Hypoxia-Inducible Factor 1α Regulates the Transforming Growth Factor β1/ SMAD Family Member 3 Pathway to Promote Breast Cancer Progression

Jianheng Peng; Xiaolin Wang; Liang Ran; Junlong Song; Rong Luo; Yongh

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자료유형: 학술저널

저자정보: Jianheng Peng (The First Affiliated Hospital of Chongqing Medical University) Xiaolin Wang (The First Affiliated Hospital of Chongqing Medical University) Liang Ran (The First Affiliated Hospital of Chongqing Medical University) Junlong Song (Renmin Hospital of Wuhan University) Rong Luo (The First Affiliated Hospital of Chongqing Medical University) Yongh (The First Affiliated Hospital of Chongqing Medical University)

저널정보: 한국유방암학회 Journal of Breast Cancer Journal of Breast Cancer Vol.21 No.3

발행연도: 2018.1

수록면: 259 - 266 (8page)

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Purpose: The transforming growth factor β1 (TGF-β1)/SMAD family member 3 (SMAD3) pathway, and hypoxia-inducible factor 1α (HIF-1α) are two key players in various types of malignancies including breast cancer. The TGF-β1/SMAD3 pathway can interact with HIF-1α in some diseases; however, their interaction in breast cancer is still unknown. Therefore, our study aimed to investigate the interactions between the TGF-β1/SMAD3 pathway and HIF-1α in breast cancer. Methods: Expression of HIF-1α in serum of breast cancer patients and healthy controls was detected by quantitative reverse transcription polymerase chain reaction, and the diagnostic value of HIF-1α for breast cancer was evaluated by receiver operating characteristic curve analysis. Breast cancer cell lines overexpressing SMAD3 and HIF-1α were established. Cell apoptosis and proliferation following different treatments were detected by 3-(4,5-dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide, and cell counting kit-8, respectively. Expression of related proteins was detected by western blot. Results: Serum levels of HIF-1α were higher in breast cancer patients than in normal controls. Both SMAD3 and HIF-1α overexpression inhibited cell apoptosis and promoted cell proliferation. Treatment with inhibitors of HIF-1α and SMAD3 promoted apoptosis in breast cancer cells and inhibited their proliferation. Overexpression of HIF-1α promoted the expression of TGF-β1 and SMAD3, while SMAD3 overexpression did not significantly affect expression of HIF-1α or TGF-β1. Conclusion: HIF-1α serves as an upstream regulator of the TGF-β1/SMAD3 pathway and promotes the growth of breast cancer.

참고문헌 (21)

참고문헌 신청

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