MicroRNA-199 suppresses cell proliferation, migration and invasion by downregulating RGS17 in hepatocellular carcinoma

Zhang, Wei; Shen, Qian; Yang, Guowei; Zhu, Liang; Zhou, Bo; Wang, Jianhua; Liu, Rong; Zhang, Yan; Qu, Xu-Dong

doi:10.1016/j.gene.2018.03.053

Cited by 44 publications

(35 citation statements)

References 28 publications

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“…In the network, miR‐199b‐5p, miR‐199b‐3p and miR‐636 had rich external connections. Studies had reported that the miR‐199 family, as a tumor suppressor, inhibited tumor growth and metastasis [39–43]. Our group also found that miR‐199b‐5p suppressed cell proliferation, migration and invasion by down‐regulating DDR1 in PCa (S. H. Zhao, L. M. Luo, X. Qian, Z. G. Zhu, J. M. Wang, Y.…”

Section: Discussionmentioning

confidence: 55%

Identifying the key genes and microRNAs in prostate cancer bone metastasis by bioinformatics analysis

et al. 2020

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Prostate adenocarcinoma (PCa) is the most common cause of death due to malignancy among men, and bone metastasis is the leading cause of mortality in patients with PCa. Therefore, identifying the causes and molecular mechanism of bone metastasis is important for early detection, diagnosis and personalized therapy. In this study, we systematically analyzed molecular correlates of bone metastasis by bioinformatics analysis. A total of 12 differentially expressed microRNAs (miRNAs) and 102 differentially expressed genes were identified. Five miRNAs had prognostic significance in biochemical recurrence‐free survival (miR‐636, miR‐491‐5p, miR‐199b‐5p, miR‐199b‐3p, miR‐28‐3p). The differentially expressed genes were significantly enriched in extracellular matrix, cell‐substrate adhesion, collagen and integrin. Seven hub genes (VCAN, COL3A1, COL1A1, APOE, COL1A2, SDC1, THY1) with worse biochemical recurrence‐free survival and one hub gene (MMP9) with worse overall survival were detected. miR‐636, a novel oncogene, was found to be up‐regulated in bone metastatic PCa tissues and also predominately up‐regulated in human PCa cell lines. miR‐636 promoted cellular invasion and migration, and may promote bone metastasis via targeting MBNL2, TNS1 and STAB1. In conclusion, we have successfully defined molecular signatures of bone metastasis in PCa.

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Section: Discussionmentioning

confidence: 55%

Identifying the key genes and microRNAs in prostate cancer bone metastasis by bioinformatics analysis

et al. 2020

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“…For instance, a microarray showed that miR-384 was down-regulated in laryngeal carcinoma [25]. Another research implies mir-384 might play an important role in metastasis of melanoma by binding to the 3′UTR of HDAC3 [26]. Recently, it was reported that miR-384 exerted tumor-suppressive functions by binding to the 3′UTR of PIWIL4 in glioma [27].…”

Section: Discussionmentioning

confidence: 99%

MiR-384 inhibits the proliferation of colorectal cancer by targeting AKT3

et al. 2018

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BackgroundGrowing evidence suggests that MiRNAs play essential roles in the initiation and progression of colorectal cancer (CRC). The aberrant expression of miR-384 has been reported in some cancers. However, the role and mechanism of miR-384 in CRC proliferation remains unknown.MethodsThe expression of miR-384 was detected in CRC and their paired normal tissues by real-time PCR. In vivo and in vitro assays were conducted to confirm the role of miR-384 in the proliferation of CRC. Bioinformatics analysis, luciferase reporter assays, western blot and in vitro assays were used to confirm that AKT3 was the target gene of miR-384. Finally, Spearman’s correlation analyses was carried out to analyze the relationship between miR-384 expression and AKT3 expression in CRC.ResultsMiR-384 was down‑regulated in CRC tissues. The in vivo and vitro functional assays verified that the ectopic upregulation of miR-384 inhibited the proliferation of CRC and the inhibition of miR-384 promoted the proliferation of CRC. Bioinformatics analysis, luciferase reporter assays, western blot and in vitro functional assays confirmed AKT3 as the target gene of miR-384. The expression of miR-384 was negatively correlated with the expressions of AKT3.ConclusionOur study verified that miR-384 could significantly suppress the proliferation of CRC by directing targeting AKT3.Electronic supplementary materialThe online version of this article (10.1186/s12935-018-0628-6) contains supplementary material, which is available to authorized users.

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“…For example, miR-1468 promoted HCC development via activating AKT signaling [13]. Additionally, miR-199 acted as a tumor suppressor in HCC by down-regulating the expression of regulators of G-protein signaling 17 [14]. To get a whole picture of the expression of miRNAs in HCC, we performed miRNA-seq to screen the miRNAs with aberrant expression in HCC tissues compared with that of corresponding normal tissues.…”

Section: Introductionmentioning

confidence: 99%

MiR-505 suppressed the growth of hepatocellular carcinoma cells via targeting IGF-1R

et al. 2019

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Hepatocellular carcinoma (HCC) is one of the most common cancers globally. An increasing body of evidence has demonstrated the critical function of microRNAs (miRNAs) in the initiation and progression of human cancers. Here, we showed that miR-505 was down-regulated in HCC tissues and cell lines. Reduced expression of miR-505 was significantly correlated with the worse prognosis of HCC patients. Overexpression of miR-505 suppressed the proliferation, colony formation and induced apoptosis of both HepG2 and Huh7 cells. Further mechanism study uncovered that miR-505 bound the 3′-untranslated region (3′-UTR) of the insulin growth factor receptor (IGF-1R) and inhibited the expression of IGF-1R in HCC cells. The down-regulation of IGF-1R by miR-505 further suppressed the phosphorylation of AKT at the amino acid S473. Consistently, the abundance of glucose transporter (GLUT) 1 (GLUT1) was reduced with the overexpression of miR-505. Down-regulation of GLUT1 by miR-505 consequently attenuated the glucose uptake, lactate production and ATP generation of HCC cells. Collectively, our results demonstrated the tumor suppressive function of miR-505 possibly via inhibiting the glycolysis of HCC cells. These findings suggested miR-505 as an interesting target for designing anti-cancer strategy in HCC.

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MicroRNA-199 suppresses cell proliferation, migration and invasion by downregulating RGS17 in hepatocellular carcinoma

Cited by 44 publications

References 28 publications

Identifying the key genes and microRNAs in prostate cancer bone metastasis by bioinformatics analysis

Identifying the key genes and microRNAs in prostate cancer bone metastasis by bioinformatics analysis

MiR-384 inhibits the proliferation of colorectal cancer by targeting AKT3

MiR-505 suppressed the growth of hepatocellular carcinoma cells via targeting IGF-1R

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