MiR-141 Suppresses the Migration and Invasion of HCC Cells by Targeting Tiam1

Liu, Ying; Ding, Yi; Huang, Jing; Wang, Shuang; Ni, Weijian; Guan, Jian; Li, Qisheng; Zhang, Yuqin; Ding, Yan‐Qing; Chen, Bin; Chen, Longhua

doi:10.1371/journal.pone.0088393

Cited by 78 publications

(81 citation statements)

References 36 publications

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“…Based on in situ hybridization (ISH) analysis, miR-141 was downregulated in hepatocellular carcinoma samples, and patients with low miR-141 expression had poorer overall survival rate. Moreover, functional analysis showed that miR-141 could inhibit the migration and invasion of HCC cells by targeting Tiam1 [29]. Also, Du et al [30] found significantly downregulated miR-141 in 80% (28/35) of primary gastric cancer tissues compared to pair-matched adjacent non-tumor tissues; overexpression of miR-141 with its precursors significantly inhibited the proliferation of gastric cancer cells.…”

Section: Discussionmentioning

confidence: 99%

“…Hu et al [35] reported that microRNA-141 could regulate Smad interacting protein 1 (SIP1) and inhibit migration and invasion of colorectal cancer cells, suggesting that miR-141 acted as a tumor suppressor gene in CRC. However, two studies on >100 CRC samples founded elevated levels of circulating miR-141 were associated with liver metastasis of CRC and poor prognosis [29,36]. Further, the combination of miR-141 levels with CEA levels improved the accuracy of CRC diagnosis [29].…”

Section: Discussionmentioning

confidence: 99%

“…However, two studies on >100 CRC samples founded elevated levels of circulating miR-141 were associated with liver metastasis of CRC and poor prognosis [29,36]. Further, the combination of miR-141 levels with CEA levels improved the accuracy of CRC diagnosis [29]. These data indicated that miR-141 may promote distant metastasis of CRC.…”

Section: Discussionmentioning

confidence: 99%

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MicroRNA-141 regulates the tumour suppressor DLC1 in colorectal cancer

Wu¹,

Zhu²,

Sun³

et al. 2015

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Our previous study has showed that DLC1 acts as a functional tumor suppressor in colorectal cancer (CRC) cell lines. The aims of this study were to determine whether DLC1 is a target of MicroRNA (miRNA) regulation and to evaluate the role of this mechanism in CRC. By bioinformatics approach and literature, miR-141 was chosen for further study. The miR-141 mimic, miR-141 inhibitor were synthesized and transfected to Lovo cells. Cell growth was determined by MTT and in vivo models. The flow cytometric analysis for cell cycle determination and transwell assays for evaluating the cell invasion were used. Luciferase reporter assays and Western blots showed that DLC1 was a direct target of miR-141 in CRC. The expression levels of miR-141 were obviously up-regulated in CRC tissues compared to non-cancerous tissues, while DLC1 expression levels were down-regulated in a high proportion of clinical samples (14/18). In addition, correlation analyses revealed negative correlation between miR-141 levels and DLC1 expression levels in CRC tissues. MiR-141 overexpression promoted cell growth in vitro and in vivo, promoted cell cycle progression and invasion in Lovo cells. Furthermore, re-introduction of DLC1 in miR-141-overexpressing Lovo cells decreased growth rate of cells, increase of the percentage in G0/G1 phase and decreased the number of migrating cells. In conclusion, we demonstrated that miR-141 is up-regulated in CRC and acts as a functional oncogene by targeting DLC1.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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MicroRNA-141 regulates the tumour suppressor DLC1 in colorectal cancer

Wu¹,

Zhu²,

Sun³

et al. 2015

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“…The best therapeutic interventions against HCC are surgery and transplantation, while other strategies do not seem to be helpful. 28 Furthermore, prognosis and diagnosis of HCC is only possible in the late stages of the disease when therapeutic options are least effective. New Figure 1.…”

Section: Discussionmentioning

confidence: 99%

Bioinformatics prediction and experimental validation of microRNA-20a targeting Cyclin D1 in hepatocellular carcinoma

et al. 2017

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Hepatocellular carcinoma is the major form of primary liver cancer, which is the second and sixth leading cause of cancer-related death in men and women, respectively. Extensive research indicates that Wnt/β-catenin signaling pathway, which plays a pivotal role in growth, development, and differentiation of hepatocellular carcinoma, is one of the major signaling pathways that is dysregulated in hepatocellular carcinoma. Cyclin D1 is a proto-oncogene and is one of the major regulators of Wnt signaling pathway, and its overexpression has been detected in various types of cancers including hepatocellular carcinoma. Using several validated bioinformatic databases, we predicted that the microRNAs are capable of targeting 3′-untranslated region of Cyclin D1 messenger RNA. According to the results, miR-20a was selected as the highest ranking microRNA targeting Cyclin D1 messenger RNA. Luciferase assay was recruited to confirm bioinformatic prediction results. Cyclin D1 expression was first assessed by quantitative real-time polymerase chain reaction in HepG2 cell line. Afterward, HepG2 cells were transduced by lentiviruses containing miR-20a. Then, the expression of miR-20a and Cyclin D1 was evaluated. The results of luciferase assay demonstrated targeting of 3′-untranslated region of Cyclin D1 messenger RNA by miR-20a. Furthermore, 238-fold decline in Cyclin D1 expression was observed after lentiviral induction of miR-20a in HepG2 cells. The results highlighted a considerable effect of miRNA-20a induction on the down-regulation of Cyclin D1 gene. Our results suggest that miR-20a can be used as a novel candidate for therapeutic purposes and a biomarker for hepatocellular carcinoma diagnosis.

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“…As an oncogene or a tumor-suppressor gene, miR-141 has been reported to be either upregulated (ovarian and colorectal cancers) (14,15) or downregulated (prostate, renal cell and hepatocellular carcinoma) (16)(17)(18) in various types of cancers. Recently, a study showed that downregulated miR-141 may confer cisplatin resistance in esophageal squamous cell carcinoma (19).…”

Section: Introductionmentioning

confidence: 99%

miR-141 confers docetaxel chemoresistance of breast cancer cells via regulation of EIF4E expression

et al. 2015

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Abstract. Resistance to docetaxel, a chemotherapy drug for breast cancer (BC) treatment, occurs in ~50% of patients, and the underlying molecular mechanisms of drug resistance are not fully understood. Gene regulation through miR-141 has been proven to play an important role in cancer drug resistance. The present study investigated the role of miR-141 expression in BC cells of acquired docetaxel resistance. Inhibition of miR-141 enhanced the response to docetaxel in docetaxel-resistant cells (MCF-7/DTX and MDA-MB-231/DTX, respectively), whereas overexpression of miR-141 confered resistance in docetaxelsensitive cells (MCF-7 and MDA-MB-231, respectively). By directly targeting the eukaryotic translation initiation factor 4E (EIF4E) mRNA, miR-141 acts on genes that are necessary for drug induced apoptosis rendering the cells drug resistant. Modulation of miR-141 expression was correlated with EIF4E expression changes and a direct interaction of miR-141 with EIF4E was shown by a luciferase assay. Thus, the present study is the first to show an increased expression of miR-141 in an acquired model of docetaxel resistance in BC. This serves as a mechanism of acquired docetaxel resistance in BC cells, possibly through direct interactions with EIF4E, therefore presenting a potential therapeutic target for the treatment of docetaxel resistant BC.

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MiR-141 Suppresses the Migration and Invasion of HCC Cells by Targeting Tiam1

Cited by 78 publications

References 36 publications

MicroRNA-141 regulates the tumour suppressor DLC1 in colorectal cancer

MicroRNA-141 regulates the tumour suppressor DLC1 in colorectal cancer

Bioinformatics prediction and experimental validation of microRNA-20a targeting Cyclin D1 in hepatocellular carcinoma

miR-141 confers docetaxel chemoresistance of breast cancer cells via regulation of EIF4E expression

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