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标题:Distinct subgroup of the Ras family member 3 (DIRAS3) expression impairs metastasis and induces autophagy of gastric cancer cells in mice.
时间:2019-08-13 23:30:52
DOI:10.1007/s00432-018-2708-3
PMID:30043279
作者:Jingping Qiu;Xiaoting Li;Yingjian He;Dan Sun;Wenhui Li
出版源: Journal of Cancer Research and Clinical Oncology ,2018
摘要:Distinct subgroup of the Ras family member 3 (DIRAS3) expression impairs metastasis and induces autophagy of gastric cancer cells in micePurpose Distinct subgroup of the Ras family member 3 (DIRAS3), also called Aplasia Ras homolog member I, is a tumor suppressor gene that induces autophagy in several cancer cell lines....
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目录:
  • Distinct subgroup of the Ras family member 3 (DIRAS3) expression impairs metastasis and induces autophagy of gastric cancer cells in mice
    • Abstract
      • Purpose
      • Methods
      • Results
      • Conclusions
    • Background
    • Methods
      • Patients
      • Tissue microarray
      • Immunohistochemistry
      • Cell culture and overexpression transfection constructs
      • Quantitative real-time reverse transcriptase PCR (qRT-PCR)
      • Western blotting
      • Epigenetic modifiers 5-AZA-dC and TSA
      • Mouse models of subcutaneous xenograft
      • Mouse model of hematogenous metastasis
      • Statistical analysis
    • Results
      • DIRAS3, LC3B-II and p62 protein amounts are associated with the clinicopathological characteristics in gastric cancer
      • BGC-823 showed the lowest expression of DIRAS3 together with the strongest metastatic abilities among GC cell lines
      • DIRAS3 overexpression inhibits proliferation, migration and invasion of BGC-823 cells possibly associated with promoting autophagy
      • DIRAS3 knockdown increases proliferation and migration in MKN-45 cells
      • DIRAS3 overexpression regulates the biological behavior of BGC-823 cells via multiple signaling pathways
      • DIRAS3 overexpression inhibits the growth of subcutaneous tumors
      • DIRAS3 inhibits lung and liver metastases in nude mice
    • Discussion
    • References

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