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May-2015 Volume 11 Issue 5

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Article

Akt regulation of Aven contributes to the sensitivity of cancer cells to chemotherapeutic agents

  • Authors:
    • Kyoung‑Youn Han
    • Jee Won Hwang
    • Gyu‑Un Bae
    • Su‑Nam Kim
    • Yong Kee Kim
  • View Affiliations / Copyright

    Affiliations: Research Center for Cell Fate Control, College of Pharmacy, Sookmyung Women's University, Seoul 140‑742, Republic of Korea, Natural Products Research Center, Korea Institute of Science and Technology, Gangneung Institute, Gangneung, Gangwon‑do 210‑340, Republic of Korea
  • Pages: 3866-3871
    |
    Published online on: January 8, 2015
       https://doi.org/10.3892/mmr.2015.3158
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Abstract

In the present study, it was demonstrated that the protein level of the apoptosis inhibitor Aven is regulated by the Akt signaling pathway, evidenced by the observation that Aven levels were significantly increased in MCF7 constitutively active (CA)‑Akt cells and significantly inhibited following treatment with LY294002. This increase in Aven appears not to be mediated by transcriptional regulation and protein stabilization. However, the level of Aven was inversely correlated with the level of cathepsin D, which is a protease responsible for generating the C‑terminal of Aven, ΔN‑Aven, indicating that the level of Aven appears to be regulated by cathepsin D activity. It has previously been reported that ΔN‑Aven is the active form of Aven, which functions as an anti‑apoptotic molecule. Notably, low levels of ΔN‑Aven were detected in MCF7 CA‑Akt cells, which were more sensitive to anticancer drugs. Taken together, the current results suggest that the expression of Aven is regulated by the Akt signaling pathway through cathepsin D activity, which contributes to the sensitivity of cancer cells to chemotherapeutic agents.
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Copy and paste a formatted citation
Spandidos Publications style
Han KY, Hwang JW, Bae GU, Kim SN and Kim YK: Akt regulation of Aven contributes to the sensitivity of cancer cells to chemotherapeutic agents. Mol Med Rep 11: 3866-3871, 2015.
APA
Han, K., Hwang, J.W., Bae, G., Kim, S., & Kim, Y.K. (2015). Akt regulation of Aven contributes to the sensitivity of cancer cells to chemotherapeutic agents. Molecular Medicine Reports, 11, 3866-3871. https://doi.org/10.3892/mmr.2015.3158
MLA
Han, K., Hwang, J. W., Bae, G., Kim, S., Kim, Y. K."Akt regulation of Aven contributes to the sensitivity of cancer cells to chemotherapeutic agents". Molecular Medicine Reports 11.5 (2015): 3866-3871.
Chicago
Han, K., Hwang, J. W., Bae, G., Kim, S., Kim, Y. K."Akt regulation of Aven contributes to the sensitivity of cancer cells to chemotherapeutic agents". Molecular Medicine Reports 11, no. 5 (2015): 3866-3871. https://doi.org/10.3892/mmr.2015.3158
Copy and paste a formatted citation
x
Spandidos Publications style
Han KY, Hwang JW, Bae GU, Kim SN and Kim YK: Akt regulation of Aven contributes to the sensitivity of cancer cells to chemotherapeutic agents. Mol Med Rep 11: 3866-3871, 2015.
APA
Han, K., Hwang, J.W., Bae, G., Kim, S., & Kim, Y.K. (2015). Akt regulation of Aven contributes to the sensitivity of cancer cells to chemotherapeutic agents. Molecular Medicine Reports, 11, 3866-3871. https://doi.org/10.3892/mmr.2015.3158
MLA
Han, K., Hwang, J. W., Bae, G., Kim, S., Kim, Y. K."Akt regulation of Aven contributes to the sensitivity of cancer cells to chemotherapeutic agents". Molecular Medicine Reports 11.5 (2015): 3866-3871.
Chicago
Han, K., Hwang, J. W., Bae, G., Kim, S., Kim, Y. K."Akt regulation of Aven contributes to the sensitivity of cancer cells to chemotherapeutic agents". Molecular Medicine Reports 11, no. 5 (2015): 3866-3871. https://doi.org/10.3892/mmr.2015.3158
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