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10.18632/oncotarget.13234

http://scihub22266oqcxt.onion/10.18632/oncotarget.13234
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C5348403!5348403 !27833078
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suck abstract from ncbi


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pmid27833078
      Oncotarget 2016 ; 7 (49 ): 81423-81434
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  • Dapper homolog 1 alpha suppresses metastasis ability of gastric cancer through inhibiting planar cell polarity pathway #MMPMID27833078
  • Liu Y ; Zhang J ; Yu W ; Zhang X ; Wang G ; Zhao Z
  • Oncotarget 2016[Dec]; 7 (49 ): 81423-81434 PMID27833078 show ga
  • Dapper homolog 1 alpha (DACT1?) is a member of DACT family and an important regulator in the planar cell polarity pathway. We aim to clarify its functional role in metastasis ability of gastric cancer. DACT1? was silenced in all gastric cancer cell lines (8/8), but expressed in normal gastric tissue. Ectopic expression of DACT1? in silenced gastric cancer cell lines (AGS, BGC823 and MGC803) by stable transfection significantly suppressed cancer cell spreading (P < 0.05), migration (P < 0.01) and invasion (P < 0.01). These effects were associated with downregulation of planar cell polarity pathway related genes involved in cell proliferation (PDGFB, VEGFA), adhesion (ITGA1, ITGA2, ITGA3, ITGB3) and migration/invasion (PLAU, MMP9, MCAM, Dvl-2 and JNK). DACT1? promoter methylation was detected in 205 gastric cancers and 20 normal controls by direct bisulfite genomic sequencing. DACT1? methylation was detected in 29.3% (60/205) of gastric cancer patients, but not in normal tissues. DACT1? methylation was associated with poor survival of gastric cancer patients. In conclusion, DACT1? plays a pivotal role as a potential tumor suppressor in migration and invasion of gastric cancer. DACT1? methylation may serve as a biomarker for the prognosis of gastric cancer.
  • |*Cell Movement [MESH]
  • |*Cell Plasticity [MESH]
  • |Adaptor Proteins, Signal Transducing/genetics/*metabolism [MESH]
  • |Cell Line, Tumor [MESH]
  • |Cell Proliferation [MESH]
  • |Cell Shape [MESH]
  • |DNA Methylation [MESH]
  • |Female [MESH]
  • |Gene Expression Regulation, Neoplastic [MESH]
  • |Humans [MESH]
  • |Kaplan-Meier Estimate [MESH]
  • |Male [MESH]
  • |Neoplasm Invasiveness [MESH]
  • |Nuclear Proteins/genetics/*metabolism [MESH]
  • |Phenotype [MESH]
  • |Proportional Hazards Models [MESH]
  • |Signal Transduction [MESH]
  • |Stomach Neoplasms/genetics/*metabolism/mortality/pathology [MESH]
  • |Time Factors [MESH]
  • |Transfection [MESH]


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