已发表论文

lncRNA DSCAM-AS1 可下调 miR-216b 以促进结直肠腺癌细胞的迁移和侵袭

 

Authors Liu F, Jia J, Sun L, Yu Q, Duan H, Jiao D, Gong Z, Zhu S, Jiang K, He Y, Chen L, Zhang Y, Sun H

Received 24 April 2019

Accepted for publication 1 July 2019

Published 21 August 2019 Volume 2019:12 Pages 6789—6795

DOI https://doi.org/10.2147/OTT.S213301

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Ms Shreya Arora

Peer reviewer comments 2

Editor who approved publication: Dr Nicola Silvestris

Background: It has been reported that lncRNA DSCAM-AS1 plays an oncogenic role in breast cancer. In the present study we explored the role of DSCAM-AS1 in colorectal adenocarcinoma (CRA).
Methods: Gene expression was analyzed by qPCR and Western blot. Overexpression experiments were performed to analyze gene interactions. Transwell assays were performed to analyze cell invasion and migration. Methylation-specific PCR (MSP) was performed to analyze DNA methylation.
Results: It was observed that DSCAM-AS1 was upregulated in the primary tumor tissues than in paired non-tumor tissues (within 2 cm around tumors) and was further increased with tumor metastasis. miR-216b was downregulated in primary tumor and further downregulated with tumor metastasis. miR-216b was inversely correlated with DSCAM-AS1 in tumor tissues, but not in non-tumor tissues. In cells of CRA cell lines, DSCAM-AS1 overexpression resulted in the downregulation of miR-216b, while miR-216b overexpression did not significantly affect DSCAM-AS1. DSCAM-AS1 overexpression did not significantly affect cancer cell proliferation but promoted cell migration and invasion. miR-216b inhibited cancer cell migration and invasion and significantly reduced the effects of DSCAM-AS1 overexpression. Methylation-specific PCR showed that DSCAM-AS1 overexpression promoted the methylation of miR-216b gene.
Conclusion: DSCAM-AS1 may downregulate miR-216b to promote the migration and invasion of CRA cells.
Keywords: colorectal adenocarcinoma, lncRNA DSCAM-AS1, miR-216b




Figure 3 miR-216b was downregulated in tumor tissue and...