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• W2890536615 abstract "Abstract Background Concerns about breast cancer had become the most dangerous cancer to women over the world, more and more anti‐cancer agents are developed to treat this malignancy. Pharmorubicin is a cytotoxic drug, widely used in the treatment of breast cancer, but its role is limited because of chemoresistance produced by cells. This study focused on exploring the influence of autophagy on the resistance of pharmorubicin in breast cancer cells. Methods The cell survival of breast cancer cells was detected by MTT . The mRNA expression of heme oxygenase‐1 ( HO ‐1) was tested by qRT ‐ PCR . The protein expression of HO ‐1, autophagic proteins ( LC 3‐I, LC 3‐ II and Beclin‐1), PI 3K and Akt was detected by Western blot. Cell autophagy was examined by Cyto‐ ID Autophagy Detection Kit. Results After being treated with pharmorubicin, the expression of HO ‐1 and autophagy related proteins was significantly enhanced, but the cell survival ratio in the two cell lines decreased. After autophagy was inhibited, HO ‐1 expression in two cells was down‐regulated. When pharmorubicin‐resistant cells were transfected with si‐ HO ‐1, the cell survival decreased and the protein expression of HO ‐1, autophagic proteins ( LC 3‐ II / LC 3‐I and Beclin‐1) as well as autophagy were all down‐regulated, while in pharmorubicin‐resistant cells transfected with pc DNA 3.1‐ HO ‐1, the results were reverse. When the PI 3K or Akt was inhibited, PI 3K, p‐Akt, HO ‐1, autophagic proteins and autophagy were decreased remarkably. Conclusion It was proved that HO ‐1 induction mediated chemoresistance of pharmorubicin in breast cancer cells by promoting autophagy via PI 3K/Akt pathway." @default.
• W2890536615 created "2018-09-27" @default.
• W2890536615 creator A5020232432 @default.
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• W2890536615 date "2018-09-14" @default.
• W2890536615 modified "2023-10-09" @default.
• W2890536615 title "Heme oxygenase-1 induction mediates chemoresistance of breast cancer cells to pharmorubicin by promoting autophagy via PI3K/Akt pathway" @default.
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• W2890536615 doi "https://doi.org/10.1111/jcmm.13800" @default.
• W2890536615 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6201364" @default.
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