Open AccessKnockdown of long non-coding RNA metastasis associated lung adenocarcinoma transcript 1 inhibits the proliferation and migration of bladder cancer cells by modulating the microRNA-34a/cyclin D1 axis
Author(s) -
Ye Liu,
Saiyue Gao,
Qingyan Du,
Qingsong Zhao
Publication year - 2018
Publication title -
international journal of molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.048
H-Index - 90
eISSN - 1791-244X
pISSN - 1107-3756
DOI - 10.3892/ijmm.2018.3959
Subject(s) - malat1 , gene knockdown , cyclin d1 , cancer research , cell cycle , biology , cell growth , oncogene , metastasis , downregulation and upregulation , microrna , adenocarcinoma , cell migration , long non coding rna , cell , cancer , cell culture , gene , genetics , biochemistry
Long non‑coding RNA (lncRNA) metastasis associated lung adenocarcinoma transcript 1 (MALAT1) has been demonstrated to participate in the development and progression of some common cancer types, including bladder cancer (BC). However, the regulatory mechanism of MALAT1 underlying BC growth and metastasis remains to be fully elucidated. The present study revealed that MALAT1 was significantly upregulated in BC tissues and cell lines compared with the adjacent non‑tumour tissues and the normal urinary tract epithelial cell line SV‑HUC‑1, respectively. The expression levels of MALAT1 were higher in stage III‑IV BC tissues when compared with that in stage I‑II tissues. Furthermore, knockdown of MALAT1 significantly inhibited BC cell proliferation and migration by targeting microRNA (miR)‑34a. The expression levels of miR‑34a were significantly decreased in BC tissues and cell lines compared with that of adjacent non‑tumour tissues and SV‑HUC‑1 cells. In addition, the expression of miR‑34a was inversely correlated with the expression of MALAT1 in BC tissues. The present study revealed that cyclin D1 (CCND1) was identified as a target gene of miR‑34a, and its expression was negatively mediated by miR‑34a in BC cells. Notably, the upregulation of CCND1 impaired the effect of MALAT1 inhibition on BC cell proliferation and migration. In addition, the expression levels of CCND1 were significantly increased in BC tissues and cell lines. In conclusion, the present findings demonstrated that the knockdown of lncRNA MALAT1 inhibits the proliferation and migration of BC cells by modulating the miR‑34a/CCND1 axis, suggesting that the MALAT1/miR‑34a/CCND1 axis may be a potential therapeutic target for BC treatment.