CALL FOR PAPERS Physiology and GI Cancer Mitochondrial STAT3 contributes to transformation of Barrett’s epithelial cells that express oncogenic Ras in a p53-independent fashion

نویسندگان

  • Chunhua Yu
  • Xiaofang Huo
  • Agoston T. Agoston
  • Xi Zhang
  • Arianne L. Theiss
  • Edaire Cheng
  • Qiuyang Zhang
  • Alexander Zaika
  • Thai H. Pham
  • David H. Wang
  • Peter E. Lobie
  • Robert D. Odze
  • Stuart J. Spechler
  • Rhonda F. Souza
چکیده

Chunhua Yu, Xiaofang Huo, Agoston T. Agoston, Xi Zhang, Arianne L. Theiss, Edaire Cheng, Qiuyang Zhang, Alexander Zaika, Thai H. Pham, David H. Wang, Peter E. Lobie, Robert D. Odze, Stuart J. Spechler, and Rhonda F. Souza Esophageal Diseases Center, Veterans Affairs North Texas Health Care System and the University of Texas Southwestern Medical Center, Dallas, Texas; Department of Medicine, Veterans Affairs North Texas Health Care System and the University of Texas Southwestern Medical Center, Dallas, Texas; Department of Surgery, Veterans Affairs North Texas Health Care System and the University of Texas Southwestern Medical Center, Dallas, Texas; Department of Pathology, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massacusetts; Harold C. Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center, Dallas, Texas; Baylor Research Institute, Baylor University Medical Center, Dallas, Texas; Department of Pediatrics, Children’s Medical Center and the University of Texas Southwestern Medical Center, Dallas, Texas; Departments of Surgery and Cancer Biology, Vanderbilt University Medical Center and the Vanderbilt-Ingram Cancer Center, Nashville, Tennessee; and Cancer Science Institute of Singapore, National University of Singapore, Yong Loo Lin School of Medicine, Singapore

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Mitochondrial STAT3 contributes to transformation of Barrett's epithelial cells that express oncogenic Ras in a p53-independent fashion.

Metaplastic epithelial cells of Barrett's esophagus transformed by the combination of p53-knockdown and oncogenic Ras expression are known to activate signal transducer and activator of transcription 3 (STAT3). When phosphorylated at tyrosine 705 (Tyr705), STAT3 functions as a nuclear transcription factor that can contribute to oncogenesis. STAT3 phosphorylated at serine 727 (Ser727) localizes ...

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The MEK-ERK Pathway Is Necessary for Serine Phosphorylation of Mitochondrial STAT3 and Ras-Mediated Transformation

Activating mutations in the RasGTPases are the most common oncogenic lesions in human cancer. Similarly, elevated STAT3 expression and/or phosphorylation are observed in the majority of human cancers. We recently found that activated Ras requires a mitochondrial rather than a nuclear activity of STAT3 to support cellular transformation. This mitochondrial activity of STAT3 was supported by phos...

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Background Recent studies revealed that tumor-associated macrophages (TAMs) play a decisive role in the regulation of tumor progression by manipulating tumor oncogenesis, angiogenesis and immune functions within tumor microenvironments. Signal transducer and activator of transcription 3 (STAT3), which is a point of convergence for numerous oncogenic signalling pathways, is constitutively activ...

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Constitutive CCND1/CDK2 Activity Substitutes for p53 Loss, or MYC or Oncogenic RAS Expression in the Transformation of Human Mammary Epithelial Cells

Cancer develops following the accumulation of genetic and epigenetic alterations that inactivate tumor suppressor genes and activate proto-oncogenes. Dysregulated cyclin-dependent kinase (CDK) activity has oncogenic potential in breast cancer due to its ability to inactivate key tumor suppressor networks and drive aberrant proliferation. Accumulation or over-expression of cyclin D1 (CCND1) occu...

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Resistance of carcinoma cells to anoikis, apoptosis that is normally induced by detachment of nonmalignant epithelial cells from the extracellular matrix, is thought to be critical for carcinoma progression. Molecular mechanisms that control anoikis of nonmalignant and cancer cells are understood poorly. In an effort to understand them we found that detachment of nonmalignant intestinal epithel...

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تاریخ انتشار 2015