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- W3132199547 abstract "Aim. The main objective of this article was to evaluate the association of voltage-dependent anion channel 1 (VDAC1) with Cytochrome C (Cytc) expression, various clinicopathological features, and prognosis in breast cancer (BC) patients. Meanwhile, the correlation of Cytc expression with various clinical features and 5-year disease-free survival (5-DFS) of BC was also investigated. Methods. In vivo, expression of VDAC1 and Cytc was examined in 219 BC tissues and 100 benign breast lesions by immunohistochemical (IHC) analysis. In vitro, MTT and wound healing migration assay were performed to detect the effect of VDAC1 on BC cells. Results. Expression of VDAC1 is conversely associated with Cytc in BC ( <math xmlns=http://www.w3.org/1998/Math/MathML id=M1> <mi>P</mi> <mo>=</mo> <mn>0.011</mn> </math> ), especially in triple-negative breast cancer (TNBC) ( <math xmlns=http://www.w3.org/1998/Math/MathML id=M2> <mi>P</mi> <mo>=</mo> <mn>0.004</mn> </math> ). Knockdown of VDAC1 inhibited proliferation ( <math xmlns=http://www.w3.org/1998/Math/MathML id=M3> <mi>P</mi> <mo><</mo> <mn>0.001</mn> </math> ) and migration ( <math xmlns=http://www.w3.org/1998/Math/MathML id=M4> <mi>P</mi> <mo><</mo> <mn>0.05</mn> </math> ) of MCF-7 cells. High expression of VDAC1 and low expression of Cytc had a significant association with multiple clinicopathological parameters ( <math xmlns=http://www.w3.org/1998/Math/MathML id=M5> <mi>P</mi> <mo><</mo> <mn>0.05</mn> </math> ) and poor 5-DFS ( <math xmlns=http://www.w3.org/1998/Math/MathML id=M6> <mi>P</mi> <mo><</mo> <mn>0.001</mn> </math> ) in BC. Conclusion. VDAC1 was elevated in BC tissues and conversely associated with Cytc. Detection of VDAC1 may provide guidance for the poor prognosis of BC, especially TNBC." @default.
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- W3132199547 date "2021-02-17" @default.
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- W3132199547 title "VDAC1 Conversely Correlates with Cytc Expression and Predicts Poor Prognosis in Human Breast Cancer Patients" @default.
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- W3132199547 doi "https://doi.org/10.1155/2021/7647139" @default.
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