SF3B4 is regulated by microRNA-133b and promotes cell proliferation and metastasis in hepatocellular carcinoma

Liu, Zhiyong; Li, Wei; Pang, Yanan; Zhou, Zaixin; Liu, Shupeng; Cheng, Kai; Qin, Qin; Yin, Jianfei; Liu, Shanrong

doi:10.1016/j.ebiom.2018.10.067

Cited by 40 publications

(40 citation statements)

References 37 publications

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“…Accumulating evidence indicates that miR expression reflects the physiological and pathological alterations in patients with cancer . Numerous studies have identified key miRs that are directly involved in cell proliferation, migration, invasion and metastasis in CRC …”

Section: Introductionmentioning

confidence: 99%

“…12 Numerous studies have identified key miRs that are directly involved in cell proliferation, migration, invasion and metastasis in CRC. 13,14 In our study, the vital role of VPS33B in vitro and in vivo was explored in CRC. We found VPS33B could interact with potential tumor suppressor NESG1 to suppress cell proliferation, invasion, migration, intrahepatic metastasis and increase sensitivity to cisplatin (DDP) via regulating the EGFR/RAS/ERK/c-Myc/p53/miR-133a-3p feedback loop.…”

Section: Introductionmentioning

confidence: 99%

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VPS33B negatively modulated by nicotine functions as a tumor suppressor in colorectal cancer

Chen

Liu

Wang

et al. 2019

Intl Journal of Cancer

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The biological role of vacuolar protein sorting 33B (VPS33B) has not been examined in colorectal cancer (CRC). We report that VPS33B was downregulated in dextran sulfate sodium/azoxymethane (DSS/AOM) ‐induced CRC mice models and nicotine‐treated CRC cells via the PI3K/AKT/c‐Jun pathway. Reduced VPS33B is an unfavorable factor promoting poor prognosis in human CRC patients. VPS33B overexpression suppressed CRC proliferation, intrahepatic metastasis and chemoresistance of cisplatin (DDP) in vivo and in vitro through modulating the epidermal growth factor receptor (EGFR)/RAS/ERK/c‐Myc/p53/miR‐133a‐3p feedback loop and the downstream cell cycle or EMT‐related factors. Furthermore, NESG1 as a newly identified tumor suppressor interacted with VPS33B via colocalization in the cytoplasm, and it was stimulated by VPS33B through the downregulation of RAS/ERK/c‐Jun‐mediated transcription. NESG1 also activated VPS33B expression via the RAS/ERK/c‐Jun pathway. Suppression of NESG1 increased cell growth, migration and invasion via the reversion of the VPS33B‐modulating signal in VPS33B‐overexpressed cells. Taken together, VPS33B as a tumor suppressor is easily dysregulated by chemical carcinogens and it interacts with NESG1 to modulate the EGFR/RAS/ERK/c‐Myc/p53/miR‐133a‐3p feedback loop and thus suppress the malignant phenotype of CRC.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

VPS33B negatively modulated by nicotine functions as a tumor suppressor in colorectal cancer

Chen

Liu

Wang

et al. 2019

Intl Journal of Cancer

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“…HCC carcinogenesis is a complex pathological process which associated with speci c tumor genes, multiple signaling cascades as well as epigenetic modi cations [22,23]. In recent years, bioinformatics analyses have been widely used to identify novel diagnostic markers and therapeutic targets for many cancers [24,25], which provide helpful tools for tumor researches.…”

Section: Discussionmentioning

confidence: 99%

Identification of Key Genes and Evaluation of Their Prognosis Potential in Hepatocellular Carcinoma by Integrated Bioinformatics Analysis

Liu

et al. 2020

Preprint

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Abstract Background Hepatocellular carcinoma (HCC) is a malignancy causing highly death rate in the world. Despite the development of treatment strategies for HCC, prognosis of this malignancy remains unsatisfactory. In this study, we aimed to identify the target genes associated with the prognosis of HCC patients. Methods Three expression profiles of HCC tissues were extracted from the Gene Expression Omnibus database to explore the differentially expressed genes (DEGs) using GEO2R method. Functional enrichment analysis was performed to reveal the biological characteristics of DEGs. Protein-protein interaction (PPI) network was constructed using Cytoscape software. The survival curve of identified DEGs were tested by Kaplan-Meier analysis. Results We identified 15 DEGs (CYP39A1, CYR61, FOS, FOXO1, GADD45B, ID1, IL1RAP, MT1M, PHLDA1, RND3, SDS, SOCS2, TAT, S100P, and SPINK1) in HCC tissues. Prognosis analysis showed that 4 DEGs (FOXO1,SPINK1༌SOCS2, and TAT) correlated with overall survival time of HCC patients, which might serve as therapeutic targets for HCC patients. Conclusions By integrated bioinformatics analysis, we proposed a novel way to reveal key genes that closely relate to HCC development.

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“…Chen et al (2018) demonstrated that miR-590-5p inhibited HCC chemoresistance by targeting yes-associated protein 1 (YAP1). MiR-133b promotes cell proliferation and metastasis in HCC by regulating splicing factor 3b subunit 4 (SF3B4) (Liu et al, 2018b). MiR-3650 suppresses HCC migration and epithelial-mesenchymal transition (EMT) by directly targeting neurofascin (Wu et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

Downregulation of miR-193a-3p is involved in the pathogenesis of hepatocellular carcinoma by targeting CCND1

Wang

Huang

et al. 2020

PeerJ

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Background Hepatocellular carcinoma (HCC) is the second-highest cause of malignancy-related death worldwide, and many physiological and pathological processes, including cancer, are regulated by microRNAs (miRNAs). miR-193a-3p is an anti-oncogene that plays an important part in health and disease biology by interacting with specific targets and signals. Methods In vitro assays were performed to explore the influences of miR-193a-3p on the propagation and apoptosis of HCC cells. The sequencing data for HCC were obtained from The Cancer Genome Atlas (TCGA), and the expression levels of miR-193a-3p in HCC and non-HCC tissues were calculated. The differential expression of miR-193a-3p in HCC was presented as standardized mean difference (SMD) with 95% confidence intervals (CIs) in Stata SE. The impact of miR-193a-3p on the prognoses of HCC patients was determined by survival analysis. The potential targets of miR-193a-3p were then predicted using miRWalk 2.0 and subjected to enrichment analyses, including Gene Ontology (GO) annotation, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, and Protein-Protein Interaction (PPI) network analysis. The interaction between miR-193a-3p and one predicted target, Cyclin D1 (CCND1), was verified by dual luciferase reporter assays and Pearson correlation analysis. Results MiR-193a-3p inhibited the propagation and facilitated the apoptosis of HCC cells in vitro. The pooled SMD indicated that miR-193a-3p had a low level of expression in HCC (SMD: −0.88, 95% CI [−2.36 −0.59]). Also, HCC patients with a higher level of miR-193a-3p expression tended to have a favorable overall survival (OS: HR = 0.7, 95% CI [0.43–1.13], P = 0.14). For the KEGG pathway analysis, the most related pathway was “proteoglycans in cancer”, while the most enriched GO term was “protein binding”. The dual luciferase reporter assays demonstrated the direct interaction between miR-193a-3p and CCND1, and the Pearson correlation analysis suggested that miR-193a-3p was negatively correlated with CCND1 in HCC tissues (R = − 0.154, P = 0.002). Conclusion miR-193a-3p could suppress proliferation and promote apoptosis by targeting CCND1 in HCC cells. Further, miR-193a-3p can be used as a promising biomarker for the diagnosis and treatment of HCC in the future.

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SF3B4 is regulated by microRNA-133b and promotes cell proliferation and metastasis in hepatocellular carcinoma

Cited by 40 publications

References 37 publications

VPS33B negatively modulated by nicotine functions as a tumor suppressor in colorectal cancer

VPS33B negatively modulated by nicotine functions as a tumor suppressor in colorectal cancer

Identification of Key Genes and Evaluation of Their Prognosis Potential in Hepatocellular Carcinoma by Integrated Bioinformatics Analysis

Downregulation of miR-193a-3p is involved in the pathogenesis of hepatocellular carcinoma by targeting CCND1

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