The CALM and CALM/AF10 interactor CATS is a marker for proliferation

Archangelo, Leticia Fröhlich; Hölzel, Michael; Hawranek, Thomas; Kremmer, Elisabeth; Przemeck, Gerhard K. H.; Eick, Dirk; Deshpande, Aniruddha J.; Buske, Christian; Angelis, Martin Hrabé de; Saad, Sara Teresinha Olalla; Bohlander, Stefan K.

doi:10.1016/j.molonc.2008.08.001

Cited by 35 publications

(58 citation statements)

References 56 publications

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“…To investigate the requirement of Cdks for rRNA processing, we applied an RNAi approach for the selective knockdown of individual Cdks. U2OS cells were transfected with siRNA targeting mRNAs of Cdk1 to Cdk16 or with control siRNA for mRNAs of luciferase, CATS, and the rRNA processing factor Pes1 (29,30) (Fig. 1, supplemental Fig.…”

Section: Resultsmentioning

confidence: 99%

Cyclin-dependent Kinase 9 Links RNA Polymerase II Transcription to Processing of Ribosomal RNA

Burger

Mühl

Michaela

et al. 2013

Journal of Biological Chemistry

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Background: Processing of ribosomal RNA is sensitive to Cdk inhibitors. Results: Inhibition of Cdk9 activity blocks 47 S rRNA processing and stabilizes a 3Ј extended 47 S primary transcript. Defective 3Ј processing negatively feeds back on RNAPI transcription. Conclusion: Cdk9 facilitates processing of 47 S rRNA by RNAPII-dependent synthesis of U8 snoRNA. Significance: Cdk9 may be a critical regulator of rRNA processing to harmonize RNAPII transcription activity with a ribosome biogenesis rate.

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Section: Resultsmentioning

confidence: 99%

Cyclin-dependent Kinase 9 Links RNA Polymerase II Transcription to Processing of Ribosomal RNA

Burger

Mühl

Michaela

et al. 2013

Journal of Biological Chemistry

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“…Thus, GOLM1 has been suggested as a putative tissue and urine biomarker of prostate cancer (36)(37)(38)(39) and shown to induce migration and invasion of prostate cancer cells (40). C1orf116 has been reported as highly expressed in prostate cancer tissue (41), whereas FAM64A is highly expressed in leukemia and lymphoma, and known to promote cell division (42,43). Moreover, we found that high expression of the predicted miR-452 target gene OAZ2 was associated with high recurrence risk after radical prostatectomy in the patient cohort from Taylor and colleagues.…”

Section: Discussionmentioning

confidence: 99%

Hypermethylation of theGABRE∼miR-452∼miR-224Promoter in Prostate Cancer Predicts Biochemical Recurrence after Radical Prostatectomy

Kristensen

Haldrup

Strand

et al. 2014

Clinical Cancer Research

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Purpose: Available tools for prostate cancer diagnosis and prognosis are suboptimal and novel biomarkers are urgently needed. Here, we investigated the regulation and biomarker potential of the GABRE$miR-452$miR-224 genomic locus.Experimental Design: GABRE/miR-452/miR-224 transcriptional expression was quantified in 80 nonmalignant and 281 prostate cancer tissue samples. GABRE$miR-452$miR-224 promoter methylation was determined by methylation-specific qPCR (MethyLight) in 35 nonmalignant, 293 prostate cancer [radical prostatectomy (RP) cohort 1] and 198 prostate cancer tissue samples (RP cohort 2). Diagnostic/prognostic biomarker potential of GABRE$miR-452$miR-224 methylation was evaluated by ROC, Kaplan-Meier, uni-and multivariate Cox regression analyses. Functional roles of miR-224 and miR-452 were investigated in PC3 and DU145 cells by viability, migration, and invasion assays and gene-set enrichment analysis (GSEA) of posttransfection transcriptional profiling data.Results: GABRE$miR-452$miR-224 was significantly downregulated in prostate cancer compared with nonmalignant prostate tissue and had highly cancer-specific aberrant promoter hypermethylation (AUC ¼ 0.98). Functional studies and GSEA suggested that miR-224 and miR-452 inhibit proliferation, migration, and invasion of PC3 and DU145 cells by direct/indirect regulation of pathways related to the cell cycle and cellular adhesion and motility. Finally, in uni-and multivariate analyses, high GABRE$miR-452$miR-224 promoter methylation was significantly associated with biochemical recurrence in RP cohort 1, which was successfully validated in RP cohort 2.Conclusion: The GABRE$miR-452$miR-224 locus is downregulated and hypermethylated in prostate cancer and is a new promising epigenetic candidate biomarker for prostate cancer diagnosis and prognosis. Tumor-suppressive functions of the intronic miR-224 and miR-452 were demonstrated in two prostate cancer cell lines, suggesting that epigenetic silencing of GABRE$miR-452$miR-224 may be selected for in prostate cancer. Clin Cancer Res; 20(8); 2169-81. Ó2014 AACR.

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“…This study reveals a previously unreported function of FAM64A in the regulation of inflammation and tumorigenesis and provides a potential therapeutic target for inflammatory diseases and cancer. levels strongly correlate with cell proliferation in both malignant and normal cells (18). FAM64A is a multifunctional protein that is involved in regulation of cell cycle progression, subcellular localization of the leukemogenic fusion protein CALM/AF10, and tumorigenesis (18)(19)(20)(21)(22).…”

Section: Significancementioning

confidence: 99%

“…levels strongly correlate with cell proliferation in both malignant and normal cells (18). FAM64A is a multifunctional protein that is involved in regulation of cell cycle progression, subcellular localization of the leukemogenic fusion protein CALM/AF10, and tumorigenesis (18)(19)(20)(21)(22). In a screen for proteins that regulate STAT3 activity, we identified FAM64A as a positive regulator of STAT3, which modulates binding of STAT3 to the promoters of its target genes.…”

Section: Significancementioning

confidence: 99%

FAM64A positively regulates STAT3 activity to promote Th17 differentiation and colitis-associated carcinogenesis

Zhang

et al. 2019

Proc. Natl. Acad. Sci. U.S.A.

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STAT3 is a transcription factor that plays central roles in various physiological processes, including differentiation of Th cells. Its deregulation results in serious diseases, including inflammatory diseases and cancer. The mechanisms related to how STAT3 activity is regulated remain enigmatic. Here we show that overexpression of FAM64A potentiates IL-6-induced activation of STAT3 and expression of downstream target genes, whereas deficiency of FAM64A has the opposite effects. FAM64A interacts with STAT3 in the nucleus and regulates binding of STAT3 to the promoters of its target genes. Deficiency of Fam64a significantly impairs differentiation of Th17 but not Th1 or induced regulatory T cells (iTreg). In addition, Fam64a deficiency attenuates experimental autoimmune encephalomyelitis (EAE) and dextran sulfate sodium (DSS)-induced colitis, which is correlated with decreased differentiation of Th17 cells and production of proinflammatory cytokines. Furthermore, Fam64a deficiency suppresses azoxymethane (AOM)/DSS-induced colitis-associated cancer (CAC) in mice. These findings suggest that FAM64A regulates Th17 differentiation and colitis and inflammation-associated cancer by modulating transcriptional activity of STAT3.

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The CALM and CALM/AF10 interactor CATS is a marker for proliferation

Cited by 35 publications

References 56 publications

Cyclin-dependent Kinase 9 Links RNA Polymerase II Transcription to Processing of Ribosomal RNA

Cyclin-dependent Kinase 9 Links RNA Polymerase II Transcription to Processing of Ribosomal RNA

Hypermethylation of theGABRE∼miR-452∼miR-224Promoter in Prostate Cancer Predicts Biochemical Recurrence after Radical Prostatectomy

FAM64A positively regulates STAT3 activity to promote Th17 differentiation and colitis-associated carcinogenesis

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