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

Qiao, Wenhui; Cao, Nong; Yang, Lei

doi:10.3892/ol.2017.6558

Cited by 32 publications

(28 citation statements)

References 35 publications

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“…32 They are involved in various processes such as angiogenesis, 33 cell growth, 34 and movement. 36 miR-744 can inhibit GC cell proliferation and invasion through targeting neurotrophic factor. 10,11 miR-154 is able to repress GC cell development by inhibiting MTDH.…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA NEAT1‐modulated miR‐506 regulates gastric cancer development through targeting STAT3

Tan

Wang

Liu

et al. 2019

J of Cellular Biochemistry

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Accumulating evidence has indicated that lncRNA NEAT1 exerts critical roles in cancers. So far, the detailed biological role and mechanisms of NEAT1 which are responsible for human gastric cancer (GC) is still largely unknown. Here, we observed that NEAT1 and STAT3 expression were significantly upregulated in human gastric cancer cells including BGC823, SGC-7901, AGS, MGC803 and MKN28 cells compared to normal gastric epithelial cells GES-1 while miR-506 was downregulated. We inhibited NEAT1 and observed that NEAT1 inhibition was able to repress the growth, migration and invasion of gastric cancer cells. Reversely, overexpression of NEAT1 exhibited an increase ability of gastric cancer progression in BGC823 and SGC-7901 cells. Bioinformatics analysis, dual luciferase reporter assays, RIP assays and RNA pull-down tests validated the negative binding correlation between NEAT1 and miR-506. In addition, it was found that miR-506 can modulate expression of NEAT1 in vitro. STAT3 was predicted as an mRNA target of miR-506 and miR-506 mimics can suppress STAT3 mRNA expression. Subsequently, it was observed that downregulation of NEAT1 can restrain gastric cancer development by decreasing STAT3 which can be reversed by miR-506 inhibitors. Therefore, it was hypothesized in our study that NEAT1 can be recognized as a ceRNA to modulate STAT3 by sponging miR-506 in gastric cancer. In conclusion, we implied that NEAT1 can serve as an important biomarker in gastric cancer diagnosis and treatment. This article is protected by copyright. All rights reserved.

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Section: Discussionmentioning

confidence: 99%

Long noncoding RNA NEAT1‐modulated miR‐506 regulates gastric cancer development through targeting STAT3

Tan

Wang

Liu

et al. 2019

J of Cellular Biochemistry

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“…As miRNAs have been observed to regulate the proliferation, migration, invasion and other biological processes, a close association between miRNA expression and tumor progression has been reported (19). For instance, Qiao et al (20) reported that miR-154 inhibited the growth and metastasis of gastric cancer cells by directly targeting metadherin (20). Cao et al (17) revealed that miR-552 promoted tumor cell proliferation and migration by directly targeting dachshund family transcription factor 1 via the Wnt/β-catenin signaling pathway in colorectal cancer (17).…”

Section: Discussionmentioning

confidence: 99%

LIMD2 targeted by miR‑34a promotes the proliferation and invasion of non‑small cell lung cancer cells

Wang

et al. 2018

Mol Med Report

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A previous study indicated that LIM domain containing 2 (LIMD2) is an oncogene in a variety of human cancers, including breast, bladder and thyroid cancers, and melanoma; however, the role of LIMD2 in non‑small cell lung cancer (NSCLC) remains largely unknown. In the present study, by reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) analysis, it was demonstrated that LIMD2 was significantly upregulated in NSCLC tissues compared with adjacent normal tissues. Consistently, LIMD2 was also upregulated in NSCLC cell lines. Furthermore, the present study reported that knockdown of LIMD2 significantly inhibited the proliferation and invasion of H1299 and A549 cells by Cell Counting Kit‑8 and Transwell assays. In addition, the expression of LIMD2 was determined to be regulated by microRNA (miR)‑34a in the present study. RT‑qPCR and western blot analysis indicated that overexpression of miR‑34a notably reduced the mRNA and protein expression levels of LIMD2 in H1299 and H549 cells. Additionally, the present study reported an inverse correlation between the expression of LIMD2 and miR‑34a in NSCLC tissues. A luciferase reporter assay also demonstrated that miR‑34a directly targeted the mRNA expression of LIMD2 in NSCLC cells. Finally, miR‑34a was revealed to possess a tumor suppressive role in NSCLC cells. Collectively, the results of the present study revealed that LIMD2 promoted NSCLC progression and was regulated by miR‑34a.

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“…Additionally, reduced levels of miR-154 levels in colorectal cancer tissues compared with non-cancerous tissues has been reported and this low expression has been shown to be significantly correlated with aggressive clinicopathological characteristics such as large tumor size, positive lymph node metastasis, and advanced clinical stage (27). Low expression of miR-154 and its association with cell proliferation, migration and invasion has also been described in prostate cancer (28). miR-154 may also function as a tumor suppressor in non-small cell lung cancer (NSCLC) by binding to B-cell-specific Moloney murine leukemia virus insertion site 1 (BMI-1) (29).…”

Section: Luciferase Reporter Assay Verifying the Predicted Interactiomentioning

confidence: 95%

Down-regulation of NAMPT expression by miR-154 reduces the viability of breast cancer cells and increases their susceptibility to doxorubicin

Bolandghamtpour

Nourbakhsh²,

Mousavizadeh

et al. 2019

Preprint

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Background Nicotinamide phosphoribosyltransferase (NAMPT) acts as an important enzyme in the salvage pathway of nicotinamide adenine dinucleotide (NAD) biosynthesis. Deregulation of NAD could be associated with progression of many cancers including breast cancer. Here, we evaluated the effect of NAMPT inhibition via miR-154 on survival of breast cancer cells. Methods Breast cancer cell lines including MCF-7 and MDA-MB-231 were transfected with miR-154 mimic, inhibitor and their negative controls. Using real-time PCR and western blotting techniques the expression levels of NAMPT and miR-154 were determined and compared with the untreated cells. NAD levels were measured by an enzymatic method. Subsequently, colorimetric methods and flow cytometry were performed to evaluate cell viability and apoptosis. Bioinformatics analyses were performed to investigate whether NAMPT 3′-UTR is a direct target of miR-154 and the findings were confirmed by luciferase reporter assay. Results According to the obtained results, NAMPT 3′-UTR was identified as a direct target of miR-154 and the levels of this miRNA was inversely associated with NAMPT expression both at mRNA and protein levels in breast cancer cell lines. Functionally, miR-154 inhibited the NAD salvage pathway leading to a remarkable decrease in cell survival and induction of apoptosis. Co-treatment of breast cancer cells with doxorubicin and miR-154 mimic significantly reduced cell viability compared to treatment with doxorubicin alone in both cell lines. Conclusions Hence, it was concluded that the inhibition of NAD production by miR-154 might be introduced as a promising therapeutic strategy for the treatment of breast cancer either alone or in combination with other conventional chemotherapeutic agents.

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

Cited by 32 publications

References 35 publications

Long noncoding RNA NEAT1‐modulated miR‐506 regulates gastric cancer development through targeting STAT3

Long noncoding RNA NEAT1‐modulated miR‐506 regulates gastric cancer development through targeting STAT3

LIMD2 targeted by miR‑34a promotes the proliferation and invasion of non‑small cell lung cancer cells

Down-regulation of NAMPT expression by miR-154 reduces the viability of breast cancer cells and increases their susceptibility to doxorubicin

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