Abstract
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.
Highlights
Colorectal cancer (CRC) is the third most common malignancy and the third leading cause in cancerinduced deaths in the United States with an estimated 135,430 new cases and 50,260 deaths in 2017 [1, 2]
We firstly demonstrated that BRAF-activated noncoding RNA (BANCR) and chromosomal segregation 1-like (CSE1L) expressions were both up-regulated in CRC tumor tissues, and CSE1L expression was positively associated with BANCR expression and clinicopathological factors of CRC
CSE1L expression was positively associated with BANCR expression in 32 cases of CRC tumor tissues (Fig. 1C)
Summary
Colorectal cancer (CRC) is the third most common malignancy and the third leading cause in cancerinduced deaths in the United States with an estimated 135,430 new cases and 50,260 deaths in 2017 [1, 2]. Both genetic and environmental changes have been considered to be involved in the etiology of CRC [3]. BRAF-activated noncoding RNA (BANCR), a 693 bp lncRNA located on chromosome 9, has been identified as an oncogene or a tumor suppressor in a variety of human malignancies, such as lung cancer, gastric cancer, colorectal cancer, thyroid cancer, melanoma, hepatocellular carcinoma and osteosarcoma [7]. In the present study, we aimed to further investtigate the roles and molecular basis of BANCR in CRC progression
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