MicroRNA-212-3p inhibits the Proliferation and Invasion of Human Hepatocellular Carcinoma Cells by Suppressing CTGF expression

Chen, Jianqing; Ou, Yang-liu; Huang, Zhiping; Hong, Yong‐Gang; Tao, Yuan‐Ping; Wang, Zhenguang; Ni, Jingwei; Hao, Liqiang; Lin, Hui

doi:10.1038/s41598-019-46088-w

Cited by 25 publications

(24 citation statements)

References 30 publications

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“…Moreover, we found that miR-195/497 cluster decreased the formation of regulatory transcription complex containing Yap and Smad3, while decreasing their common target genes, such as the gene-encoding CTGF ( Luo, 2017 ). Various studies have revealed that CTGF is critical in cancer progression and initiation ( Chen et al, 2019 ; Pu et al, 2019 ; Zhou et al, 2020 ).…”

Section: Discussionmentioning

confidence: 99%

Silencing of lncRNA MIR497HG via CRISPR/Cas13d Induces Bladder Cancer Progression Through Promoting the Crosstalk Between Hippo/Yap and TGF-β/Smad Signaling

Zhuang

Liu

et al. 2020

Front. Mol. Biosci.

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A subset of long non-coding RNAs (lncRNAs), categorized as miRNA-host gene lncRNAs (lnc-miRHGs), is processed to produce miRNAs and involved in cancer progression. This work aimed to investigate the influences and the molecular mechanisms of lnc-miRHGs MIR497HG in bladder cancer (BCa). The miR-497 and miR-195 were derived from MIR497HG. We identified that lnc-miRHG MIR497HG and two harbored miRNAs, miR-497 and miR-195, were downregulated in BCa by analyzing The Cancer Genome Atlas and our dataset. Silencing of MIR497HG by CRISPR/Cas13d in BCa cell line 5637 promoted cell growth, migration, and invasion in vitro. Conversely, overexpression of MIR497HG suppressed cell progression in BCa cell line T24. MiR-497/miR-195 mimics rescued significantly the oncogenic roles of knockdown of MIR497HG by CRISPR/Cas13d in BCa. Mechanistically, miR-497 and miR-195 co-ordinately suppressed multiple key components in Hippo/Yap and transforming growth factor β signaling and particularly attenuated the interaction between Yap and Smad3. In addition, E2F4 was proven to be critical for silencing MIR497HG transcription in BCa cells. In short, we propose for the first time to reveal the function and mechanisms of MIR497HG in BCa. Blocking the pathological process may be a potential strategy for the treatment of BCa.

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Section: Discussionmentioning

confidence: 99%

Silencing of lncRNA MIR497HG via CRISPR/Cas13d Induces Bladder Cancer Progression Through Promoting the Crosstalk Between Hippo/Yap and TGF-β/Smad Signaling

Zhuang

Liu

et al. 2020

Front. Mol. Biosci.

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“…However, the effects, if any, in HCC remained unclear. Thus, Chen et al (2019) examined the relationship between miRNA-212-3p and CCN2 in the hepatic TME. The authors showed that microRNA-212-3p inhibited proliferation of HCC cell lines through suppression of CCN2.…”

Section: Micro-rna Involvement In Hsc Activation In the Hepatic Tmementioning

confidence: 99%

Hepatic Stellate Cells and Hepatocarcinogenesis

Barry

Baldeosingh

Lamm

et al. 2020

Front. Cell Dev. Biol.

112

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Hepatic stellate cells (HSCs) are a significant component of the hepatocellular carcinoma (HCC) tumor microenvironment (TME). Activated HSCs transform into myofibroblastlike cells to promote fibrosis in response to liver injury or chronic inflammation, leading to cirrhosis and HCC. The hepatic TME is comprised of cellular components, including activated HSCs, tumor-associated macrophages, endothelial cells, immune cells, and non-cellular components, such as growth factors, proteolytic enzymes and their inhibitors, and other extracellular matrix (ECM) proteins. Interactions between HCC cells and their microenvironment have become topics under active investigation. These interactions within the hepatic TME have the potential to drive carcinogenesis and create challenges in generating effective therapies. Current studies reveal potential mechanisms through which activated HSCs drive hepatocarcinogenesis utilizing matricellular proteins and paracrine crosstalk within the TME. Since activated HSCs are primary secretors of ECM proteins during liver injury and inflammation, they help promote fibrogenesis, infiltrate the HCC stroma, and contribute to HCC development. In this review, we examine several recent studies revealing the roles of HSCs and their clinical implications in the development of fibrosis and cirrhosis within the hepatic TME.

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“…For involvement of specific regulatory elements in the CCN2 gene we refer to Leask et al ( 2009 ). Furthermore, CCN2 expression can be regulated at the posttranscriptional and posttranslational level by various factors, including VEGF (Kondo et al 2006 ), hypoxia (Kondo et al 2002 ), tumor necrosis factor α (TNF-α), interferon gamma (IFN-γ) (Cooker et al 2007 ; Laug et al 2012 ), and a host of different microRNAs (miRNAs) (Cai et al 2018 ; Che et al 2019 ; Chen et al 2016 , 2019 ; Ernst et al 2010 ; Fox et al 2013 ; He et al 2017 ; Mu et al 2016 ; Qiao et al 2017 ; Sun et al 2016 ). For example, CCN2 and miRNA-21 are components of a positive feedback loop in pancreatic stellate cells, that may serve as an amplification mechanism for enhanced collagen production (Charrier et al 2014a ).…”

Section: Introductionmentioning

confidence: 99%

CCN2 (Cellular Communication Network factor 2) in the bone marrow microenvironment, normal and malignant hematopoiesis

Leguit

Raymakers²,

Hebeda

et al. 2021

J. Cell Commun. Signal.

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CCN2, formerly termed Connective Tissue Growth Factor, is a protein belonging to the Cellular Communication Network (CCN)-family of secreted extracellular matrix-associated proteins. As a matricellular protein it is mainly considered to be active as a modifier of signaling activity of several different signaling pathways and as an orchestrator of their cross-talk. Furthermore, CCN2 and its fragments have been implicated in the regulation of a multitude of biological processes, including cell proliferation, differentiation, adhesion, migration, cell survival, apoptosis and the production of extracellular matrix products, as well as in more complex processes such as embryonic development, angiogenesis, chondrogenesis, osteogenesis, fibrosis, mechanotransduction and inflammation. Its function is complex and context dependent, depending on cell type, state of differentiation and microenvironmental context. CCN2 plays a role in many diseases, especially those associated with fibrosis, but has also been implicated in many different forms of cancer. In the bone marrow (BM), CCN2 is highly expressed in mesenchymal stem/stromal cells (MSCs). CCN2 is important for MSC function, supporting its proliferation, migration and differentiation. In addition, stromal CCN2 supports the maintenance and longtime survival of hematopoietic stem cells, and in the presence of interleukin 7, stimulates the differentiation of pro-B lymphocytes into pre-B lymphocytes. Overexpression of CCN2 is seen in the majority of B-acute lymphoblastic leukemias, especially in certain cytogenetic subgroups associated with poor outcome. In acute myeloid leukemia, CCN2 expression is increased in MSCs, which has been associated with leukemic engraftment in vivo. In this review, the complex function of CCN2 in the BM microenvironment and in normal as well as malignant hematopoiesis is discussed. In addition, an overview is given of data on the remaining CCN family members regarding normal and malignant hematopoiesis, having many similarities and some differences in their function.

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MicroRNA-212-3p inhibits the Proliferation and Invasion of Human Hepatocellular Carcinoma Cells by Suppressing CTGF expression

Cited by 25 publications

References 30 publications

Silencing of lncRNA MIR497HG via CRISPR/Cas13d Induces Bladder Cancer Progression Through Promoting the Crosstalk Between Hippo/Yap and TGF-β/Smad Signaling

Silencing of lncRNA MIR497HG via CRISPR/Cas13d Induces Bladder Cancer Progression Through Promoting the Crosstalk Between Hippo/Yap and TGF-β/Smad Signaling

Hepatic Stellate Cells and Hepatocarcinogenesis

CCN2 (Cellular Communication Network factor 2) in the bone marrow microenvironment, normal and malignant hematopoiesis

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