Long non-coding RNA MIAT promotes gastric cancer growth and metastasis through regulation of miR-141/DDX5 pathway

Abstract

BackgroundThe objective of this study was to investigate the role and mechanism of long non-coding RNA MIAT in gastric cancer (GC).MethodsReal-time PCR was used to determine MIAT level in 120 GC tissues, and in two gastric cancer cell lines. The clinicopathological characteristics of MIAT in GC patients were analyzed. Small interfering RNA specific for MIAT (si-MIAT) and lentivector for si-MIAT was performed to down-regulate MIAT expression in GC cells and in animal tumor model, respectively. The interaction of MIAT and miR-141 was measured by RNA pull-down assay and RNA immunoprecipitation. The biological function of si-MIAT on GC cell growth and metastasis were explored through flow cytometry assay, invasion and migration assay in vitro.ResultsMIAT was highly expressed in GC tissues and cell lines and correlated with differentiation degree, TNM stage, distant metastasis, and lymph node metastasis. MIAT knockdown inhibited GC growth and metastasis both in vitro and in vivo. Furthermore, MIAT acted as miR-141 sponge and regulated its target gene DDX5 expression. In BGC-823 and MGC-803 cells with si-MIAT, DDX5 overexpression resulted in an increase of cell proliferation, migration and invasion.ConclusionsOur data indicated that MIAT played an oncogenic role in GC growth and metastasis, and could serve as a novel molecular target for treating GC.Electronic supplementary materialThe online version of this article (10.1186/s13046-018-0725-3) contains supplementary material, which is available to authorized users.

Long non‑coding RNA MIAT promotes gastric cancer proliferation and metastasis via modulating the miR‑331‑3p/RAB5B pathway

“…However, the detailed role and molecular mechanisms of MIAT in GC remain to be elucidated. MIAT was revealed to be upregulated in GC tissues, which is consistent with previous reports ( 25 ). In the present study, it was also demonstrated that high expression of MIAT was correlated with late TNM stage, lymphatic metastasis and a poor prognosis.…”

“…Knockdown of MIAT suppresses cell biological behaviours in gastric cancer via a mechanism involving the miR-29a-3p/HDAC4 axis ( 30 ). Moreover, MIAT promotes gastric cancer growth and metastasis via regulation of the miR-141/DDX5 pathway ( 25 ). The current results also extend the regulatory mechanism of MIAT function.…”

lncRNA MIAT promotes cell invasion and migration in esophageal cancer

“…Furthermore a previous study demonstrated that MIAT is significantly increased in cancer lesions (11). In digestive tract cancer, previous studies have determined that MIAT is highly expressed in gastric cancer (12,13), colorectal cancer (14) and hepatocellular carcinoma (15,16).…”

Long non‑coding RNA MIAT competitively binds miR‑150‑5p to regulate ZEB1 expression in osteosarcoma

“…The myocardial infarction associated transcript (MIAT) may be expressed in postmitotic retinal precursor cells and mitotic progenitors (15). With regards to human malignancies, MIAT upregulation has been observed in conditions including neuroendocrine prostatic and gastric cancer (16,17). However, the role of MIAT in the regulation of osteosarcoma remains unresolved.…”