Downregulation of LINC00958 inhibits proliferation, invasion and migration, and promotes apoptosis of colorectal cancer cells by targeting miR‑3619‑5p

Sun,Ye; Liu,Yi; Cai,Yun; Han,Pingping; Wang,Rui; Cao,Lijun; He,Shuixiang

doi:10.3892/or.2020.7707

Downregulation of LINC00958 inhibits proliferation, invasion and migration, and promotes apoptosis of colorectal cancer cells by targeting miR‑3619‑5p

Authors:
- Ye Sun
- Yi Liu
- Yun Cai
- Pingping Han
- Rui Wang
- Lijun Cao
- Shuixiang He
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Affiliations: Department of Traditional Chinese Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, P.R. China, Department of Gastroenterology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, P.R. China
Published online on: July 29, 2020 https://doi.org/10.3892/or.2020.7707
Pages: 1574-1582
Copyright: © Sun et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

The aberrant expression of long non‑coding RNAs (lncRNAs), including LINC00958, has been demonstrated in several types cancers. The present study aimed to investigate the role of LINC00958 in colorectal cancer (CRC) and identify the possible underlying mechanisms. The expression of LINC00958 and microRNA (miR)‑3619‑5p was detected in several human CRC cell lines using reverse transcription‑quantitative PCR. Then, short hairpin RNA (shRNA)‑LINC00958 was transfected into the cells. The results revealed that the expression of LINC00958 was notably upregulated, whereas miR‑3619‑5p was downregulated in CRC cells. Transfection with shRNA‑LINC00958 inhibited the proliferation, invasion and migration of CRC cells. Moreover, the rate of apoptosis was enhanced, accompanied by a decrease in the expression of Bcl‑2 and an increase in the expression of Bax and caspase‑3. A luciferase reporter assay was conducted to verify the target binding site between LINC00958 and miR‑3619‑5p. The luciferase reporter assay confirmed that miR‑3619‑5p could be directly targeted by LINC00958. Furthermore, the miR‑3619‑5p inhibitor reversed the effects of LINC00958 silencing on proliferation, invasion, migration and apoptosis. Taken together, the findings suggest that the downregulation of LINC00958 suppresses the proliferation, invasion and migration, and promotes the apoptosis of CRC cells by targeting miR‑3619‑5p in vitro, which provides a theoretical basis and therapeutic strategy for the treatment of CRC.

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