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. 2019 Sep 12;9(49):28775-28782.
doi: 10.1039/c9ra05572j. eCollection 2019 Sep 9.

Retracted Article: Aclarubicin regulates glioma cell growth and DNA damage through the SIRT1/PI3K/AKT signaling pathway

Jun-Feng Huo  1 , Xiao-Bing Chen  1
Affiliations

Retracted Article: Aclarubicin regulates glioma cell growth and DNA damage through the SIRT1/PI3K/AKT signaling pathway

Jun-Feng Huo et al. RSC Adv. .

Retraction in

Abstract

Aclarubicin (ACR), an anthracycline anti-tumor agent, is known to play important roles in cancer. Evidence has suggested that ACR has therapeutic effects on rats intracranially implanted with C6 glioma cells. However, the function and mechanism of ACR in glioma cells remain elusive. In this study, we examined the effects of ACR on glioma cell growth, apoptosis, and DNA damage. Our results showed that treatment with different concentrations of ACR (1, 2, and 5 μM) markedly impeded glioma cell survival, significantly decreased cell proliferation, and increased cell apoptosis and caspase-3 activity. Furthermore, ACR treatment promoted DNA damage through phosphorylation of ATM and CHK1 in U87 and U251 cells. Treatment with ACR also increased sirtuin 1 (SIRT1) expression and inhibited phosphatidylinositol 3'-kinase (PI3K)/AKT pathway activation. Interestingly, we found that AKT overexpression reversed the effects of ACR on glioma cell survival, proliferation, apoptosis, and DNA damage. Thus, our data suggest that ACR induces apoptosis and DNA damage in U87 and U251 cells through the SIRT1/PI3K/AKT signaling pathway.

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Conflict of interest statement

There is no conflict of interest to be declared by the authors.

Figures

Fig. 1
Fig. 1. Structure of ACR.
Fig. 2
Fig. 2. ACR suppressed cell growth and promoted cell apoptosis in U87 and U251 cells. (A and B) The CellTiter-Blue kit was used to detect cell survival. (C) CCK-8 assay was used to measure cell proliferation. (D) Cell death detection ELISA assay was used to detect cell apoptosis. (E) Caspase-3/CPP32 colorimetric assay kit was used to measure caspase-3 activity. For cell survival analysis, U87 and U251 cells were treated with 1, 2, and 5 μM ACR for 1, 6, 12, and 24 h. For evaluation of cell proliferation, apoptosis, and caspase-3 activity, U87 and U251 cells were treated with 5 μM ACR for 12 h. Control cells were left untreated. *p < 0.05 compared with the control group.
Fig. 3
Fig. 3. ACR increased U87 and U251 cell DNA damage. Western blotting was used to measure the protein expression of pATM, pCHK1, ATM, and CHK1 in U87 (A) and U251 (B) cells. U87 and U251 cells were treated with 5 μM ACR for 12 h. Control cells were left untreated. *p < 0.05 compared with the control group.
Fig. 4
Fig. 4. ACR induced the activation of SIRT1/PI3K/AKT signaling pathway in U87 and U251 cells. Western blotting was used to measure the protein expression of SIRT1, pAKT, and AKT in U87 (A) and U251 (B) cells. U87 and U251 cells were transfected with control or SIRT1 siRNA for 48 h and then treated with 5 μM ACR for 12 h. Control cells were left untreated. *p < 0.05 compared with the control group, #p < 0.05 compared with the ACR group.
Fig. 5
Fig. 5. Overexpression of PI3K/AKT reversed the effects of ACR in U87 cells. (A) Western blotting was used to measure the protein expression of pAKT and AKT. (B) CellTiter-Blue kit was used to detect cell survival. (C) CCK-8 assay was used to measure cell proliferation. (D) Cell death detection ELISA assay was used to detect cell apoptosis. (E) Caspase-3/CPP32 colorimetric assay kit was used to measure caspase-3 activity. (F) Western blotting was used to measure the protein expression of pATM and pCHK1. U87 cells were transfected with pcDNA3.1 or pcDNA3.1-AKT vector for 48 h and then treated with 5 μM ACR for 12 h. Control cells were left untreated. *p < 0.05 compared with the control group, #p < 0.05 compared with the ACR group.
Fig. 6
Fig. 6. Schematic model of ACR-mediated regulation of glioma cell growth and DNA damage via the SIRT1/PI3K/AKT signaling pathway.
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