis and enhances adriamycin resistance in colorectal cancer
- 1 Department of Colorectal Surgery, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, Shenyang 110042, China
- 2 Department of Orthopedics, The Affiliated Hospital of Liaoning University of Traditional Chinese Medicine, Shenyang 110032, China
- 3 Department of Colorectal Surgery, Harbin Medical University Cancer Hospital, Harbin 150081, China
received: May 25, 2018 ; accepted: August 13, 2018 ; published: August 22, 2018 ;https://doi.org/10.18632/aging.101530
How to Cite
Copyright: Ma et al. This is an open‐access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Colorectal cancer (CRC) is the third most common malignancy in the United States. Chemotherapeutic resistance is a massive obstacle for cancer treatment. The roles and molecular basis of long non-coding RNA BRAF-activated noncoding RNA (BANCR) in CRC progression and adriamycin (ADR) resistance have not been extensively identified. In this study, we found that BANCR and CSE1L expressions were upregulated in CRC tumor tissues. Meanwhile, CSE1L expression was correlated with depth of CRC. BANCR silencing suppressed cell proliferation and invasion capacity, increased apoptotic rate and potentiated cell sensitivity to ADR. CSE1L downregulation triggered a reduction of cell proliferation and invasion ability, and an increase of apoptosis rate and cell sensitivity to ADR. CSE1L overexpression attenuated si-BANCR-mediated anti-proliferation, anti-invasion and pro-apoptosis effects in CRC cells. BANCR acted as a molecular sponge of miR-203 to sequester miR-203 away from CSE1L in CRC cells, resulting in the upregulation of CSE1L expression. CSE1L knockdown inhibited expressions of DNA-repair-related proteins (53BP1 and FEN1) in HCT116 cells. BANCR knockdown also inhibited tumor growth and enhanced ADR sensitivity in CRC mice model. In conclusion, BANCR knockdown suppressed CRC progression and strengthened chemosensitization of CRC cells to ADR possibly by regulating miR-203/CSE1L axis, indicating that BANCR might be a promising target for CRC treatment.
CRC: colorectal cancer; ADR: adriamycin; CSE1L: chromosomal segregation 1-like; lncRNAs: long non-coding RNAs; CAS: cellular apoptosis susceptibility; FBS: fetal bovine serum; NC: nitrocellulose; FEN1: flap endonuclease 1.