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

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.

journal_name

Mol Med Rep

authors

Han KY,Hwang JW,Bae GU,Kim SN,Kim YK

doi

10.3892/mmr.2015.3158

subject

Has Abstract

pub_date

2015-05-01 00:00:00

pages

3866-71

issue

5

eissn

1791-2997

issn

1791-3004

journal_volume

11

pub_type

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