MiRNA-206 inhibits hepatocellular carcinoma cell proliferation and migration but promotes apoptosis by modulating cMET expression

Wang, Yuanxi; Tai, Qin-wen; Zhang, Jinhui; Kang, Junsheng; Gao, Feng; Zhong, Feng; Cai, Liquan; Fang, Fa; Gao, Yi

doi:10.1093/abbs/gmy119

Cited by 43 publications

(31 citation statements)

References 33 publications

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“…According to Wei’s research, miR-206 expression in RCC cells and tissues was both notably downregulated; miR-206 suppressed the growth, proliferation and migration in RCC cell lines.26 Similarly, Cai et al investigated that downregulating miR-206 expression had an effect on suppressing proliferation and invasion in ccRCC.27 Those research indicated miR-206 was a critical factor in tumorgenesis and development. Besides, miR-206 inhibited proliferation and migration on hepatocellular carcinoma cells.28 In the current research, we also suggested that miR-206 played a crucial role as a suppression factor in RCC. Furthermore, miR-206 could act as a downstream effector of circZFR, as its expression was negatively regulated by circZFR, and the effects of circZFR silence on RCC cell lines were attenuated when miR-206 was silenced.…”

Section: Discussionsupporting

confidence: 65%

<p>Silencing circZFR inhibits the proliferation, migration and invasion of human renal carcinoma cells by regulating miR-206</p>

Wang¹,

Gao²,

Liu³

2019

OTT

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BackgroundRenal cell carcinoma (RCC) is the most prevalent kind of kidney cancer. At present, the most efficient treatment mean is surgery. 40% patients with clear cell RCC (ccRCC) relapse after surgery. Identifying novel therapeutic markers and spots for early detection and treatment of RCC is necessary.MethodsqRT-PCR was utilized to quantify circZFR and miR-206 expression in CAKI-1 and ACHN cells. Cell viability was detected by CCK-8 assay. Colony formation capacity was measured by colony formation assay. Transwell assay was utilized to investigate migration and invasion capacity. Expression of migration and apoptosis-associated proteins was quantified by Western blot.ResultsAs a result, circZFR was highly expressed in RCC tissues and cells. Si-circZFR suppressed cell growth, migration and invasion of experimental cells. In addition, knockdown of circZFR upregulated miR-206 expression. Moreover, the antigrowth, antimigrating and anti-invasive effects of si-circZFR were attenuated when downregulating miR-206. Furthermore, Met is the target gene of miR-206 in experimental cells. The suppression on these signaling pathways was acted by targeting miR-206/Met axis.ConclusionThe results demonstrated si-circZFR inhibited cell growth, migration and invasion in experimental cells by up-regulating of miR-206. Furthermore, si-circZFR suppressed Wnt/β-catenin and PI3K/AKT pathways via targeting miR-206/Met axis.

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Section: Discussionsupporting

confidence: 65%

<p>Silencing circZFR inhibits the proliferation, migration and invasion of human renal carcinoma cells by regulating miR-206</p>

Wang¹,

Gao²,

Liu³

2019

OTT

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“…Conversely, inhibition of miR-206 inhibition enhances expression of protein tyrosine phosphatase 1B (PTP1B) that plays an oncogenic role in HCC, in HepG2, and Huh7 cells [148]. MiR-206 also directly targets the c-Met gene for silencing and restoration of c-Met expression reverses the inhibitory effect of miR-206 on HCC [149]. Nrf2, involved in cellular antioxidant defense systems, protects against excessive ROS damage to macromolecules and consequent senescence and apoptosis.…”

Section: Effect Of Thyroid Hormone On the Role Of Oxidative Stressmentioning

confidence: 99%

Roles of Thyroid Hormone-Associated microRNAs Affecting Oxidative Stress in Human Hepatocellular Carcinoma

Huang

Wang

Yeh

et al. 2019

IJMS

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Oxidative stress occurs as a result of imbalance between the generation of reactive oxygen species (ROS) and antioxidant genes in cells, causing damage to lipids, proteins, and DNA. Accumulating damage of cellular components can trigger various diseases, including metabolic syndrome and cancer. Over the past few years, the physiological significance of microRNAs (miRNA) in cancer has been a focus of comprehensive research. In view of the extensive level of miRNA interference in biological processes, the roles of miRNAs in oxidative stress and their relevance in physiological processes have recently become a subject of interest. In-depth research is underway to specifically address the direct or indirect relationships of oxidative stress-induced miRNAs in liver cancer and the potential involvement of the thyroid hormone in these processes. While studies on thyroid hormone in liver cancer are abundantly documented, no conclusive information on the potential relationships among thyroid hormone, specific miRNAs, and oxidative stress in liver cancer is available. In this review, we discuss the effects of thyroid hormone on oxidative stress-related miRNAs that potentially have a positive or negative impact on liver cancer. Additionally, supporting evidence from clinical and animal experiments is provided.

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“…LIHC, liver hepatocellular carcinoma; OS, overall survival. development and progression of LIHC by affecting cell cycle and proliferation, metastasis and invasion, drug resistance and inhibition of apoptosis (49)(50)(51). It has been demonstrated that the levels of let-7c are lower in LIHC tissues than in the corresponding normal adjacent tissues (52).…”

Section: Discussionmentioning

confidence: 99%

Effect of let‑7c on the PI3K/Akt/FoxO signaling pathway in hepatocellular carcinoma

Wang

2020

Oncol Lett

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The early diagnosis and treatment of liver hepatocellular carcinoma (LIHC) remains a major challenge. Therefore, it is of great significance to strengthen basic research on LIHC in order to improve the prevention and treatment of the disease. Numerous studies have indicated that the PI3K/Akt and FoxO signaling pathways mediate proliferation, survival and migration during the development of LIHC. Therefore, they have become a target for LIHC treatment. Furthermore, let-7c has been demonstrated to repress cell proliferation, migration and invasion, and to induce G 1 phase arrest and apoptosis of LIHC cells. However, the mechanism of its action is not clear. In the present study, the association between let-7c and the PI3K/Akt/FoxO signaling pathway, as well as their roles in the development of LIHC were investigated using The Cancer Genome Atlas and various public databases (Tumor-miRNA-Pathway, OncomiR, DIANA-TarBase v8, KOBAS 3.0, ONCOMINE, Kaplan-Meier plotter, LinkedOmics, UALCAN and cBioPortal). The effects of let-7c-5p on PI3K/Akt/FoxO signaling pathway-related target genes were analyzed following overexpression of let-7c-5p in the MHCC-97H cell line via reverse transcription-quantitative PCR, and the let-7c-5p target genes belonging to the PI3K/Akt/FOXO signaling pathway in LIHC were screened out. GO and KEGG enrichment analyses of these target genes was performed using g:Profiler, gOST. In addition, GeneMANIA and Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) databases were used to determine the gene-gene and protein-protein interaction networks, respectively. The data demonstrated that cyclin B2 (CCNB2), cyclin E2 (CCNE2), cyclin dependent kinase 4 (CDK4), homer scaffold protein 1 (HOMER1), heat shock protein 90 α family class A member 1 (HSP90AA1), neuroblastoma RAS viral oncogene homolog (NRAS), protein phosphatase 2 catalytic subunit α (PPP2CA), protein kinase AMP-activated catalytic subunit α2 (PRKAA2) and Rac family small GTPase 1 (RAC1) may be target genes of let-7c-5p. These genes, particularly CCNE2, were associated with poor overall survival and could be promising candidate biomarkers for disease and poor prognosis in LIHC. Among them, seven genes (CCNE2, CDK4, HSP90AA1, NRAS, PPP2CA, PRKAA2 and RAC1) belonged to the PI3K-Akt signaling pathway and four genes (CCNB2, HOMER1, NRAS and PRKAA2) belonged to the FoxO signaling pathway. The majority of these genes were closely associated with the cell cycle and their elevated expression may aggravate cell cycle disorders. Therefore, let-7c may be considered to be an anti-oncogene of LIHC. The present study may provide novel targets and strategies for the diagnosis and treatment of LIHC.

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MiRNA-206 inhibits hepatocellular carcinoma cell proliferation and migration but promotes apoptosis by modulating cMET expression

Cited by 43 publications

References 33 publications

<p>Silencing circZFR inhibits the proliferation, migration and invasion of human renal carcinoma cells by regulating miR-206</p>

<p>Silencing circZFR inhibits the proliferation, migration and invasion of human renal carcinoma cells by regulating miR-206</p>

Roles of Thyroid Hormone-Associated microRNAs Affecting Oxidative Stress in Human Hepatocellular Carcinoma

Effect of let‑7c on the PI3K/Akt/FoxO signaling pathway in hepatocellular carcinoma

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