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Metformin potentiates rapamycin and cisplatin in gastric cancer in mice

Guanzhen Yu1,2, Wenzheng Fang1,3, Tian Xia4,5

  • 1Department of Medical Oncology, Changzheng Hospital, Shanghai 200070, China.

Oncotarget
|April 25, 2015
PubMed

Insights

Metformin shows potential for gastric cancer treatment by inhibiting tumor growth and enhancing chemotherapy effects. This study highlights its role in regulating key cancer-related pathways and gene expression.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Gastric cancer is characterized by dysregulated signaling pathways, including the AMPK and mTOR pathways.
  • Specific molecular markers like PTEN, MMP7, and DCN1 are altered in gastric cancer tissues.

Purpose of the Study:

  • To investigate the effects of metformin on molecular markers and tumor growth in gastric cancer.
  • To evaluate metformin's efficacy alone and in combination with cisplatin or rapamycin for gastric cancer treatment.

Main Methods:

  • Analysis of protein and gene expression in human gastric cancer tissues versus noncancerous tissues.
  • In vivo studies using mouse models to assess metformin's impact on tumor growth.
  • Evaluation of combination therapies involving metformin, cisplatin, and rapamycin.

Main Results:

  • Metformin down-regulated phosphorylated AMPK (pAMPKα) and PTEN while up-regulating p-mTOR, p-S6, p-4EBP1, MMP7, and DCN1 in gastric cancer tissues.
  • Metformin inhibited tumor growth in mice.
  • Combination therapies with metformin and either cisplatin or rapamycin demonstrated enhanced tumor growth reduction compared to monotherapy.

Conclusions:

  • Metformin influences key molecular pathways (AMPK and mTOR) and gene expression (PTEN, MMP7, FN1) relevant to gastric cancer.
  • Metformin exhibits potential as a therapeutic agent for gastric cancer, particularly when combined with cisplatin or rapamycin.
Keywords:
experimental therapygastric cancergene expressionmetforminmouse model

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