We are analyzing https://link.springer.com/article/10.1186/s13046-019-1405-7.

Title:
The JAK2/STAT3/CCND2 Axis promotes colorectal Cancer stem cell persistence and radioresistance | Journal of Experimental & Clinical Cancer Research
Description:
Background Radiotherapy (RT) is a highly effective multimodal nonsurgical treatment that is essential for patients with advanced colorectal cancer (CRC). Nevertheless, cell subpopulations displaying intrinsic radioresistance survive after RT. The reactivation of their proliferation and successful colonization at local or distant sites may increase the risk of poor clinical outcomes. Recently, radioresistant cancer cells surviving RT were reported to exhibit a more aggressive phenotype than parental cells, although the underlying mechanisms remain unclear. Methods By investigating public databases containing CRC patient data, we explored potential radioresistance-associated signaling pathways. Then, their mechanistic roles in radioresistance were investigated through multiple validation steps using patient-derived primary CRC cells, human CRC cell lines, and CRC xenografts. Results Janus kinase (JAK)/signal transducer and activator of transcription (STAT) signaling was activated in radioresistant CRC tissues in correlation with local and distant metastases. JAK2 was preferentially overexpressed in the CRC stem cell subpopulation, which was accompanied by the phosphorylation of STAT proteins, especially STAT3. JAK2/STAT3 signaling played an essential role in promoting tumor initiation and radioresistance by limiting apoptosis and enhancing clonogenic potential. Mechanistically, the direct binding of STAT3 to the cyclin D2 (CCND2) promoter increased CCND2 transcription. CCND2 expression was required for persistent cancer stem cell (CSC) growth via the maintenance of an intact cell cycle and proliferation with low levels of DNA damage accumulation. Conclusion Herein, we first identified JAK2/STAT3/CCND2 signaling as a resistance mechanism for the persistent growth of CSCs after RT, suggesting potential biomarkers and regimens for improving outcomes among CRC patients.
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Keywords {🔍}

cells, cancer, crc, jak, ccnd, cell, fig, expression, cdv, signaling, additional, article, file, jakstat, radioresistance, stat, cscs, google, scholar, analysis, hct, figure, knockdown, tissues, radiation, cas, stem, treatment, dna, data, primary, performed, genes, tumor, multiple, assay, lovo, potential, compared, stattic, csc, pathway, activation, growth, population, gse, control, silencing, pathways, tumors,

Topics {✒️}

verification number e1cd-b820–6327-66ea-e39p il-6/jak/stat3 signalling axis jeong-seok nam nl/cgi-bin/r2/main c-jun n-terminal kinase jak2/stat3/ccnd2 signaling contributes poly adp-ribose polymerase fluorescence-activated cell sorting induce epithelial–mesenchymal transition performing real-time qpcr cd44+cd24– stem cell patient-derived primary crc patient-derived crc cells jak2/stat3/ccnd2 axis dna double-stranded breaks article google scholar identified jak2/stat3/ccnd2 signaling substantial life-threatening event aberrant jak/stat signaling real-time qpcr analysis d-type cyclins consist mitogen-activated protein kinases γh2ax+ dna-damaged cells d-type cyclin family small-cell lung cancer extracellular signal-regulated kinases augmenting rt-induced apoptosis supplementary tables s1-s14 jak/stat signaling pathway article download pdf jak2/stat3 signaling played intrinsic jak2/stat3 signaling targeting jak2/stat3 reduces stem marker-negative cells putative csc markers jak/stat signaling components activate jak/stat signaling deplete dna replication-stressed high jak2/stat3 levels dna damage-sensing mechanisms full size image targeting jak2/stat3 signaling sphere-cultured hct116 cells shjak2-transfected cancer cells small-molecule inhibitor jak2-depleted cells compared jak2/stat3 signaling pathway rt-induced signaling network csc-enriched ccnd2 expression csc-enriched spheres compared

Schema {🗺️}

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         description:Radiotherapy (RT) is a highly effective multimodal nonsurgical treatment that is essential for patients with advanced colorectal cancer (CRC). Nevertheless, cell subpopulations displaying intrinsic radioresistance survive after RT. The reactivation of their proliferation and successful colonization at local or distant sites may increase the risk of poor clinical outcomes. Recently, radioresistant cancer cells surviving RT were reported to exhibit a more aggressive phenotype than parental cells, although the underlying mechanisms remain unclear. By investigating public databases containing CRC patient data, we explored potential radioresistance-associated signaling pathways. Then, their mechanistic roles in radioresistance were investigated through multiple validation steps using patient-derived primary CRC cells, human CRC cell lines, and CRC xenografts. Janus kinase (JAK)/signal transducer and activator of transcription (STAT) signaling was activated in radioresistant CRC tissues in correlation with local and distant metastases. JAK2 was preferentially overexpressed in the CRC stem cell subpopulation, which was accompanied by the phosphorylation of STAT proteins, especially STAT3. JAK2/STAT3 signaling played an essential role in promoting tumor initiation and radioresistance by limiting apoptosis and enhancing clonogenic potential. Mechanistically, the direct binding of STAT3 to the cyclin D2 (CCND2) promoter increased CCND2 transcription. CCND2 expression was required for persistent cancer stem cell (CSC) growth via the maintenance of an intact cell cycle and proliferation with low levels of DNA damage accumulation. Herein, we first identified JAK2/STAT3/CCND2 signaling as a resistance mechanism for the persistent growth of CSCs after RT, suggesting potential biomarkers and regimens for improving outcomes among CRC patients.
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            Radioresistance
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            Immunology
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            Oncology
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      headline:The JAK2/STAT3/CCND2 Axis promotes colorectal Cancer stem cell persistence and radioresistance
      description:Radiotherapy (RT) is a highly effective multimodal nonsurgical treatment that is essential for patients with advanced colorectal cancer (CRC). Nevertheless, cell subpopulations displaying intrinsic radioresistance survive after RT. The reactivation of their proliferation and successful colonization at local or distant sites may increase the risk of poor clinical outcomes. Recently, radioresistant cancer cells surviving RT were reported to exhibit a more aggressive phenotype than parental cells, although the underlying mechanisms remain unclear. By investigating public databases containing CRC patient data, we explored potential radioresistance-associated signaling pathways. Then, their mechanistic roles in radioresistance were investigated through multiple validation steps using patient-derived primary CRC cells, human CRC cell lines, and CRC xenografts. Janus kinase (JAK)/signal transducer and activator of transcription (STAT) signaling was activated in radioresistant CRC tissues in correlation with local and distant metastases. JAK2 was preferentially overexpressed in the CRC stem cell subpopulation, which was accompanied by the phosphorylation of STAT proteins, especially STAT3. JAK2/STAT3 signaling played an essential role in promoting tumor initiation and radioresistance by limiting apoptosis and enhancing clonogenic potential. Mechanistically, the direct binding of STAT3 to the cyclin D2 (CCND2) promoter increased CCND2 transcription. CCND2 expression was required for persistent cancer stem cell (CSC) growth via the maintenance of an intact cell cycle and proliferation with low levels of DNA damage accumulation. Herein, we first identified JAK2/STAT3/CCND2 signaling as a resistance mechanism for the persistent growth of CSCs after RT, suggesting potential biomarkers and regimens for improving outcomes among CRC patients.
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         Radioresistance
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         Cancer stem cells (CSCs)
         Cancer Research
         Immunology
         Apoptosis
         Oncology
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