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Down‐regulation of LncRNA CCAT1 enhances radiosensitivity via regulating miR‐148b in breast cancer
Author(s) -
Lai Yong,
Chen Yang,
Lin Yuanhong,
Ye Ling
Publication year - 2018
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.10890
Subject(s) - radiosensitivity , radioresistance , breast cancer , gene knockdown , cancer research , cancer , microrna , oncology , biomarker , medicine , biology , chemistry , apoptosis , radiation therapy , gene , biochemistry
LncRNA colon‐cancer‐associated transcript‐1 (CCAT1) was proved to be a potential prognostic biomarker for breast cancer progression. However, the role of CCAT1 in regulating radiosensitivity of breast cancer and its underlying mechanism have not been investigated. The present study showed that CCAT1 was up‐regulated and miR‐148b was down‐regulated in radioresistant breast cancer tissues compared with radiosensitive breast cancer tissues. Radiation treatment triggered a significant increase in CCAT1 and an obvious decrease in miR‐148b. CCAT1 down‐regulation reduced colony formation rates and caspase3 activity in breast cancer cells under irradiation. Moreover, CCAT1 could negatively regulate miR‐148b expression. Furthermore, overexpression of miR‐148b suppressed colony survival fraction and caspase3 expression under irradiation in breast cancer cells, which was exacerbated by CCAT1 knockdown. Taken together, this study demonstrated that CCAT1 down‐regulation improved radiosensitivity of breast cancer cells via negatively regulating miR‐148b expression, providing a crucial clue for lncRNA‐miRNA interaction in the mechanism of radiosensitivity of breast cancer.