MiR-30a-5p promotes cholangiocarcinoma cell proliferation through targeting SOCS3

Zhang, Jia Wei; Wang, Xing; Li, Gao Chao; Wang, Dong; Han, Song; Zhang, Yao Dong; Luo, Chen; Wang, Hong Wei; Jiang, Wang Jie; Li, Chang Xian; Li, Xiangcheng

doi:10.7150/jca.41437

Cited by 36 publications

(24 citation statements)

References 28 publications

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“…In several studies, BCL2 has been reported to act as a target gene of multiple miRNAs, including miR‐153, miR‐136 and miR‐365 . BCL2 has also been elucidated to be a target gene of miR‐15b in condylar hyperplasia and liver cancer . miR‐15b has been shown to play a role in the development of multidrug resistance in gastric cancer cells, at least in part by modulation of apoptosis via targeting BCL2 .…”

Section: Discussionmentioning

confidence: 99%

miR‐15b enhances the proliferation and migration of lung adenocarcinoma by targeting BCL2

et al. 2020

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Background: Lung adenocarcinoma (LUAD) is a subtype of lung cancer (LC), which is the most common tumor worldwide. Accumulating evidence has elucidated an important role of microRNAs (miRNAs) in mediating the development and progression of several tumors. The purpose of this study was to explore the role and underlying mechanism of miR-15b in LUAD. Methods: CCK-8 and Transwell assays were conducted to measure the capacities of cell viability and migration in SPC-A1 cells. Luciferase assay was utilized to verifymiR-15b direct binding to BCL2 mRNA 3 0 -UTR. Results: We determined that miR-15b was overexpressed in LUAD and miR-15b overexpression predicted a significantly worse outcome in patients with LUAD. miR-15b improved LUAD growth in vitro and vivo. miR-15b enhanced cell migration and epithelial-mesenchymal transition (EMT) in LUAD. miR-15b promoted cell viability, migration and EMT through inhibiting BCL2 expression by targeting to its mRNA 3 0 -UTR. BCL2 reversed functions of miR-15b on promoting cell proliferation, migration and EMT in SPC-A1 cells. Conclusions: miR-15b promoted cell viability, migration and EMT by targeting BCL2 in LUAD. The newly identified miR-15b/BCL2 axis provides a novel insight into the pathogenesis of LUAD.

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Section: Discussionmentioning

confidence: 99%

miR‐15b enhances the proliferation and migration of lung adenocarcinoma by targeting BCL2

et al. 2020

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“…Therefore, miRNAs may be used as tumor suppressor genes to regulate the pathophysiological process of CAA. On the contrary, Zhang et al have found that the expression of miR-30a-5p was increased in both CCA tissues and cells, and it could promote the proliferation of CCA cells by inhibiting SOCS3 [ 28 ]. The mechanisms of the above studies all focused on that miRNAs can inhibit, attenuate, or eliminate the expression of downstream genes.…”

Section: Discussionmentioning

confidence: 99%

Novel miRNA Predicts Survival and Prognosis of Cholangiocarcinoma Based on RNA-seq Data and In Vitro Experiments

Yao

Jiao

Liu

et al. 2020

BioMed Research International

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Accumulating evidence has demonstrated that microRNAs (miRNAs or miRs) play an important role in the diagnosis and prognosis of tumors. In the case of cholangiocarcinoma (CCA), miRNAs may serve as potential tumor biomarkers and therapeutic targets. Based on The Cancer Genome Atlas (TCGA) database, fold change >2 was used to screen out miRNAs with differential expression in patients with CCA. Univariate and multivariate Cox regression analyses identified miR-3913-5p as an independent prognostic factor in patients with CCA. Overall survival and progression-free survival of patients with CCA were analyzed based on clinical data from TCGA database. In addition, four datasets were combined to identify 21 possible target genes of miR-3913, and Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses were conducted to predict potential pathways and functions of the molecular target genes. Subsequently, the miRNAs associated with survival were selected to build the miRNA-mRNA expression network. Furthermore, the differential expression of miR-3913-5p in CCA cells and normal bile duct epithelial cells was confirmed through in vitro experiments. The possible target genes (RNF24 and SIGLEC) were further screened by reverse transcription-quantitative PCR. In addition, functional experiments showed that miR-3913-5p might be an oncogene that affects the proliferation and migration of CCA cells by inhibiting and mimicking miR-3913-5p. Therefore, miR-3913 may serve as a biomarker for the diagnosis and prognosis of patients with CCA.

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“…miRNA is involved in the pathophysiological process in many diseases by negative regulation of target genes [15].To found the potential target gene of miR-27a-3p in CCA, we used two independent algorithms, TargetScan (www.targetscan.org/), and mirbase (www.mirbase.org/), and found that ING5 could be a potential gene of miR-27a-3p target (Fig. 4A).…”

Section: Ing5 Directly Target Mir-27a-3pmentioning

confidence: 99%

miR-27a-3p attenuates induce autophagy-related cell death by suppressing Inhibitor of growth family 5 in cholangiocarcinoma

Zhang

Kang

et al. 2020

Preprint

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Background MicroRNAs (miRNAs) are abnormally expressed in human tumors, including cholangiocarcinoma (CCA). miR-27a-3p was observed up-regulated in CCA, but its functions in CCA are largely unknown.Methods CCK8 assay, Colony formation assays and Ki-67 staining was employed to detect the cell growth. The autophagy and proliferation relative-protein analyzed by western blot. The immunofluorescence staining was applied to analyze the expression level of LC3 I/II. Tumor xenografts was used to test the role of miR-27a-3p. Luciferase reporter assay, western bolt and qRT-PCR showed the relationship between miR-27a-3p and ING5.Results miR-27a-3p expression was increased in human CCA tissues. Inhibition of miR-27a-3p suppressed the proliferative capacity of CCA cells, silencing of miR-27a-3p dramatically induced cell death and suppressed tumor growth in vivo. The proteins, such as Beclin-1, p62, p21, p-p53, CDK4 and CDK6, were decreased upon miR-27a-3p inhibitor transfection. Western blot assay and immunofluorescence analysis were showed the induced-autophagy after transfecting with miR-27a-3p or inhibitor of growth family 5 (ING5) in RBE. ING5 as a direct miR-27a-3p target in CCA. Co-transfect of miR-27a-3p and ING5 can reverse CCA cell death which induced by miR-27a-3p inhibitor alone.Conclusions miR-27a-3p promotes oncogenesis of CCA by triggering autophagy-related cell death by interacting with ING5 directly.

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MiR-30a-5p promotes cholangiocarcinoma cell proliferation through targeting SOCS3

Cited by 36 publications

References 28 publications

miR‐15b enhances the proliferation and migration of lung adenocarcinoma by targeting BCL2

miR‐15b enhances the proliferation and migration of lung adenocarcinoma by targeting BCL2

Novel miRNA Predicts Survival and Prognosis of Cholangiocarcinoma Based on RNA-seq Data and In Vitro Experiments

miR-27a-3p attenuates induce autophagy-related cell death by suppressing Inhibitor of growth family 5 in cholangiocarcinoma

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