Effects of hnRNP A2/B1 Knockdown on Inhibition of Glioblastoma Cell Invasion, Growth and Survival

Deng, Jinmu; Chen, Song; Wang, Feng; Zhao, Hongxin; Xie, Zongyi; Xu, Zhongye; Zhang, Qingtao; Liang, Ping; Zhai, Xuan; Yuan, Chao

doi:10.1007/s12035-014-9080-3

Cited by 48 publications

(47 citation statements)

References 41 publications

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“…It was over-expressed in glioma and correlated with advanced glioma grades. Moreover, knockdown of hnRNP A2/B1 reduced glioblastoma cell viability, adhesion, migration, invasion and tumor formation in mice [17,18]. In this study, ␤-asarone inhibited the expression of both hnRNP H1 and hnRNP A2/B1, indicating these two proteins may be served as the candidate targets for the anti-tumor effect of ␤-asarone.…”

Section: Verification Of Differentially Expressed Proteins By Rt-pcrmentioning

confidence: 49%

Proteomic analysis of β-asarone induced cytotoxicity in human glioblastoma U251 cells

Chen

Ning

et al. 2015

Journal of Pharmaceutical and Biomedical Analysis

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Section: Verification Of Differentially Expressed Proteins By Rt-pcrmentioning

confidence: 49%

Proteomic analysis of β-asarone induced cytotoxicity in human glioblastoma U251 cells

Chen

Ning

et al. 2015

Journal of Pharmaceutical and Biomedical Analysis

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“…We previously discovered that the level of HNRNPA2B1 expression is higher in pancreatic cancer than in non-lesion tissue, as are other cancers, such as lung cancer [36], hepatocellular carcinoma [16] and glioblastoma [37]. Based on our study, we chose several pancreatic carcinoma cell lines to simulate different types of pancreatic cancers and generated models of HNRNPA2B1 depletion and overexpression using Crispr/Cas9 genetic technology.…”

Section: Discussionmentioning

confidence: 99%

HNRNPA2B1 regulates the epithelial–mesenchymal transition in pancreatic cancer cells through the ERK/snail signalling pathway

et al. 2017

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BackgroundHeterogeneous nuclear ribonucleoprotein A2B1 (HNRNPA2B1) is closely related to tumour occurrence and development, oncogene expression, apoptosis inhibition and invasion and metastasis capacities. However, its function in the epithelial–mesenchymal transition (EMT) of pancreatic cancer is not fully understood.MethodsBy comparing various wild-type pancreatic cancer cell lines, we determined which have a higher expression level of HNRNPA2B1 accompanied by the higher expression of N-cadherin and vimentin and lower expression of E-cadherin. Therefore, to elucidate the role of HNRNPA2B1 in EMT, we generated models of HNRNPA2B1 knockdown and overexpression in different types of pancreatic cancer cell lines (MIA Paca-2, PANC-1 and Patu-8988) and examined changes in expression of EMT-related factors, including CDH1, CDH2, vimentin and snail.ResultsThe results show that HNRNPA2B1 promotes EMT development by down-regulating E-cadherin and up-regulating N-cadherin and vimentin, and also stimulates the invasion capacity and inhibits viability in human pancreatic cancer cell lines, the similar results in vivo experiments. Moreover, we found that HNRNPA2B1 likely regulates EMT progression in pancreatic carcinoma via the ERK/snail signalling pathway.ConclusionsThe results of this work suggest that HNRNPA2B1 inhibition has potential antitumour effects, which warrants in-depth investigation.

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“…hnRNPA2B1 protein is highly expressed in glioma tissues, correlated with glioma grades and related to poor prognosis [75]. Mechanically, hnRNPA2B1 promotes GBM cell viability, adhesion, migration, invasion, chemoresistance to TMZ and tumorigenecity as well as protects cells from apoptosis and reactive oxygen species (ROS) generation possibly via downregulating tumor suppressors such as cellular FLICE (FADD-like IL-1β-converting enzyme)-inhibitory protein (c-FLIP), bridging integrator 1 (BIN1) and WW domain containing oxidoreductase (WWOX), and upregulating phospho-signal transducer and activator of transcription 3 (p-STAT3), matrix metallopeptidase 2 (MMP-2), and the proto-oncogene RON (also known as macrophage stimulating 1 receptor, MST1R) [74,75]. These results indicate that hnRNPC and hnRNPA2B1 are possible m 6 A readers that contribute to GBM pathogenesis.…”

Section: Hnrnpc and Hnrnpa2b1mentioning

confidence: 99%

The Emerging Roles of RNA Modifications in Glioblastoma

Dong

Cui

2020

Cancers

103

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Glioblastoma (GBM) is a grade IV glioma that is the most malignant brain tumor type. Currently, there are no effective and sufficient therapeutic strategies for its treatment because its pathological mechanism is not fully characterized. With the fast development of the Next Generation Sequencing (NGS) technology, more than 170 kinds of covalent ribonucleic acid (RNA) modifications are found to be extensively present in almost all living organisms and all kinds of RNAs, including ribosomal RNAs (rRNAs), transfer RNAs (tRNAs) and messenger RNAs (mRNAs). RNA modifications are also emerging as important modulators in the regulation of biological processes and pathological progression, and study of the epi-transcriptome has been a new area for researchers to explore their connections with the initiation and progression of cancers. Recently, RNA modifications, especially m6A, and their RNA-modifying proteins (RMPs) such as methyltransferase like 3 (METTL3) and α-ketoglutarate-dependent dioxygenase alkB homolog 5 (ALKBH5), have also emerged as important epigenetic mechanisms for the aggressiveness and malignancy of GBM, especially the pluripotency of glioma stem-like cells (GSCs). Although the current study is just the tip of an iceberg, these new evidences will provide new insights for possible GBM treatments. In this review, we summarize the recent studies about RNA modifications, such as N6-methyladenosine (m6A), N6,2′O-dimethyladenosine (m6Am), 5-methylcytosine (m5C), N1-methyladenosine (m1A), inosine (I) and pseudouridine (ψ) as well as the corresponding RMPs including the writers, erasers and readers that participate in the tumorigenesis and development of GBM, so as to provide some clues for GBM treatment.

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Effects of hnRNP A2/B1 Knockdown on Inhibition of Glioblastoma Cell Invasion, Growth and Survival

Cited by 48 publications

References 41 publications

Proteomic analysis of β-asarone induced cytotoxicity in human glioblastoma U251 cells

Proteomic analysis of β-asarone induced cytotoxicity in human glioblastoma U251 cells

HNRNPA2B1 regulates the epithelial–mesenchymal transition in pancreatic cancer cells through the ERK/snail signalling pathway

The Emerging Roles of RNA Modifications in Glioblastoma

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