MicroRNA-218 inhibits the proliferation, migration, and invasion and promotes apoptosis of gastric cancer cells by targeting LASP1

Wang, Lele; Wang, Lei; Wang, Xiaoying; Shang, Di; Yin, Shengjie; Sun, Lili; Ji, Hongbo

doi:10.1007/s13277-016-5388-0

Cited by 21 publications

(19 citation statements)

References 32 publications

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“…Previous studies have demonstrated that miRNAs negatively regulate target gene expression by binding to the 3'UTR of target genes (26)(27)(28). In the present study, MTDH was identified as a novel target gene of miR-154 in GC.…”

Section: Discussionsupporting

confidence: 51%

MicroRNA-154 inhibits the growth and metastasis of gastric cancer cells by directly targeting MTDH

Qiao¹,

Cao²,

Yang³

2017

Oncology Letters

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Abstract. MicroRNAs (miRNAs) are a group of non-protein-coding, highly conserved single-stranded RNA molecules. The abnormal expression of miRNAs has been demonstrated to have an important function in the carcinogenesis and progression of gastric cancer. microRNA-154 (miR-154) has been reported to be downregulated in non-small cell lung, colorectal and prostate cancer. However, the expression and roles of miR-154 in gastric cancer remain to be established. The present study measured the expression levels of miR-154 in gastric cancer tissues and cell lines. miR-154 was found to be significantly downregulated in gastric cancer tissues and cell lines. In addition, functional studies indicated that the overexpression of miR-154 inhibited the proliferation, migration and invasion of gastric cancer cells. Using TargetScan, a dual luciferase reporter assay, reverse transcription-quantitative polymerase chain reaction and western blot analysis, metadherin (MTDH) was revealed as a novel miR-154 target. In addition, knocking down MTDH lead to a similar effect as overexpressing-154 in gastric cells. The present findings indicate that miR-154 was downregulated in gastric cancer, and inhibited tumor behaviors of gastric cancer cells partially through the downregulation of MTDH. Therefore, the miR-154/MTDH axis may be a novel therapeutic to treat patients with gastric cancer.

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Section: Discussionsupporting

confidence: 51%

MicroRNA-154 inhibits the growth and metastasis of gastric cancer cells by directly targeting MTDH

Qiao¹,

Cao²,

Yang³

2017

Oncology Letters

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“…MiR-218 upregulation inhibited the proliferation and invasion and induced apoptosis of pancreatic cancer cells [30]. Interestingly, miR-218 could suppress cell proliferation, migration and invasion in gastric cancer and prostate cancer [31,32]. Moreover, our gene microarray analysis showed that ANLN downregulation induced miR-218 expression.…”

Section: Introductionmentioning

confidence: 97%

ANLN-induced EZH2 upregulation promotes pancreatic cancer progression by mediating miR-218-5p/LASP1 signaling axis

Wang

Dai

Gong

et al. 2019

J Exp Clin Cancer Res

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Background: Pancreatic cancer is a highly lethal malignancy with poor prognosis. Anillin (ANLN), an actin binding protein, is upregulated and plays an important role in many malignant tumors. However, the precise role of ANLN in pancreatic cancer remains unclear. Methods: The expression of ANLN and its association with pancreatic cancer patient survival were analyzed using an online database and confirmed by immunohistochemistry. The ANLN protein expression in pancreatic cancer cell lines was detected by Western blot. Cell proliferation, colony formation and transwell assays in vitro and in vivo tumor growth were used to determine the role of ANLN in pancreatic cancer. Gene expression microarray analysis and a series of in vitro assays were used to elucidate the mechanisms of ANLN regulating pancreatic cancer progression.Results: We found that the ANLN expression was significantly upregulated in pancreatic cancer tissues and cell lines. The high expression of ANLN was associated with tumor size, tumor differentiation, TNM stage, lymph node metastasis, distant metastasis and poor prognosis in pancreatic cancer. ANLN downregulation significantly inhibited cell proliferation, colony formation, migration, invasion and tumorigenicity in nude mice. Meanwhile, we found that ANLN knockdown inhibited several cell-cell adhesion related genes, including the gene encoding LIM and SH3 protein 1 (LASP1). LASP1 upregulation partially reversed the tumor-suppressive effect of ANLN downregulation on pancreatic cancer cell progression. Moreover, we found that ANLN downregulation induced the expression of miR-218-5p which inhibited LASP1 expression through binding to its 3'UTR. We also found that ANLN-induced enhancer of zeste homolog 2 (EZH2) upregulation was involved in regulating miR-218-5p/LASP1 signaling axis. EZH2 upregulation or miR-218-5p downregulation partially reversed the tumor-suppressive effect of ANLN downregulation on pancreatic cancer cell progression. Conclusion: ANLN contributed to pancreatic cancer progression by regulating EZH2/miR-218-5p/LASP1 signaling axis. These findings suggest that ANLN may be a candidate therapeutic target in pancreatic cancer.

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“…A previous study reported that >50% of known miRNAs are located at genomic regions or in fragile sites closely correlated with cancer (11). Additional studies reported that miRNAs were abnormally expressed in a variety of human cancers, such as HCC (12), gastric cancer (13), colorectal cancer (14), glioma (15) and bladder cancer (16). These dysregulated miRNAs may act as oncogenes or tumor suppressors in tumorigenesis and tumor development, which depends on tumor type and the roles of their target genes (17,18).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-302a inhibits cell proliferation and invasion, and induces cell apoptosis in hepatocellular carcinoma by directly targeting VEGFA

Qin

Zha

Fan

et al. 2017

Molecular Medicine Reports

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Hepatocellular carcinoma (HCC) is the fifth most common cancer and the third most common cause of cancer‑related mortality worldwide. An increasing number of studies have demonstrated that microRNAs may be used as diagnostic, therapeutic and prognostic targets for human cancers, including HCC. The present study aimed to evaluate microRNA (miR)‑302a expression and function in HCC, and its underlying mechanisms. The results revealed that miR‑302a was expressed at low levels in HCC tissues and cell lines. Reduced miR‑302a expression was correlated with tumor‑node‑metastasis stage and lymph node metastasis in patients with HCC. Additionally, overexpression of miR‑302a reduced cell proliferation and invasion, and induced apoptosis in HCC cells. Vascular endothelial growth factor A (VEGFA) was demonstrated to be a direct target gene of miR‑302a. VEGFA was highly expressed in HCC tissues and inversely correlated with miR‑302a expression. Knockdown of VEGFA expression led to reduced HCC cell proliferation and invasion, and increased apoptosis rates, similar to miR‑302a overexpression, which suggested that VEGFA may be a functional downstream target of miR‑302a in HCC. These data suggested that this newly identified miR‑302a/VEGFA axis may be involved in HCC formation and progression. The present results also provide novel potential targets for the treatments of patients with HCC.

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MicroRNA-218 inhibits the proliferation, migration, and invasion and promotes apoptosis of gastric cancer cells by targeting LASP1

Cited by 21 publications

References 32 publications

MicroRNA-154 inhibits the growth and metastasis of gastric cancer cells by directly targeting MTDH

MicroRNA-154 inhibits the growth and metastasis of gastric cancer cells by directly targeting MTDH

ANLN-induced EZH2 upregulation promotes pancreatic cancer progression by mediating miR-218-5p/LASP1 signaling axis

MicroRNA-302a inhibits cell proliferation and invasion, and induces cell apoptosis in hepatocellular carcinoma by directly targeting VEGFA

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