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      CXCR2 promotes breast cancer metastasis and chemoresistance via suppression of AKT1 and activation of COX2.

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          Abstract

          Metastasis and chemoresistance are two major causes of breast cancer death. We show here that the chemokine receptor CXCR2 was overexpressed in breast cancer cell lines and tissues. CXCR2 promoted anti-apoptosis, anti-senescence, and epithelial-to-mesenchymal transition (EMT) of breast cancer cells, leading to the enhanced metastasis and chemoresistance. Further study suggested that AKT1 and cyclooxygenase-2 (COX2; PTGS2) might mediate the CXCR2 signaling to inversely control the breast cancer metastasis and chemoresistance through the regulation of EMT, apoptosis, and senescence. Analyses of clinical data indicate that the high expression of CXCR2 was correlated with the high expression of COX2 and the low expression of AKT1, P85α, E-cadherin, and β-catenin in cancer tissues. Poor outcomes were associated with the high expression of CXCR2 or COX2 while favorable survivals were associated with the high expression of P85α, AKT1, or E-cadherin in all cancer patients. Cox multivariate analysis demonstrated that CXCR2, COX2, and AKT1 could be independent predictors for disease free survivals. All these data suggest that CXCR2 promotes breast cancer metastasis and chemoresistance via suppressing AKT1 and activating COX2. Thus, antagonists of the CXCR2 signaling molecules may be used to treat breast cancer patients particularly with high metastasis and chemoresistance.

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          Author and article information

          Journal
          Cancer Lett.
          Cancer letters
          Elsevier BV
          1872-7980
          0304-3835
          January 01 2018
          : 412
          Affiliations
          [1 ] Cancer Institute, Fudan University Shanghai Cancer Center, Shanghai, 200032, China; Department of Breast Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China; Department of Oncology, Shanghai Medical College, Fudan University, 200032, China.
          [2 ] Cancer Institute, Fudan University Shanghai Cancer Center, Shanghai, 200032, China; Department of Oncology, Shanghai Medical College, Fudan University, 200032, China.
          [3 ] Department of Breast Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China; Department of Oncology, Shanghai Medical College, Fudan University, 200032, China.
          [4 ] Cancer Institute, Fudan University Shanghai Cancer Center, Shanghai, 200032, China; Department of Breast Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China; Department of Oncology, Shanghai Medical College, Fudan University, 200032, China. Electronic address: zhimingshao@yahoo.com.
          [5 ] Department of Breast Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China; Department of Oncology, Shanghai Medical College, Fudan University, 200032, China. Electronic address: genghongdi@yahoo.com.
          [6 ] Cancer Institute, Fudan University Shanghai Cancer Center, Shanghai, 200032, China; Department of Oncology, Shanghai Medical College, Fudan University, 200032, China; Central Laboratory, The Fifth People's Hospital of Shanghai, Fudan University, 200240, China. Electronic address: yanggong@fudan.edu.cn.
          Article
          S0304-3835(17)30583-9
          10.1016/j.canlet.2017.09.030
          28964785

          CXCR2, COX2, Breast cancer, AKT1, Metastasis

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