Effect of hnRNPA2/B1 on the proliferation and apoptosis of glioma U251 cells via the regulation of AKT and STAT3 pathways

Yin, Daixia; Kong, Cheng; Chen, Muhu

doi:10.1042/bsr20190318

Cited by 16 publications

(11 citation statements)

References 39 publications

(42 reference statements)

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“…While hnRNPA1 and hnRNPA2/B1 have been widely studied, studies on hnRNPA0 and hnRNPA3 are limited. Notably, hnRNPAB and its subgroups are closely associated with malignant biological behaviors such as proliferation and apoptosis reduction, as well as poor patient prognosis in various cancer types (16)(17)(18)(19)(20)(21). Our previous study confirmed the upregulation of hnRNPAB expression in CRC tissues compared with adjacent tissues, which was closely associated with poor prognosis (21).…”

Section: Microrna-8063 Targets Heterogeneous Nuclear Ribonucleoprotein Ab To Inhibit the Self-renewal Of Colorectal Cancer Stem Cells Viamentioning

confidence: 55%

MicroRNA‑8063 targets heterogeneous nuclear ribonucleoprotein AB to inhibit the self‑renewal of colorectal cancer stem cells via the Wnt/β‑catenin pathway

et al. 2021

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The presence of cancer stem cells (CSCs) is a major cause of therapeutic failure in a variety of cancer types, including colorectal cancer (CRC). However, the underlying mechanisms that regulate the self-renewal of colorectal cancer stem cells (CRCSCs) remain unclear. Our previous study utilized CRCSCs and their parent cells; through gene microarray screening and bioinformatics analysis, we hypothesized that microRNA (miR)-8063 may bind to, and regulate the expression of, heterogeneous nuclear ribonucleoprotein AB (hnRNPAB) to facilitate the regulation of CRCSC self-renewal. The aim of the present study was to confirm this conjecture through relevant experiments. The results indicated that compared with that in parent cells, miR-8063 expression was significantly downregulated in CRCSCs, while hnRNPAB expression was increased. Furthermore, hnRNPAB was identified as a direct target of miR-8063 using a dual-Luciferase assay. Overexpression of hnRNPAB promoted the acquisition of CSC characteristics in CRC cells (increased colony formation ability, enhanced tumorigenicity, and upregulated expression of CSC markers), as well as the upregulation of key proteins (Wnt3a, Wnt5a and β-catenin) in the Wnt/β-catenin signaling pathway. Similarly, after silencing miR-8063 in CRC cells, the characteristics of CSC were altered, and the expression of hnRNPAB protein was promoted. However, post overexpression of miR-8063 in CRCSCs, the self-renewal ability of CSCs was weakened with the downregulation of hnRNPAB protein, Wnt3a, Wnt5a and β-catenin. These results suggest that as a tumor suppressor, miR-8063 is involved in regulating the self-renewal of CRCSCs, where loss of miR-8063 expression weakens its inhibition on hnRNPAB, which leads to the activation of Wnt/β-catenin signaling to promote the self-renewal of CRCSCs.

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Section: Microrna-8063 Targets Heterogeneous Nuclear Ribonucleoprotein Ab To Inhibit the Self-renewal Of Colorectal Cancer Stem Cells Viamentioning

confidence: 55%

MicroRNA‑8063 targets heterogeneous nuclear ribonucleoprotein AB to inhibit the self‑renewal of colorectal cancer stem cells via the Wnt/β‑catenin pathway

et al. 2021

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“…demonstrated that HNRNPA2B1 can mediate the packaging of miR-30b-3p into extracellular vesicles and promotes the ability of GBM cells to resist TMZ ( 148 ). It was also shown that knockdown of HNRNPA2B1 in GBM cells could lead to the inactivation of AKT and STAT3 signaling pathways in tumor cells, reduce the expression of Bcl-2 and PCNA, and thus inhibit the growth of GBM cells, and the establishment of xenograft tumor models using GBM cells with knockdown of HNRNPA2B1 also revealed that knockdown of HNRNPA2B1 could inhibit the progression of GBM in vivo ( 149 ). Analysis of GBM samples with different m6A scores using K-M analysis showed that overall survival was significantly higher in the group with low m6AScore than in the group with high m6AScore, while the P-value for m6AScore was lower than 0.05 (HR>1) in both uni- and mul-tivariate Cox analysis.…”

Section: M6a Modification and Glioblastomamentioning

confidence: 99%

The Potential Value of m6A RNA Methylation in the Development of Cancers Focus on Malignant Glioma

et al. 2022

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N6-methyladenosine (m6A) RNA methylation is an epigenetic modification that has emerged in the last few years and has received increasing attention as the most abundant internal RNA modification in eukaryotic cells. m6A modifications affect multiple aspects of RNA metabolism, and m6A methylation has been shown to play a critical role in the progression of multiple cancers through a variety of mechanisms. This review summarizes the mechanisms by which m6A RNA methylation induced peripheral cancer cell progression and its potential role in the infiltration of immune cell of the glioblastoma microenvironment and novel immunotherapy. Assessing the pattern of m6A modification in glioblastoma will contribute to improving our understanding of microenvironmental infiltration and novel immunotherapies, and help in developing immunotherapeutic strategies.

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“…Downregulation of hnRNP A2/B1 expression in the glioma cell line U251 further induced apoptosis of tumour cells. They found that the regulation of proliferation and apoptosis of glioma cells was mainly achieved by regulating AKT and TAT3 signalling pathways [ 47 ].…”

Section: Introductionmentioning

confidence: 99%

Interaction between m6A methylation and noncoding RNA in glioma

Tao

Wen

et al. 2022

Cell Death Discov.

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Glioma is considered to be the most common brain malignancy in the central nervous system. At present, the aetiology of glioma is not clear. Due to its rapidly growth and easily recurrence, the prognosis of patients with glioma is very poor. N6-methyladenosine (m6A) methylation is an internal reversible modification in most RNAs, including messenger RNAs (mRNAs) and noncoding RNAs (ncRNAs). Recent studies have shown that the m6A regulators are abnormal expressed, and are extensively involved in the progression of glioma by targeting ncRNAs. Moreover, as the most important epigenetic regulators, ncRNAs can also affect the function of m6A regulators in glioma. This review summarized the expression and function of certain common m6A regulators in glioma. Also, the current review sum up the mutual interactions between m6A regulators and ncRNAs in glioma.

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Effect of hnRNPA2/B1 on the proliferation and apoptosis of glioma U251 cells via the regulation of AKT and STAT3 pathways

Cited by 16 publications

References 39 publications

MicroRNA‑8063 targets heterogeneous nuclear ribonucleoprotein AB to inhibit the self‑renewal of colorectal cancer stem cells via the Wnt/β‑catenin pathway

MicroRNA‑8063 targets heterogeneous nuclear ribonucleoprotein AB to inhibit the self‑renewal of colorectal cancer stem cells via the Wnt/β‑catenin pathway

The Potential Value of m6A RNA Methylation in the Development of Cancers Focus on Malignant Glioma

Interaction between m6A methylation and noncoding RNA in glioma

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