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The RNA binding protein MEX3A controls G1/S transition via regulating RB/E2F pathway in clear cell renal cell carcinoma

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE175409 | GEO | 2021/05/25

REPOSITORIES: GEO

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RNA-binding protein MEX3A controls G1/S transition via regulating the RB/E2F pathway in clear cell renal cell carcinoma.

Project description:MEX3A is an RNA-binding protein that mediates mRNA decay through binding to 3' untranslated regions. However, its role and mechanism in clear cell renal cell carcinoma remain unknown. In this study, we found that MEX3A expression was transcriptionally activated by ETS1 and upregulated in clear cell renal cell carcinoma. Silencing MEX3A markedly reduced clear cell renal cell carcinoma cell proliferation in vitro and in vivo. Inhibiting MEX3A induced G1/S cell-cycle arrest. Gene set enrichment analysis revealed that E2F targets are the central downstream pathways of MEX3A. To identify MEX3A targets, systematic screening using enhanced cross-linking and immunoprecipitation sequencing, and RNA-immunoprecipitation sequencing assays were performed. A network of 4,000 genes was identified as potential targets of MEX3A. Gene ontology analysis of upregulated genes bound by MEX3A indicated that negative regulation of the cell proliferation pathway was highly enriched. Further assays indicated that MEX3A bound to the CDKN2B 3' untranslated region, promoting its mRNA degradation. This leads to decreased levels of CDKN2B and an uncontrolled cell cycle in clear cell renal cell carcinoma, which was confirmed by rescue experiments. Our findings revealed that MEX3A acts as a post-transcriptional regulator of abnormal cell-cycle progression in clear cell renal cell carcinoma.

| S-EPMC8703191 | biostudies-literature

The RNA binding protein MEX3A controls G1/S transition via regulating RB/E2F pathway in clear cell renal cell carcinoma [eCLIP-Seq]

Project description:Flag_eCLIP_Seq was performed in MEX3A-flag overexpressing ACHN cells.

2021-05-25 | GSE175407 | GEO

The RNA binding protein MEX3A controls G1/S transition via regulating RB/E2F pathway in clear cell renal cell carcinoma [RIP-Seq]

Project description:Flag_RIP_Seq was performed in MEX3A-flag overexpressing ACHN cells.

2021-05-25 | GSE175405 | GEO

The RNA binding protein MEX3A controls G1/S transition via regulating RB/E2F pathway in clear cell renal cell carcinoma [RNA-Seq]

Project description:RNA-Seq was performed after siRNA transfection in ACHN cells.

2021-05-25 | GSE175404 | GEO

The RNA binding protein MEX3A controls G1/S transition via regulating RB/E2F pathway in clear cell renal cell carcinoma

Project description:The RNA binding protein MEX3A controls G1/S transition via regulating RB/E2F pathway in clear cell renal cell carcinoma

| PRJNA732318 | ENA

The RNA binding protein MEX3A controls G1/S transition via regulating RB/E2F pathway in clear cell renal cell carcinoma [RNA-Seq]

Project description:The RNA binding protein MEX3A controls G1/S transition via regulating RB/E2F pathway in clear cell renal cell carcinoma [RNA-Seq]

| PRJNA732307 | ENA

The RNA binding protein MEX3A controls G1/S transition via regulating RB/E2F pathway in clear cell renal cell carcinoma [RIP-Seq]

Project description:The RNA binding protein MEX3A controls G1/S transition via regulating RB/E2F pathway in clear cell renal cell carcinoma [RIP-Seq]

| PRJNA732308 | ENA

The RNA binding protein MEX3A controls G1/S transition via regulating RB/E2F pathway in clear cell renal cell carcinoma [eCLIP-Seq]

Project description:The RNA binding protein MEX3A controls G1/S transition via regulating RB/E2F pathway in clear cell renal cell carcinoma [eCLIP-Seq]

| PRJNA732353 | ENA

Comprehensive bioinformatics analysis of the E2F family in human clear cell renal cell carcinoma.

Project description:Clear cell renal cell carcinoma (ccRCC) originates from renal tubular epithelial cells and is the most common pathological renal cell carcinoma type with the worst prognosis. The relationship between the expression, prognosis and mechanism of ccRCC and the E2F family remains challenging. In the present study, RNA sequencing and clinical data of ccRCC from The Cancer Genome Atlas and two datasets, GSE36895 and GSE53757, from the Gene Expression Omnibus were used to identify the role of the E2F family in ccRCC. A total of 10 groups of tumor tissues and paired-normal tissues from patients with ccRCC were verified by reverse transcription-quantitative PCR. the expression, tumor grade and stage, prognosis and regulatory mechanism of the E2F family in ccRCC were analyzed. It was found that the expression levels of E2F1 to 4 and 6 to 8 were higher in ccRCC tissues than in normal tissues, whereas the expression level of E2F5 was lower in the former than in the latter. The expression levels of E2F1 to 8 were correlated with tumor stage and grade. Low expression of E2F1 to 5 and 7 to 8 was significantly associated with longer overall survival, disease-specific survival and progression-free survival times. The data revealed that the E2F family rarely has genetic mutations. The expression of E2F1, E2F2, E2F5, E2F7 and E2F8 was significantly correlated with DNA methylation, and E2F1 to E2F7 were significantly correlated with copy number and the data showed that the expression of E2Fs was significantly correlated with the cell cycle. The results of the present study suggested that E2F family genes may be potential targets for ccRCC molecular diagnosis and targeted therapy.

| S-EPMC9478613 | biostudies-literature

CtIP activates its own and cyclin D1 promoters via the E2F/RB pathway during G1/S progression.

Project description:Cell cycle progression from G(1) to S phase is mainly controlled by E2F transcription factors and RB family proteins. Previously we showed that the presence of CtIP is essential for G(1)/S transition in primary mouse blastocysts, as well as in NIH 3T3 cells. However, how CtIP executes this function remains to be elucidated. Here we show that in NIH 3T3 cells the expression of CtIP is regulated by the E2F/RB pathway during late G(1) and S phases. The presence of wild-type CtIP, but not the E157K mutant form, which failed to interact with RB, enhanced its own promoter activity. Chromatin immunoprecipitation analysis indicated that the recruitment of CtIP to its promoter occurs concomitantly with TFIIB, a component of the RNA polymerase II complex, and with dissociation of RB from the promoter during late G(1) and G(1)/S transition. Similar positive regulation of cyclin D1 expression by CtIP was also observed. Consistently, cells expressing the CtIP(E157K) protein alone exhibited growth retardation, an increase in the G(1) population, and a decrease in the S-phase population. Taken together, these results suggest that, contrary to the postulated universal corepressor role, CtIP activates a subset of E2F-responsive promoters by releasing RB-imposed repression and therefore promotes G(1)/S progression.

| S-EPMC1446954 | biostudies-literature

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