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Article

Caveolin-1 plays a key role in the oleanolic acid-induced apoptosis of HL-60 cells

  • Authors:
    • Wei Ma
    • Di-Di Wang
    • Li Li
    • Yu-Kuan Feng
    • Hong-Mei Gu
    • Gui-Ming Zhu
    • Jin-Hua Piao
    • Yu Yang
    • Xu Gao
    • Peng-Xia Zhang
  • View Affiliations / Copyright

    Affiliations: School of Basic Medicine, Jiamusi University, Jiamusi 154000, P.R. China, Department of Biology, Mudanjiang Medical University, Mudanjiang 157011, P.R. China, Department of Biochemistry, Harbin Medical University, Harbin 150086, P.R. China
  • Pages: 293-301
    |
    Published online on: May 15, 2014
       https://doi.org/10.3892/or.2014.3177
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Abstract

Our previous study found that caveolin-1 (CAV-1) protein expression is upregulated during oleanolic acid (OA)-induced inhibition of proliferation and promotion of apoptosis in HL-60 cells. CAV-1 is the main structural protein component of caveolae, playing important roles in tumorigenesis and tumor development. It has been shown that cav-1 expression is lower in leukemia cancer cell lines SUP-B15, HL-60, THP-1 and K562 and in chronic lymphocytic leukemia primary (CLP) cells when compared with normal white blood cells, with the lowest cav-1 expression level found in HL-60 cells. To study the effects of cav-1 in HL-60 cells and the effects of cav-1 overexpression on OA drug efficacy, cav-1 was overexpressed in HL-60 cells using lentiviral-mediated transfection combined with OA treatment. The results showed that cav-1 overexpression inhibited HL-60 cell proliferation, promoted apoptosis, arrested the cell cycle in the G1 phase and inhibited activation of the PI3K/AKT/mTOR signaling pathway. Overexpression of CAV-1 also increased HL-60 cell sensitivity to OA. To further verify whether OA affects HL-60 cells via the activation of downstream signaling pathways by CAV-1, cav-1 gene expression was silenced using RNAi, and the cells were treated with OA to examine its efficacy. The results showed that after cav-1 silencing, OA had little effect on cell activity, apoptosis, the cell cycle and phosphorylation of HL-60 cells. This study is the first to show that CAV-1 plays a crucial role in the effects of OA on HL-60 cells.
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Copy and paste a formatted citation
Spandidos Publications style
Ma W, Wang D, Li L, Feng Y, Gu H, Zhu G, Piao J, Yang Y, Gao X, Zhang P, Zhang P, et al: Caveolin-1 plays a key role in the oleanolic acid-induced apoptosis of HL-60 cells. Oncol Rep 32: 293-301, 2014.
APA
Ma, W., Wang, D., Li, L., Feng, Y., Gu, H., Zhu, G. ... Zhang, P. (2014). Caveolin-1 plays a key role in the oleanolic acid-induced apoptosis of HL-60 cells. Oncology Reports, 32, 293-301. https://doi.org/10.3892/or.2014.3177
MLA
Ma, W., Wang, D., Li, L., Feng, Y., Gu, H., Zhu, G., Piao, J., Yang, Y., Gao, X., Zhang, P."Caveolin-1 plays a key role in the oleanolic acid-induced apoptosis of HL-60 cells". Oncology Reports 32.1 (2014): 293-301.
Chicago
Ma, W., Wang, D., Li, L., Feng, Y., Gu, H., Zhu, G., Piao, J., Yang, Y., Gao, X., Zhang, P."Caveolin-1 plays a key role in the oleanolic acid-induced apoptosis of HL-60 cells". Oncology Reports 32, no. 1 (2014): 293-301. https://doi.org/10.3892/or.2014.3177
Copy and paste a formatted citation
x
Spandidos Publications style
Ma W, Wang D, Li L, Feng Y, Gu H, Zhu G, Piao J, Yang Y, Gao X, Zhang P, Zhang P, et al: Caveolin-1 plays a key role in the oleanolic acid-induced apoptosis of HL-60 cells. Oncol Rep 32: 293-301, 2014.
APA
Ma, W., Wang, D., Li, L., Feng, Y., Gu, H., Zhu, G. ... Zhang, P. (2014). Caveolin-1 plays a key role in the oleanolic acid-induced apoptosis of HL-60 cells. Oncology Reports, 32, 293-301. https://doi.org/10.3892/or.2014.3177
MLA
Ma, W., Wang, D., Li, L., Feng, Y., Gu, H., Zhu, G., Piao, J., Yang, Y., Gao, X., Zhang, P."Caveolin-1 plays a key role in the oleanolic acid-induced apoptosis of HL-60 cells". Oncology Reports 32.1 (2014): 293-301.
Chicago
Ma, W., Wang, D., Li, L., Feng, Y., Gu, H., Zhu, G., Piao, J., Yang, Y., Gao, X., Zhang, P."Caveolin-1 plays a key role in the oleanolic acid-induced apoptosis of HL-60 cells". Oncology Reports 32, no. 1 (2014): 293-301. https://doi.org/10.3892/or.2014.3177
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