Down-Regulation of MiR-30c Promotes the Invasion of Non-Small Cell Lung Cancer by Targeting MTA1

Xia, Yang; Chen, Qiyou; Zhong, Zhaodong; Xu, C.; Wu, Chen; Liu, Bin; Chen, Yijiang

doi:10.1159/000354452

Cited by 46 publications

(29 citation statements)

References 31 publications

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“…This suggests that miRNAs are central regulators of cancer. Xia et al [27] recently Figure 3. miR-125a-3p suppresses the proliferation of NSCLC cells by inhibiting MTA1 (A) MTT assay, (B) colony formation assay, and (C) EdU assay were performed in SPC-A-1 and 95D cells co-transfected with miR-125a-3p or miR-NC and si-MTA1 or scrambled siRNA.…”

Section: Discussionmentioning

confidence: 97%

miR-125a-3p targets MTA1 to suppress NSCLC cell proliferation, migration, and invasion

Zhang¹,

Zhu²,

Li³

et al. 2015

ABBS

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Metastasis-associated gene 1 (MTA1) is associated with cell growth, metastasis, and survival in nonsmall-cell lung cancer (NSCLC). Several previous reports have demonstrated that microRNAs affect gene expression through interaction between their seed region and the 3′-untranslated region of the target mRNA, resulting in post-transcriptional regulation. The aim of this study was to identify miRNAs that suppress malignancy in NSCLC cells by targeting MTA1. Two human NSCLC cell lines were analyzed for the expression of MTA1 by quantitative RT-PCR and western blotting after transfection with MTA1 mimics. A luciferase reporter assay was established to test the direct connection between MTA1 and its upstream miRNAs. Cell proliferation was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, 5-ethynyl-2′-deoxyuridine analysis, and colony formation assay. Cell migration and invasive capacity were evaluated by wound-healing assay and transwell assay. The miRNA/MTA1 axis was also probed by quantitative RT-PCR and western blotting in samples from eight NSCLC patients. Among the candidate miRNAs, miR-125a-3p was shown to posttranscriptionally regulate MTA1 in NSCLC cells. These data were reinforced by the luciferase reporter assay, in addition to the demonstration that MTA1 is inversely correlated with miR-125a-3p in NSCLC tissues. Furthermore, miR-125a-3p was found to inhibit NSCLC cell proliferation, migration, and invasion, through the same mechanisms of down-regulated MTA1. Our report demonstrates that miR-125a-3p inhibits the proliferation, migration, and invasion of NSCLC cells through down-regulation of MTA1, indicating the role of the miR-125a-3p/MTA1 axis in NSCLC, and may provide novel insight into the molecular mechanisms underpinning the disease and potential therapeutic targets.

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Section: Discussionmentioning

confidence: 97%

miR-125a-3p targets MTA1 to suppress NSCLC cell proliferation, migration, and invasion

Zhang¹,

Zhu²,

Li³

et al. 2015

ABBS

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“…For instance, Gu and his co-workers verified that miR-150 induced cell proliferation inhabitation and apoptosis in NSCLC by targeting BAK1 [19]. Meanwhile, our previous work has also confirmed that miR-204 and miR-30c function as regulators in the progression of NSCLC by targeting specific genes [15,16]. Recently, miR-452 was regarded as tumor suppressor in glioma [7], prostate [20] and breast malignancies [8], which was supported by our findings that miR-452 expression was significantly reduced in tumor comparing with corresponding adjacent tissues and was negatively correlated with the tumor stage and lymph nodes metastases.…”

Section: Discussionmentioning

confidence: 98%

“…Our previous studies have illustrated that invasion and metastasis are key factors influencing the rate of long-term survival of NSCLC [15,16]. Even diagnosed at early stage and surgically resected successfully, a considerable number of NSCLC patients will suffer from metastasis or recurrence.…”

Section: Discussionmentioning

confidence: 99%

Up-Regulation of MiR-452 Inhibits Metastasis of Non-Small Cell Lung Cancer by Regulating BMI1

Xia

Pan

et al. 2015

Cell Physiol Biochem

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Background/Aims: MicroRNAs (miRNAs) have been regarded as a new class of regulators in cellular processes in non-small cell lung cancer (NSCLC). However, the relationship between miR-452 and the development of NSCLC remains unclear. Methods: qRT-PCR was used to detect the expression of miR-452 and its target gene in NSCLC samples (n=60). The transwell assay was used to test the cell invasion capability. The regulation mechanism was confirmed by luciferase reporter assay and western blot assay. Results: In the current study, a relatively lower miR-452 and higher BMI1 expression levels were confirmed to be associated with advanced tumor stage and more extent of lymph nodes metastasis. In vitro, down-regulated miR-452 could enhance cell invasion capability. Furthermore, miR-452 modulated BMI1 expression by binding to its 3ʹ-UTR. The enhancement of cell invasion capability induced by down-regulated miR-452 was eliminated by repression of BMI1. Conclusions: Our results suggest that miR-452 plays a vital role in development of NSCLC, and this miR-452-BMI1 pathway might generate a novel insight into the treatment of NSCLC.

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“…miRNAs bind target mRNAs at complementary sites in their 3'-untranslated regions (3'-UTRs), thereby suppressing the expression of the target gene at the posttranscriptional level [19][20][21]. Through this mechanism, miRNAs regulate a wide range of biological processes, including cell proliferation and differentiation [22], migration, apoptosis, development, and metabolism [23][24][25]. For example, miR-545 suppress cell proliferation by targeting Cyclin D1 and CDK4 in lung cancer cells [26].…”

Section: Down-regulation Of Adam17 By Sirna Reversed the Effect Of MImentioning

confidence: 99%

Adam17, a Target of Mir-326, Promotes Emt-Induced Cells Invasion in Lung Adenocarcinoma

Cai

Wang²,

Zhang³

et al. 2015

Cell Physiol Biochem

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Background/Aims: A disintegrin and metalloprotease (ADAM) 17 has been reported to be implicated in cancer cells invasion. Nevertheless, its potential role in lung adenocarcinoma has not been addressed clearly. Methods: RT-PCR and Western blot were used to detect the expression of miR-326 and ADAM17 in lung adenocarcinoma samples (n=73). miR-326 mimics and inhibitor were tansfected in human A549 and SPCA1 cell lines. The transwell assay was used to detect the cell invasive ability. The regulation mechanism was evaluated by luciferase reporter assay. The markers of (epithelial-to-mesenchymal transition) EMT were detected by using Western blot assay. Results: We found increased expression of ADAM17 in lung adenocarcinoma and cell lines. In vitro, up-regulation of ADAM17 promoted cells invasion, while silencing of ADAM17 inhibited cells invasion. Meanwhile, ADAM17 could affect the markers of EMT. Furthermore, we confirmed that ADAM17 is a target of miR-326, which is involved in EMT and cells invasion. Conclusions: These findings revealed that ADAM17, a target of miR-326, promoted EMT-induced cells invasion in lung adenocarcinoma.

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Down-Regulation of MiR-30c Promotes the Invasion of Non-Small Cell Lung Cancer by Targeting MTA1

Cited by 46 publications

References 31 publications

miR-125a-3p targets MTA1 to suppress NSCLC cell proliferation, migration, and invasion

miR-125a-3p targets MTA1 to suppress NSCLC cell proliferation, migration, and invasion

Up-Regulation of MiR-452 Inhibits Metastasis of Non-Small Cell Lung Cancer by Regulating BMI1

Adam17, a Target of Mir-326, Promotes Emt-Induced Cells Invasion in Lung Adenocarcinoma

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