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

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

ORGANISM(S): Homo sapiens

PROVIDER: GSE175404 | GEO | 2021/05/25

REPOSITORIES: GEO

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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

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

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-05-25 | GSE175409 | 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

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

The G1/S transition is promoted by Rb degradation via the E3 ligase UBR5.

Project description:Mammalian cells make the decision to divide at the G1/S transition in response to diverse signals impinging on the retinoblastoma protein Rb, a cell cycle inhibitor and tumor suppressor. Rb is inhibited by two parallel pathways. In the canonical pathway, cyclin D-Cdk4/6 kinase complexes phosphorylate and inactivate Rb. In the second, recently discovered pathway, Rb's concentration decreases during G1 through an unknown mechanism. Here, we found that regulated protein degradation via the E3 ubiquitin ligase UBR5 is responsible for Rb's concentration drop in G1. UBR5 knockout cells have increased Rb concentration in early G1, exhibited a lower G1/S transition rate, and are more sensitive to inhibition of Cdk4/6. This last observation suggests that UBR5 inhibition can strengthen the efficacy of Cdk4/6 inhibitor-based cancer therapies.

| S-EPMC10592979 | biostudies-literature

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