We are analyzing https://link.springer.com/article/10.1007/s12015-015-9611-y.

Title:
The Role of Hypoxia and Cancer Stem Cells in Renal Cell Carcinoma Pathogenesis | Stem Cell Reviews and Reports
Description:
The cancer stem cell (CSC) model has recently been approached also in renal cell carcinoma (RCC). A few populations of putative renal tumor-initiating cells (TICs) were identified, but they are indifferently understood; however, the first and most thoroughly investigated are CD105-positive CSCs. The article presents a detailed comparison of all renal CSC-like populations identified by now as well as their presumable origin. Hypoxic activation of hypoxia-inducible factors (HIFs) contributes to tumor aggressiveness by multiple molecular pathways, including the governance of immature stem cell-like phenotype and related epithelial-to-mesenchymal transition (EMT)/de-differentiation, and, as a result, poor prognosis. Due to intrinsic von Hippel-Lindau protein (pVHL) loss of function, clear-cell RCC (ccRCC) develops unique pathological intra-cellular pseudo-hypoxic phenotype with a constant HIF activation, regardless of oxygen level. Despite satisfactory evidence concerning pseudo-hypoxia importance in RCC biology, its influence on putative renal CSC-like largely remains unknown. Thus, the article discusses a current knowledge of HIF-1α/2α signaling pathways in the promotion of undifferentiated tumor phenotype in general, including some experimental findings specific for pseudo-hypoxic ccRCC, mostly dependent from HIF-2α oncogenic functions. Existing gaps in understanding both putative renal CSCs and their potential connection with hypoxia need to be filled in order to propose breakthrough strategies for RCC treatment.
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Keywords {🔍}

pubmed, cells, cell, google, scholar, article, cancer, cas, renal, stem, tumor, rcc, hifα, central, hypoxia, cscs, carcinoma, expression, journal, human, phenotype, ccrcc, kidney, research, csc, gene, molecular, vhl, population, differentiation, epithelial, growth, clinical, markers, putative, marker, role, nature, pvhl, csclike, normal, tumors, factors, endothelial, factor, hif, signaling, mesenchymal, hypoxiainducible, treatment,

Topics {✒️}

stem cell-specific anti-human-cd133/1 hif-2α-driven pseudo-hypoxic phenotype stromal cell-derived factor-1alpha hypoxia-inducible factor-1-dependent repression hypoxia-inducible factor-2alpha knock dual-blocking epithelial-mesenchymal transition activating hypoxia-inducible factor-2α von hippel-lindau protein hypoxia-inducible factor-2alpha correlates kidney-specific stem/progenitor cells mapk/erk-dependent autocrine loop hif-1α/2α-mediated transcription complex recruiting hif-1α/2α sk-rc-42 sphere-forming resident stem/progenitor cells von hippel-lindau function hypoxia-inducible factor-1-dependent regulation hif-1α/2α-expressing subtype stem/progenitor cell pools von hippel-lindau loss hif-1α/2α signaling pathways bone marrow-derived cells tumorigenic multipotent/bipotent csc pro-metastatic emt-related genes pseudo-tubular structures mimic kidney-resident stem cells transforming growth factor-β tumor-suppressor functions unrelated renal cell carcinoma--rationale wnt/β-catenin signalling tumor necrosis factor-α modulating mir-141/zeb2 signaling normal stem/progenitor cells article download pdf renal tumor-initiating cells hypoxia-inducible factor-2a subsequent proteasome-mediated degradation von hippel-lindau von hippel--lindau von hippel-lindau nuclear hif-1α protein transforming growth factor-alpha carrying pro-angiogenic mrnas hypoxia-inducible factor-1alpha hypoxia-inducible factor 1alpha bayer healthcare/onyx pharmaceuticals pre-malignant cystic lesions cd133+/cd24+ tubular progenitors cd133+/cd24+/ctr2+ cells vhl tumor-suppressor gene

Questions {❓}

Do stem cells exist in the adult kidney?
Pharmacogenomics and cancer stem cells: a changing landscape?
The question is, what happens within putative pVHL −/− pseudo-hypoxic renal CSCs when acute/chronic hypoxia starts to develop within a tumor?
Why is the partial oxygen pressure of human tissues a crucial parameter?

Schema {🗺️}

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      headline:The Role of Hypoxia and Cancer Stem Cells in Renal Cell Carcinoma Pathogenesis
      description:The cancer stem cell (CSC) model has recently been approached also in renal cell carcinoma (RCC). A few populations of putative renal tumor-initiating cells (TICs) were identified, but they are indifferently understood; however, the first and most thoroughly investigated are CD105-positive CSCs. The article presents a detailed comparison of all renal CSC-like populations identified by now as well as their presumable origin. Hypoxic activation of hypoxia-inducible factors (HIFs) contributes to tumor aggressiveness by multiple molecular pathways, including the governance of immature stem cell-like phenotype and related epithelial-to-mesenchymal transition (EMT)/de-differentiation, and, as a result, poor prognosis. Due to intrinsic von Hippel-Lindau protein (pVHL) loss of function, clear-cell RCC (ccRCC) develops unique pathological intra-cellular pseudo-hypoxic phenotype with a constant HIF activation, regardless of oxygen level. Despite satisfactory evidence concerning pseudo-hypoxia importance in RCC biology, its influence on putative renal CSC-like largely remains unknown. Thus, the article discusses a current knowledge of HIF-1α/2α signaling pathways in the promotion of undifferentiated tumor phenotype in general, including some experimental findings specific for pseudo-hypoxic ccRCC, mostly dependent from HIF-2α oncogenic functions. Existing gaps in understanding both putative renal CSCs and their potential connection with hypoxia need to be filled in order to propose breakthrough strategies for RCC treatment.
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          Cancer stem cells
         Hypoxia-inducible factors (HIF-1α, HIF-2α)
         von Hippel-Lindau protein (pVHL)
         Epithelial-to-mesenchymal transition
         Stem Cells
         Regenerative Medicine/Tissue Engineering
         Cell Biology
         Biomedical Engineering and Bioengineering
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      name:Department of Oncology with Laboratory of Molecular Oncology, Military Institute of Medicine, Warsaw, Poland
      name:Department of Oncology with Laboratory of Molecular Oncology, Military Institute of Medicine, Warsaw, Poland
      name:School of Molecular Medicine, Medical University of Warsaw, Warsaw, Poland
      name:Department of Oncology with Laboratory of Molecular Oncology, Military Institute of Medicine, Warsaw, Poland
      name:Institute of Genetics and Biotechnology, Faculty of Biology, University of Warsaw, Warsaw, Poland
      name:Emory School of Medicine, Atlanta, USA
      name:Department of Oncology with Laboratory of Molecular Oncology, Military Institute of Medicine, Warsaw, Poland
      name:School of Molecular Medicine, Medical University of Warsaw, Warsaw, Poland
      name:Department of General Surgery and Transplantology, Medical University of Warsaw, Warsaw, Poland
      name:Institute of Genetics and Biotechnology, Faculty of Biology, University of Warsaw, Warsaw, Poland
      name:Institute of Biochemistry and Biophysics, Polish Academy of Sciences, Warsaw, Poland
      name:Department of Otolaryngology, Czerniakowski Hospital, Medical University of Warsaw, Warsaw, Poland
      name:Centre de Biophysique Moléculaire, CNRS UPR 4301, Orléans, France
      name:Department of Oncology with Laboratory of Molecular Oncology, Military Institute of Medicine, Warsaw, Poland

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