miR-137 Is Frequently Down-Regulated in Gastric Cancer and Is a Negative Regulator of Cdc42

Chen, Qingjiang; Chen, Xiaobing; Zhang, Mingzhi; Fan, Qingxia; Luo, Suxia; Cao, Xiaoqin

doi:10.1007/s10620-010-1536-3

Cited by 127 publications

(115 citation statements)

References 17 publications

(20 reference statements)

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“…Previous studies have demonstrated that a low expression of miR-137 inhibits cell growth in vivo and in vitro through G 1 phase cell cycle arrest, and impairs cell migration and invasion (7,27). To investigate the effect of miR-137 on NSCLC cell growth, the colony forming and proliferation ability of cells was determined using soft agar colony formation assays and MTT assays, respectively.…”

Section: Discussionmentioning

confidence: 99%

miR-137 inhibits the proliferation of human non-small cell lung cancer cells by targeting SRC3

Chen

Zhang

et al. 2017

Oncology Letters

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Abstract. Non-small cell lung cancer (NSCLC) is the most common type of lung cancer. The results of the present study demonstrate that high expression of microRNA (miR)-137 and low expression of steroid receptor coactivator-3 (SRC3) had a significant negative correlation in 40 NSCLC tissue samples. In addition, cell colony formation and proliferation was significantly reduced in miR-137-transfected A549 and NCI-H838 cells compared with scramble-transfected NSCLC cell lines. miR-137 was identified to induce G 1 /S cell cycle arrest and dysregulate the mRNA expression of cell cycle-associated proteins (proliferating cell nuclear antigen, cyclin E, cyclin A1, cyclin A2 and p21) in NSCLC cells. Notably, miR-137 could significantly suppress SRC3 3' untranslated region (UTR) luciferase-reporter activity, an effect that was not detectable when the putative 3'-UTR target-site was mutated, further clarifying the molecular mechanisms underlying the role of miR-137 in NSCLC. In conclusion, the results of the present study suggest that miR-137 suppresses NSCLC cell proliferation by partially targeting SRC3.

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Section: Discussionmentioning

confidence: 99%

miR-137 inhibits the proliferation of human non-small cell lung cancer cells by targeting SRC3

Chen

Zhang

et al. 2017

Oncology Letters

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“…49 For example, it has been shown that RhoA is target of miRNA-155 50,51 and miRNA-125a-3p; 52 RhoB is a target of miRNA- 21; 53 RhoBTB1 is a target of miRNA-31; 54 and Cdc42 is a target of miRNA-29 55 and miRNA-137. 56 Sometimes the same miRNA can target 2 different Rho GTPases. miRNA-185 has been reported to decrease the levels of RhoA and Cdc42, leading to inhibition of proliferation in human colorectal cancer cells.…”

Section: 43mentioning

confidence: 99%

Rho GTPases: Regulation and roles in cancer cell biology

Haga

Ridley²

2016

Small GTPases

401

390

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Rho GTPases are well known for their roles in regulating cell migration, and also contribute to a variety of other cellular responses. They are subdivided into 2 groups: typical and atypical. The typical Rho family members, including RhoA, Rac1 and Cdc42, cycle between an active GTP-bound and inactive GDP-bound conformation, and are regulated by GEFs, GAPs and GDIs, whereas atypical Rho family members have amino acid substitutions that alter their ability to interact with GTP/GDP and hence are regulated by different mechanisms. Both typical and atypical Rho GTPases contribute to cancer progression. In a few cancers, RhoA or Rac1 are mutated, but in most cancers expression levels and/or activity of Rho GTPases is altered. Rho GTPase signaling could therefore be therapeutically targeted in cancer treatment.

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“…In hepatocellular carcinoma, miR-224 promotes cell proliferation, migration and invasion, and inhibited apoptosis by regulating CDC42 expression (49). In gastric cancer, CDC42 was demonstrated to be a direct gene of miR-137 (50). In NSCLC, miR-25 and miR-137 were demonstrated, by targeting CDC42, to be important regulators in initiation and progression and NSCLC (51,52).…”

Section: Cdc42 Is Involved In Mir29a-induced Effects In Nsclc Cellsmentioning

confidence: 99%

MicroRNA-29a functions as a potential tumor suppressor through directly targeting CDC42 in non-small cell lung cancer

Wang

et al. 2017

Oncology Letters

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Abstract. The expression and function of microRNA-29a (miR-29a) have been investigated in various types of cancer. In the present study, the expression, function and underlying molecular mechanism of miR-29a were investigated in non-small cell lung cancer (NSCLC). The expression level of miR-29a in NSCLC was determined using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Cell proliferation, migration and invasion ability were determined using Cell Counting Kit-8, cell migration and invasion assays, respectively. Bioinformatics analysis and dual-luciferase reporter assays were performed to determine whether cell division cycle 42 (CDC42) is a direct target gene of miR-29a. To assess CDC42 mRNA and protein expression following transfection with miR-29a, RT-qPCR and western blotting were performed. Following knockdown of CDC42, functional assays were performed to investigate the roles of CDC42 in NSCLC. The results demonstrated that miR-29a was downregulated in NSCLC and the decreased expression level of miR-29a was significantly associated with advanced tumor-node-metastasis classification and metastasis. In addition, upregulation of miR-29a inhibited cell proliferation, migration and invasion in NSCLC, whereas downregulation of miR-29a had the opposite effects. Furthermore, CDC42 was identified as a direct target gene of miR-29a in vitro. miR-29a was demonstrated to function as a tumor suppressor in NSCLC by directly targeting CDC42 and may be investigated further as a target therapy for NSCLC.

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miR-137 Is Frequently Down-Regulated in Gastric Cancer and Is a Negative Regulator of Cdc42

Abstract: miR-137 is frequently down-regulated in gastric cancer and is a negative regulator of Cdc42.

Cited by 127 publications

References 17 publications

miR-137 inhibits the proliferation of human non-small cell lung cancer cells by targeting SRC3

miR-137 inhibits the proliferation of human non-small cell lung cancer cells by targeting SRC3

Rho GTPases: Regulation and roles in cancer cell biology

MicroRNA-29a functions as a potential tumor suppressor through directly targeting CDC42 in non-small cell lung cancer

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