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RING-finger protein 6 amplification activates JAK/STAT3 pathway by modifying SHP-1 ubiquitylation and associates with poor outcome in colorectal cancer

ABSTRACT: To elucidate whether RNF6 plays a role in colorectal cancer tumorigenesis, a RNA-seq analysis was performed to compare the gene expression profiles of RNF6 siRNA and control siRNA transfectants.

ORGANISM(S): Homo sapiens

PROVIDER: GSE107980 | GEO | 2018/03/12

REPOSITORIES: GEO

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RING-finger protein 6 amplification activates JAK/STAT3 pathway by modifying SHP-1 ubiquitylation and associates with poor outcome in colorectal cancer

Project description:RING-finger protein 6 amplification activates JAK/STAT3 pathway by modifying SHP-1 ubiquitylation and associates with poor outcome in colorectal cancer

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RNA-seq and CUT&Tag analysis of the effects of lncRNA LOC105378662 knockdown in gastric cancer cells

Project description:To elucidate whether lncRNA LOC105378662 plays a role in gastric cancer tumorigenesis, a RNA-seq analysis was performed to compare the gene expression profiles of LOC105378662 siRNA and control siRNA transfectants. And we found LOC105378662 interact with BRD7 ( bromodomain containing 7), which usually acted as a co-factor in gene transcription. Therefore, we compared the enrichment of BRD7 in MGC803 cells with LOC105378662 siRNA and control siRNA transfectants through CUT&Tag sequencing.

2024-11-24 | GSE189471 | GEO

URI1 amplification in uterine carcinosarcoma associates with chemo-resistance and poor prognosis.

Project description:Uterine carcinosarcoma (UCS) is a rare type of cancer and accounts for 5% of uterine malignancies. However, UCS patients suffer a high prevalence of chemo-resistance and a very poor prognosis compared to uterine cancer patients. URI is a chaperone with functions in transcription. We analyzed the somatic URI1 copy number variation in 57 post-menopausal non-metastatic UCS patients in comparison to 363 uterine corpus endometrial carcinomas. URI1 amplification was detected in 40% (23/57) of primary UCS and 5.5% (20/363) of uterine carcinomas. UCS patients with URI1 amplification exhibited 13% (3/23) tumor-free survival compared to 41% (14/34) in the absence of URI amplification (P=0.023). URI1 amplification (OR=6.54, P=0.027), weight (OR=1.068, P=0.024), hypertension (OR=3.35, P=0.044), and tumor stage (OR=2.358, P=0.018) associated with poor survival. Patients treated with hormone replacement therapy (OR=15.87, P=0.011) displayed enhanced overall survival. Combined radiation and chemotherapy improved patient survival (median survival=2043 days) compared to single (median survival=597 days) or no treatment (median survival=317 days, P=0.0016). Importantly, patients with URI1 amplification had poor response to adjuvant treatment compared to control group (P=0.013). Tumors with URI1 amplification displayed decreased transcription of genes encoding tumor suppressor and apoptotic regulators and increased expression of genes regulating oncogenesis, survival and metastasis. Overexpression of URI1 in a cultured cell model induced ATM expression and resistance to cisplatin. Our findings suggest that high prevalence in UCS may associate with poor prognosis and worse response to adjuvant treatment.

| S-EPMC4548345 | biostudies-literature

A novel lncRNA lncRNA-AF339830 promotes colorectal carcinogenesis and glucose metabolism by stabilizing and specifying the transcription modification pattern of c-Myc [RNA-Seq]

Project description:To elucidate whether lncRNA-AF339830 plays a role in colorectal cancer tumorigenesis, a RNA-seq analysis was performed to compare the gene expression profiles of lncRNA-AF339830 siRNA and control siRNA transfectants.

2019-07-08 | GSE119866 | GEO

A novel lncRNA lncRNA-AK096729 promotes colorectal carcinogenesis and glucose metabolism by stabilizing and specifying the transcription modification pattern of c-Myc

Project description:To elucidate whether lncRNA-AK096729 plays a role in colorectal cancer tumorigenesis, a RNA-seq analysis was performed to compare the gene expression profiles of lncRNA-AF339830 siRNA and control siRNA transfectants.

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A novel lncRNA lncRNA-AF339830 promotes colorectal carcinogenesis and glucose metabolism by stabilizing and specifying the transcription modification pattern of c-Myc [ChIP-Seq]

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Mechanism of ubiquitylation by dimeric RING ligase RNF4.

Project description:Mammalian RNF4 is a dimeric RING ubiquitin E3 ligase that ubiquitylates poly-SUMOylated proteins. We found that RNF4 bound ubiquitin-charged UbcH5a tightly but free UbcH5a weakly. To provide insight into the mechanism of RING-mediated ubiquitylation, we docked the UbcH5~ubiquitin thioester onto the RNF4 RING structure. This revealed that with E2 bound to one monomer of RNF4, the thioester-linked ubiquitin could reach across the dimer to engage the other monomer. In this model, the 'Ile44 hydrophobic patch' of ubiquitin is predicted to engage a conserved tyrosine located at the dimer interface of the RING, and mutation of these residues blocked ubiquitylation activity. Thus, dimeric RING ligases are not simply inert scaffolds that bring substrate and E2-loaded ubiquitin into close proximity. Instead, they facilitate ubiquitin transfer by preferentially binding the E2~ubiquitin thioester across the dimer and activating the thioester bond for catalysis.

| S-EPMC3326525 | biostudies-literature

Expression data from SHP specific siRNA or nonspecefic siRNA transfected rat astrocytes

Project description:To clarify the effect of SHP in LXRs-mediated signaling pathway, we performed global gene expression analysis of SHP siRNA transfected- or control siRNA transfected- astrocytes after IFN-γ and LXRs agonist. Microarray analysis revealed that expression of several genes encoding inflammatory mediators were reversed in SHP siRNA transfected-astrocytes, when compared with control siRNA transfected-astrocytes.

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HPGD associates with poor prognosis in breast cancer, induces epithelial-mesenchymal transition and promotes cell migration in cultured breast cancer cells

Project description:Effects of siRNA and shRNA treatment on gene expression in breast cancer cell lines

2012-06-01 | E-TABM-1162 | biostudies-arrayexpress

SMURF1-mediated ubiquitylation of SHP-1 promotes cell proliferation and invasion of endometrial stromal cells in endometriosis.

Project description:BackgroundEndometriosis is a widespread benign gynecological disorder. The signal transducer and activator of transcription 3 (STAT3) signaling pathway plays an important role in the pathogenesis of endometriosis through regulating proliferation and invasion of endometrial stromal cells. Furthermore, the protein tyrosine phosphatase (PTP), SH2 domain-containing phosphatase 1 (SHP-1), negatively regulates STAT3 activation. However, regulation of the SHP-1-STAT3 pathway in the pathogenesis of endometriosis remains unclear.MethodsCell proliferation and invasion were assessed by Cell Counting Kit-8 (CCK-8) assay and Transwell analysis, respectively, to investigate the role and regulation of the SHP-1-STAT3 pathway in the proliferation and invasion of endometrial stromal cells. Expression of Smad ubiquitin regulatory factor 1 (SMURF1), SHP-1, matrix metalloproteinase 2 (MMP2), MMP9, STAT3, and phospho-STAT3 (p-STAT3) level in patients with endometriosis were measured by Western blotting and/or immunohistochemical staining. The interaction between SMURF1 and SHP-1 was investigated by co-immunoprecipitation and ubiquitylation analysis.ResultsThe present study demonstrated that downregulation of SHP-1 expression in patients with endometriosis was negatively correlated with SMURF1 expression. SMURF1, an E3 ubiquitin ligase, activated the STAT3 pathway via ubiquitylation and degradation of SHP-1. Furthermore, SMURF1 promoted cell proliferation and invasion of endometrial stromal cells by activating STAT3 signaling and expression of its downstream targets, MMP2 and MMP9, whereas SHP-1 demonstrated an inverse effect. Additionally, SHP-1 inhibited SMURF1-mediated cell invasion and proliferation of endometrial stromal cells.ConclusionsOur findings indicate that SMURF1-mediated ubiquitylation of SHP-1 regulates endometrial stromal cell proliferation and invasion during endometriosis.

| S-EPMC8033391 | biostudies-literature

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