Inhibition of EGR1 inhibits glioma proliferation by targeting CCND1 promoter

Chen, Diangang; Zhu, Bo; Lv, Sheng‐Qing; Zhu, Haobo; Tang, Jinliang; Huang, Changlin; Li, Qingrui; Zhou, Pu; Wang, Donglin; Li, Guanghui

doi:10.1186/s13046-017-0656-4

Cited by 51 publications

(29 citation statements)

References 37 publications

(44 reference statements)

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“…Previous research has demonstrated that ccnd1 serves an important role in promoting the development and progress of multiple types of human cancer, such as lung adenocarcinoma, glioma and renal cell cancer (46)(47)(48)(49). a previous study indicated that mir-374a inactivated the phosphoinositide 3-kinase (Pi3K)/aKT signaling axis through inhibiting ccnd1 and suppressing the progression of colon cancer (49).…”

Section: Ccnd1 Is Required For the Proliferation And Apoptosis Of Ht-mentioning

confidence: 99%

MicroRNA‑628‑5p inhibits cell proliferation and induces apoptosis in colorectal cancer through downregulating CCND1 expression levels

Guo

Xue

2020

Mol Med Report

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Microrna (mir)-628-5p serves as an antitumor gene in a variety of cancers; however, the role of mir-628-5p in colorectal cancer remains largely unclear. The purpose of this study was to investigate the role and mechanism of mir-628-5p in colorectal cancer. reverse transcription-quantitative Pcr (RT-qPCR), colony formation assays and flow cytometric analysis were used to determine the expression levels of mir-628-5p in colorectal cancer tissues and cell lines, and the proliferative ability of colorectal cancer cells. TargetScan version 7.2 and dual-luciferase reporter assay were performed to predict and confirm mir-628-5p target genes. The expression levels of cyclin d1 (ccnd1) and related genes were determined using rT-qPcr or/and western blotting analysis. mir-628-5p mimics and ccnd1 plasmids were used to overexpress mir-628-5p and ccnd1; it was demonstrated that the expression levels of miR-628-5p were significantly downregulated in colorectal cancer tissues and cell lines. mir-628-5p mimic-transfected cells inhibited the proliferation and induced apoptosis of HT-29 cells. ccnd1, a downstream effector of mir-628-5p, promoted the proliferation and suppressed apoptosis of HT-29 cells, and the effects were reversed by mir-628-5p mimics. in conclusion, the present study suggested that colorectal cancer progression may be regulated through the mir-628-5p/ccnd1 axis, and mir-628-5p could be used as a potential diagnostic and prognostic biomarker for colorectal cancer.

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Section: Ccnd1 Is Required For the Proliferation And Apoptosis Of Ht-mentioning

confidence: 99%

MicroRNA‑628‑5p inhibits cell proliferation and induces apoptosis in colorectal cancer through downregulating CCND1 expression levels

Guo

Xue

2020

Mol Med Report

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“…The abnormal expression of CCND1 promotes cell proliferation by regulating the cell cycle [30]. Previous researchers have demonstrated that CCND1, identi ed as a proto-oncogene, has an essential role in the development of many kinds of tumours, including lung adenocarcinoma, glioma and renal cell cancer [31][32][33]. In addition, some studies have shown that overexpression of CCND1 promotes tumour cell invasion and metastasis in breast cancer gastric cancer, leading to a poor prognosis [34,35].…”

Section: Discussionmentioning

confidence: 99%

Bioinformatic analysis reveals MIR502 as a potential tumour suppressor in ovarian cancer

Wang

Ning

et al. 2020

Preprint

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Background: Ovarian cancer (OC) is a major cause of death among women due to the lack of early screening methods and its complex pathological progression. Increasing evidence has indicated that microRNAs regulate gene expression in tumours by interacting with mRNAs. Although the research regarding OC and microRNAs is extensive, the vital role of MIR502 in OC remains unclear.Methods: We integrated two microRNA expression arrays from GEO to identify differentially expressed genes. The Kaplan–Meier method was used to screen for miRNAs that had an influence on survival outcome. Upstream regulators of MIR502 were predicted by JASPAR and verified by ChIP-seq data. The LinkedOmics database was used to study genes that were correlated with MIR502. Gene Set Enrichment Analysis (GSEA) was conducted for functional annotation with GO and KEGG pathway enrichment analyses by using the open access WebGestalt tool. We constructed a PPI network by using STRING to further explore the core proteins.Results: We found that the expression level of MIR502 was significantly downregulated in OC, which was related to poor overall survival. NRF1, as an upstream regulator of MIR502, was predicted by JASPAR and verified by ChIP-seq data. In addition, anti-apoptosis and pro-proliferation genes in the Hippo signalling pathway, including CCND1, MYC, FGF1 and GLI2, were negatively regulated by MIR502, as shown in the GO and KEGG pathway enrichment results. The PPI network further demonstrated that CCND1 and MYCN were at core positions in the development of ovarian cancer. Conclusions: MIR502, which is regulated by NRF1, acts as a tumour suppressor gene to accelerate apoptosis and suppress proliferation by targeting the Hippo signalling pathway in ovarian cancer.

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“…EGR1 (Early growth response 1), also known as NGFI-A, TIS8, ZIF268, or KROX-24, is a member of the EGR family of transcription factors (18). EGR1 exhibits a dual role of a tumor suppressor or a tumor-promoting factor in various carcinomas, by regulating cell cycle progression, apoptosis and malignant transformations (19)(20)(21).…”

Section: Discussionmentioning

confidence: 99%

Targeting Phosphorylation of p21-activated Kinase 1 at Thr423 Induces Cell Cycle Arrest and Apoptosis in Cutaneous T-cell Lymphoma Cells

Wang¹,

Li²,

Zhang³

et al. 2019

Acta Derm Venerol

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SIGNIFICANCEIPA-3, a small molecular inhibitor of p21-activated kinase 1 (PAK1) phosphorylation, has anti-tumor activity in multiple cancers. However, its role in cutaneous T-cell lymphoma and the underlying molecular pathogenesis are still unclear. This study investigates the role of IPA-3 on cutaneous Tcell lymphoma cells. Pho-PAK1 overexpression is seen in patients with cutaneous T-cell lymphoma. IPA-3 treatment induces apoptosis and inhibits cell growth by inducing EGR1 expression and simultaneously down-regulating the levels of BCL-2 and pho-BAD. Therefore, pho-PAK1 may be a potential tumor marker and therapeutic target of cutaneous T-cell lymphoma.Cutaneous T-cell lymphoma (CTCL) represents a rare group of extranodal T-cell lymphoproliferative diseases. Due to poor clinical outcome of CTCL, there is an urgent need for new and improved therapies. A small molecule, IPA-3, which inhibits p21-activated kinase 1 (PAK1), has shown therapeutic potential in various types of malignancies. In the present study, the anti-tumor effect of IPA-3 and its underlying molecular mechanism was evaluated. High expression of phosphorylated-PAK1 (pho-PAK1) was seen in CTCL lesional skin compared to benign inflammatory dermatoses. IPA-3 could significantly inhibit the proliferation of 3 CTCL lines in a dose-and time-dependent manner. The percentage of apoptotic cells was higher in the treatment group. Further, IPA-3 treatment caused increased EGR1 protein levels and decreased apoptosis-related BCL-2 and pho-BAD protein levels. In summary, inhibition of pho-PAK1 has significant antitumor effects in CTCL cells and it can be explored as a future therapeutic option.

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Inhibition of EGR1 inhibits glioma proliferation by targeting CCND1 promoter

Cited by 51 publications

References 37 publications

MicroRNA‑628‑5p inhibits cell proliferation and induces apoptosis in colorectal cancer through downregulating CCND1 expression levels

MicroRNA‑628‑5p inhibits cell proliferation and induces apoptosis in colorectal cancer through downregulating CCND1 expression levels

Bioinformatic analysis reveals MIR502 as a potential tumour suppressor in ovarian cancer

Targeting Phosphorylation of p21-activated Kinase 1 at Thr423 Induces Cell Cycle Arrest and Apoptosis in Cutaneous T-cell Lymphoma Cells

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