MicroRNA‑30a suppresses the proliferation, migration and invasion of human renal cell carcinoma cells by directly targeting ADAM9

Jiang, Lining; Liu, Yabin; Ma, Chen

doi:10.3892/ol.2018.8999

Cited by 11 publications

(13 citation statements)

References 41 publications

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“…Interestingly, HIF-P4H-3 expression seems to be a favorable prognostic marker for patients with HCC [102] since its downregulation in HCC was associated with more aggressive tumor behavior and poor prognosis [103]. Altogether, the mechanisms involved in the progression of fatty liver diseases to fibrosis/cirrhosis/HCC are many and involve not only the HIF system but also the crosstalk with various other signaling pathways.…”

Section: Hypoxia Hifs and Hif-p4h In Liver Fibrosis/cirrhosis/hccmentioning

confidence: 99%

Hypoxia-Inducible Factor Prolyl 4-Hydroxylases and Metabolism

Koivunen

Kietzmann

2018

Trends in Molecular Medicine

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Hypoxia-inducible factor prolyl 4-hydroxylases (HIF-P4Hs, also known as PHDs or EglNs) are enzymes that act as cellular oxygen sensors. Inhibition of HIF-P4Hs leads to stabilization of hypoxiainducible transcription factors (HIFs) which initiate a gene expression program that allows to cope with low oxygen levels and to restore tissue oxygenation. This involves for example upregulation of erythropoiesis and angiogenesis, modulation of inflammatory responses and reprogramming of metabolism. Currently, several pharmacological HIF-P4H inhibitors are in clinical trials mainly for renal anemia. However, recent data suggest that HIF-P4H inhibitors could also be considered to treat metabolic disorders. Here we will discuss the potential of targeting HIF-P4Hs and the HIF pathway for the treatment of obesity, metabolic syndrome, atherosclerosis and fatty liver diseases. Highlights Inhibition of HIF-P4Hs, which act as molecular oxygen sensors, is the so far best understood mechanism to regulate the oxygen sensing pathway. Several HIF-P4H inhibitors are currently in phase 3 randomized clinical trials for treatment of renal anemia with no reported serious side effects until now. Recent data from preclinical, clinical and epidemiological studies support that besides anemia activation of the hypoxia response via HIF-P4H inhibition is a powerful tool to regulate metabolism and may be beneficial for conditions such as obesity, metabolic syndrome, T2D, NAFLD/NASH or liver fibrosis.

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Section: Hypoxia Hifs and Hif-p4h In Liver Fibrosis/cirrhosis/hccmentioning

confidence: 99%

Hypoxia-Inducible Factor Prolyl 4-Hydroxylases and Metabolism

Koivunen

Kietzmann

2018

Trends in Molecular Medicine

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“…Studies profiling miRNAs have noted the dysregulation of many miRNAs in ccRCC, for example, miR‐215, 17 miR‐200, 18 miR‐708, 19 miR‐199a 20 and miR‐30a, which have been reported to regulate growth, invasion and migration of ccRCC cells. Among them, miR‐30a has been proved to function as a putative tumour suppressor in ccRCC 21 . Studies have revealed that miR‐30a‐5p inhibits ccRCC aggressiveness through repression of zinc finger E‐box binding homeobox 2 (ZEB2) 22 and GRP78, 23 and miR‐30a‐3p has also been reported to suppress cellular invasion and metastasis of ccRCC via targeting autophagy related 12 (ATG12) 24 and Wnt family member 2 (WNT2) 25 .…”

Section: Introductionmentioning

confidence: 99%

SNHG12 promotes carcinogenesis of human renal cell cancer via functioning as a competing endogenous RNA and sponging miR‐30a‐3p

Liu

Zhang

et al. 2021

J Cellular Molecular Medi

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Small nucleolar RNA host gene 12 (SNHG12) has been indicated in the tumorigenesis of various human cancers, including clear cell renal cell carcinoma (ccRCC). However, the underlying mechanisms of SNHG12 driving progression of ccRCC remain incompletely understood. In the present study, we discovered that SNHG12 is up‐regulated in ccRCC and that overexpression of SNHG12 predicted poor clinical outcome of ccRCC patients. SNHG12 knockdown notably inhibited proliferation and migration of RCC cells. Furthermore, we discovered that miR‐30a‐3p, a putative ccRCC inhibitor, was competitively sponged by SNHG12. Via the crosstalk network, SNHG12 was capable of up‐regulating multiple target genes of miR‐30a‐3p, namely, RUNX2, WNT2 and IGF‐1R, which have been identified to facilitate tumorigenesis of ccRCC. Taken together, our present study suggested a novel ceRNA network, in which SNHG12 could promote the malignancy of ccRCC although competitively binding with miR‐30a‐3p and consequently release the expression of its downstream cancer‐related genes.

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“…Several miRNAs have been identi ed to participate in some important biological and pathological processes of ccRCC 15 . For instance, miR-182 16 , miR-30a 17 and miR-200c-3p 18 act as tumor suppressors to inhibit the progression of ccRCC by respectively targeting IGF1R, ADAM9 and SLC6A1, while miR-654 19 and miR-543 20 facilitate ccRCC cell proliferation and metastasis by targeting GK5 and Krüppel-like factor 6 (KLF-6), respectively. Generally speaking, miR-129-5p is considered to be a tumor suppressor and is down-regulated in prostate cancer (PC) 21 , bladder cancer (BC) 22 , etc.…”

Section: Discussionmentioning

confidence: 99%

miR-129-5p inhibits clear cell renal cell carcinoma cell proliferation, migration and invasion by targeting SPN

Gao

Wang

Zhang

et al. 2021

Preprint

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Objective: Our study aims to investigate the mechanism of the miR-129-5p/SPN axis in clear cell renal cell carcinoma (ccRCC), providing a novel direction for the targeted therapy of ccRCC. Methods: Bioinformatics methods were implemented to find the differentially expressed genes (DEGs) associated with ccRCC from TCGA database. qRT-PCR was performed to detect miR-129-5p and SPN mRNA expression, while western bot was carried out for the detection of protein expression of SPN. Bioinformatics analysis was used to predict the binding sites of miR-129-5p on SPN 3’UTR, while dual-luciferase assay was conducted to verify their binding relationship. CCK-8 assay, colony formation assay, wound healing assay and Transwell assay were employed to measure ccRCC cell proliferative ability, cell formation ability, cell migratory and invasive abilities. Flow cytometry was implemented to assess cell cycle and apoptosis. Results: miR-129-5p exhibited a significantly down-regulated expression level in ccRCC, while SPN showed a remarkably up-regulated expression level. Overexpressed miR-129-5p inhibited ccRCC cell proliferative, invasive and migratory capacities while induced cell cycle arrest in G0/G1 phase and promoted cell apoptosis. Dual-luciferase assay confirmed that there was a binding relationship between miR-129-5p and SPN. Moreover, overexpressed miR-129-5p remarkably reduced SPN expression in cancer cells, weakened the promoting effect of SPN on cell proliferation, migration, invasion and cell cycle progress, and led to enhanced cell apoptotic activity.Conclusion: Our study proves the regulatory effect of the miR-129-5p/SPN axis in ccRCC, and provides a novel potential target for precise treatment of patients with ccRCC.

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MicroRNA‑30a suppresses the proliferation, migration and invasion of human renal cell carcinoma cells by directly targeting ADAM9

Cited by 11 publications

References 41 publications

Hypoxia-Inducible Factor Prolyl 4-Hydroxylases and Metabolism

Hypoxia-Inducible Factor Prolyl 4-Hydroxylases and Metabolism

SNHG12 promotes carcinogenesis of human renal cell cancer via functioning as a competing endogenous RNA and sponging miR‐30a‐3p

miR-129-5p inhibits clear cell renal cell carcinoma cell proliferation, migration and invasion by targeting SPN

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