miR-122 Regulates Tumorigenesis in Hepatocellular Carcinoma by Targeting AKT3

Nassirpour, Rounak; Mehta, Pramod P.; Yin, Min-Jean

doi:10.1371/journal.pone.0079655

Cited by 81 publications

(67 citation statements)

References 28 publications

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“…Growing evidences have indicated that the increased or decreased expression of miRNAs is closely implicated in the tumorigenesis, metastasis, and prognosis of HCC [26,27,28]. In spite of these evidences, numerous existing studies have revealed the roles that miRNAs play in HCC; the underlying molecular mechanism responsible for the progression of malignant HCC however remains to be further explored.…”

Section: Discussionmentioning

confidence: 99%

MiR-490-5p Suppresses Cell Proliferation and Invasion by Targeting BUB1 in Hepatocellular Carcinoma Cells

Liu

et al. 2017

Pharmacology

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Objective: To verify that miR-490-5p could influence hepatocellular carcinoma (HCC) cells' proliferation, invasion, cycle, and apoptosis by targeting BUB1. Methods: Quantitative real time-PCR (QRT-PCR) was used to determine the miR-490-5p expression. Immunohistochemistry, qRT-PCR, and Western blot were employed to detect BUB1 and transforming growth factor-beta (TGFβ/Smad) signaling-related proteins expression in hepatic tissues and cells. The luciferase assay was used to confirm the targeting relationship between miR-490-5p and BUB1. The Cell Counting Kit-8, colony formation, Transwell invasion, scratch healing assays, and flow cytometry analysis were conducted to evaluate HCC cells proliferation, invasion, migration, and apoptosis alteration after transfection. Results: In HCC tissues and cells, lower expression of miR-490-5p was detected, while BUB1 was overexpressed than controls. The upregulation of miR-490-5p inhibited BUB1 expression and the overexpression of miR-490-5p or the under-expression of BUB1 inhibited HCC cells proliferation, migration, invasion, and increased the apoptosis rate. Conclusion: MiR-490-5p could regulate TGFβ/Smad signaling pathways by inhibiting BUB1, which could then inhibit HCC cells proliferation, invasion, and migration as well as decrease cell viability and increase apoptosis.

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Section: Discussionmentioning

confidence: 99%

MiR-490-5p Suppresses Cell Proliferation and Invasion by Targeting BUB1 in Hepatocellular Carcinoma Cells

Liu

et al. 2017

Pharmacology

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“…miRNAs are hypothesized to be a highly involved in mediating malignant functions in cancer development (23,24). Previous studies indicated that proliferation (25), viability (26), migration and invasion of epithelial cells (27) were decreased while miR-126 was transfected (28). In a study, reduction of miR-126 led various cancer cells to induce angiogenesis, tumor growth and metastasis (29).…”

Section: Discussionmentioning

confidence: 99%

Micro RNA-126 coordinates cell behavior and signaling cascades according to characteristics of breast cancer cells

Coşan¹,

Öner²,

Şahin³

2017

BLL

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BACKGROUND: Micro RNA-126 is known to enhance apoptotic processes and also plays a role in vascular growth through the regulation of vascular endothelial growth factor-mediated signaling, angiogenesis, and vascular integrity. OBJECTIVES: We aimed to determine the role of miR-126 in breast cancer cell lines with a variety of different characteristics to evaluate its interaction with certain cancer-related molecules and mechanisms. METHODS: To determine the effect of presence and absence of miR-126 in MCF-7 and MDA-MB-231 breast cancer cells, miR-126 mimics and inhibitor were transfected. miRNA and gene expressions were observed by using RT-PCR. Viability, proliferation, adhesion, invasion and lateral motility assays were performed to determine cell behavior changes. RESULTS: miR-126 is more effective on MDA-MB-231 cells on cell behavior. We observed an increase in miR-126 expression when miR-126 mimics was transfected to MCF-7 and MDA-MB-231 cells. Also, there was a decrease in miR-126 expression when MCF-7 and MDA-MB-231 cells were transfected with miR-126 inhibitor. Furthermore, presence and absence of miR-126 modulated the gene expressions of VEGF/PI3K/AKT and MAPK signaling in MCF-7 and MDA-MB-231. CONCLUSION: Our study showed that miR-126 is in a state of interaction with a multitude molecules playing a role in breast cancer. According to obtained data, we can say that miR-126 may be more effective in inhibition of metastatic breast cancer (Tab. 4, Fig. 3, Ref. 46). Text in PDF www.elis.sk.

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“…Subsequent studies confirmed that miRNA expression is frequently deregulated in numerous types of cancer. miR-122, a liver-specific miRNA, is downregulated in hepatocellular carcinoma, resulting in the suppression of cell migration and proliferation and the induction of cell apoptosis by targeting AKT3 (5). Upregulated miR-30b/30d contributes to melanoma cell invasion and migration by targeting polypeptide N-acetylgalactosaminyltransferase 7, leading to the progression of metastasis (6).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-96 promotes the proliferation of colorectal cancer cells and targets tumor protein p53 inducible nuclear protein 1, forkhead box protein O1 (FOXO1) and FOXO3a

Gao

Wang

2014

Molecular Medicine Reports

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Abstract. MicroRNAs (miRNAs) are a conserved class of small, endogenous, non protein-coding RNA molecules that are capable of regulating gene expression at post-transcriptional levels and are involved in diverse cellular processes, including cancer pathogenesis. It has previously been reported that miRNA-96 (miR-96) is overexpressed in human colorectal cancer (CRC). However, the underlying mechanism of miR-96 regulation in CRC remains to be elucidated. In the present study, miR-96 was confirmed to be upregulated in CRC tissues by reverse transcription quantitative polymerase chain reaction. MTT assay, colony formation assay and cell cycle analysis revealed that miR-96 overexpression led to increased tumor cell viability, colony formation ability and cell cycle progression. By contrast, inhibition of miR-96 resulted in the suppression of cell proliferation. It was also demonstrated that miR-96 reduced the messenger RNA and protein expression levels of tumor protein p53 inducible nuclear protein 1 (TP53INP1), forkhead box protein O1 (FOXO1) and FOXO3a, which are closely associated with cell proliferation. A luciferase reporter assay indicated that miR-96 inhibited luciferase intensity controlled by the 3'UTRs of TP53INP1, FOXO1 and FOXO3a. In conclusion, the results of the present study demonstrated that miR-96 contributed to CRC cell growth and that TP53INP1, FOXO1 and FOXO3a were direct targets of miR-96, suggesting that miR-96 may have the potential to be used in the development of miRNA-based therapies for CRC patients.

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miR-122 Regulates Tumorigenesis in Hepatocellular Carcinoma by Targeting AKT3

Cited by 81 publications

References 28 publications

MiR-490-5p Suppresses Cell Proliferation and Invasion by Targeting BUB1 in Hepatocellular Carcinoma Cells

MiR-490-5p Suppresses Cell Proliferation and Invasion by Targeting BUB1 in Hepatocellular Carcinoma Cells

Micro RNA-126 coordinates cell behavior and signaling cascades according to characteristics of breast cancer cells

MicroRNA-96 promotes the proliferation of colorectal cancer cells and targets tumor protein p53 inducible nuclear protein 1, forkhead box protein O1 (FOXO1) and FOXO3a

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