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cells, expression, hypoxia, rcc, fig, lnctcfl, cell, osrc, ybx, sox, formation, csc, article, pubmed, normoxia, cscs, tumor, cancer, analysis, days, google, scholar, exposed, transduced, results, additional, protein, lncrnas, phenotype, signaling, stem, progression, found, file, sunitinib, assay, cas, tissues, plasmid, data, level, oear, renal, performed, sphere, shlnctcfl, axis, therapy, patients, normal,

Topics {✒️}

hypoxia-modulated ar/lnctcfl5-2/ybx1/sox2 signals ablity ar/lnctcfl5-2/ybx1/sox2 signaling axis lnctcfl5-2-ybx1-sox2 signaling axis renal cell carcinoma org/db/gene/lnc-tcfl5-2 lnctcfl5-2-modulated ybx1/sox2 signals lncrnas including lnc-ctb-114c7 real-time rt-pcr assays cell stem cell heat-induced antigen retrieval ubiquitin-mediated degradation plays renal cell cancer cyclin-dependent kinases family sh-lnc-ctb-114c7 bio-rad cfx96 system human glyceraldehyde-3-phosphate dehydrogenase embryonic stem cell reduced proteasome-mediated degradation ar-modulated csc phenotype stem cell programs stem cell rev sh-lnctcfl5-2 suppresses tumorigenicity plasmid encoding ar-shrna1/2 renal cell carcinomas hrp-conjugated secondary antibodies lnctcfl5-2/ybx1/sox2 signaling supplement figures demonstrated quantitative real-time pcr article download pdf ar-suppressed cscs phenotypes goat anti-rat igg hypoxia-suppressed ar signaling human renal cancer hypoxia-induced csc phenotypes goat anti-mouse igg chi-ping huang cancer stem cells cancer stem-cells brain tumor-initiating cells monitor tumor growth androgen/ar signaling lnctcfl5-2/ybx1 complex translocates oe-ar oe-mutant lnctcfl5-2 lnc-ctb-114c7 osrc-2-luc cells suspended ar/lnctcfl5-2/ybx1 signals small renal masses signaling axis somatic stem cells cell growth

Questions {❓}

• Targeting the Y/CCAAT box in cancer: YB-1 (YBX1) or NF-Y?

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WebPage:
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         headline:Hypoxia increases RCC stem cell phenotype via altering the androgen receptor (AR)-lncTCFL5-2-YBX1-SOX2 signaling axis
         description:Early studies indicated that the androgen receptor (AR) could promote renal cell carcinoma (RCC) development and metastasis, but its linkage to RCC progression under hypoxia, remains unclear. Here we found AR expression in RCC cells decreased in response to hypoxia, which might then lead to increase the cancer stem cells (CSC) phenotype through the lncTCFL5-2-modulated YBX1/SOX2 signals. The consequences of such hypoxia-modulated AR/lncTCFL5-2/YBX1/SOX2 signals ablity to alter the CSC phenotype might render RCC cells more resistant to targeted therapy with Sunitinib. Mechanism dissection revealed that AR might alter the lncTCFL5-2/YBX1/SOX2 signaling through transcriptional suppression of the lncTCFL5-2 expression via the AR-response-elements (AREs) on the lncTCFL5-2 promoter. The lncTCFL5-2 interacts with YBX1 to increase its stability, which in turn increases SOX2 expression at a transcriptional level via the YBX1-response-elements (YBX1Es) on the SOX2 promoter. The in vivo mouse model with orthotopic xenografts of RCC cells also validates the in vitro data, and a human RCC sample survey demonstrated the clinical significance of the AR/lncTCFL5-2/YBX1/SOX2 signaling axis for the RCC prognosis, likely as a result of regulating CSC phenotypes. Together, these findings suggest that hypoxia may increase the RCC CSC phenotype via altering the AR/lncTCFL5-2/YBX1/SOX2 signaling axis and a potential therapy to target this newly identified signal perhaps may help improve the targeted therapy with Sunitinib to better suppress RCC progression.
         datePublished:2022-11-17T00:00:00Z
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            Renal cell carcinoma
            Cancer stem cells
            Androgen receptor
            lncTCFL5-2
            Cell Biology
            Microbiology
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            Neurobiology
            Proteomics
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      headline:Hypoxia increases RCC stem cell phenotype via altering the androgen receptor (AR)-lncTCFL5-2-YBX1-SOX2 signaling axis
      description:Early studies indicated that the androgen receptor (AR) could promote renal cell carcinoma (RCC) development and metastasis, but its linkage to RCC progression under hypoxia, remains unclear. Here we found AR expression in RCC cells decreased in response to hypoxia, which might then lead to increase the cancer stem cells (CSC) phenotype through the lncTCFL5-2-modulated YBX1/SOX2 signals. The consequences of such hypoxia-modulated AR/lncTCFL5-2/YBX1/SOX2 signals ablity to alter the CSC phenotype might render RCC cells more resistant to targeted therapy with Sunitinib. Mechanism dissection revealed that AR might alter the lncTCFL5-2/YBX1/SOX2 signaling through transcriptional suppression of the lncTCFL5-2 expression via the AR-response-elements (AREs) on the lncTCFL5-2 promoter. The lncTCFL5-2 interacts with YBX1 to increase its stability, which in turn increases SOX2 expression at a transcriptional level via the YBX1-response-elements (YBX1Es) on the SOX2 promoter. The in vivo mouse model with orthotopic xenografts of RCC cells also validates the in vitro data, and a human RCC sample survey demonstrated the clinical significance of the AR/lncTCFL5-2/YBX1/SOX2 signaling axis for the RCC prognosis, likely as a result of regulating CSC phenotypes. Together, these findings suggest that hypoxia may increase the RCC CSC phenotype via altering the AR/lncTCFL5-2/YBX1/SOX2 signaling axis and a potential therapy to target this newly identified signal perhaps may help improve the targeted therapy with Sunitinib to better suppress RCC progression.
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         Hypoxia
         Renal cell carcinoma
         Cancer stem cells
         Androgen receptor
         lncTCFL5-2
         Cell Biology
         Microbiology
         Stem Cells
         Neurobiology
         Proteomics
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            name:China Medical University/Hospital
            address:
               name:Department of Urology, China Medical University/Hospital, Taichung, Taiwan
               type:PostalAddress
            type:Organization
      name:Junhua Zheng
      affiliation:
            name:Renji Hospital, Shanghai Jiaotong University School of Medicine
            address:
               name:Department of Urology, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China
               type:PostalAddress
            type:Organization
      email:[email protected]
      name:Chawnshang Chang
      url:http://orcid.org/0000-0001-8510-3516
      affiliation:
            name:Urology, Radiation Oncology and The Wilmot Cancer Institute, University of Rochester Medical Center
            address:
               name:George Whipple Lab for Cancer Research, Departments of Pathology, Urology, Radiation Oncology and The Wilmot Cancer Institute, University of Rochester Medical Center, Rochester, USA
               type:PostalAddress
            type:Organization
            name:China Medical University/Hospital
            address:
               name:Department of Urology, China Medical University/Hospital, Taichung, Taiwan
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Urology, Shanghai Tenth People’s Hospital, Tongji University, Shanghai, China
      name:George Whipple Lab for Cancer Research, Departments of Pathology, Urology, Radiation Oncology and The Wilmot Cancer Institute, University of Rochester Medical Center, Rochester, USA
      name:George Whipple Lab for Cancer Research, Departments of Pathology, Urology, Radiation Oncology and The Wilmot Cancer Institute, University of Rochester Medical Center, Rochester, USA
      name:George Whipple Lab for Cancer Research, Departments of Pathology, Urology, Radiation Oncology and The Wilmot Cancer Institute, University of Rochester Medical Center, Rochester, USA
      name:Department of Urology, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China
      name:Department of Urology, Shanghai Tenth People’s Hospital, Tongji University, Shanghai, China
      name:Department of Urology, Shanghai Tenth People’s Hospital, Tongji University, Shanghai, China
      name:George Whipple Lab for Cancer Research, Departments of Pathology, Urology, Radiation Oncology and The Wilmot Cancer Institute, University of Rochester Medical Center, Rochester, USA
      name:George Whipple Lab for Cancer Research, Departments of Pathology, Urology, Radiation Oncology and The Wilmot Cancer Institute, University of Rochester Medical Center, Rochester, USA
      name:Department of Urology, China Medical University/Hospital, Taichung, Taiwan
      name:Department of Urology, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China
      name:George Whipple Lab for Cancer Research, Departments of Pathology, Urology, Radiation Oncology and The Wilmot Cancer Institute, University of Rochester Medical Center, Rochester, USA
      name:Department of Urology, China Medical University/Hospital, Taichung, Taiwan

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