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MACC1 decreases the chemosensitivity of gastric cancer cells to oxaliplatin by regulating FASN expression

  • Authors:
    • Jiangman Duan
    • Lishan Chen
    • Minyu Zhou
    • Jingwen Zhang
    • Li Sun
    • Na Huang
    • Jianping Bin
    • Yulin Liao
    • Wangjun Liao
  • View Affiliations / Copyright

    Affiliations: Department of Oncology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, P.R. China, Huiqiao Medical Center, Nanfang Hospital, Southern Medical University, Guangzhou 510515, P.R. China, Department of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, P.R. China
    Copyright: © Duan et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 2583-2592
    |
    Published online on: March 22, 2017
       https://doi.org/10.3892/or.2017.5519
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Abstract

The effect of chemotherapeutic agents is limited as a result of drug resistance, which demands prompt solutions provided by clinical studies. To date, the underlying mechanisms of chemotherapy resistance are relatively unknown. Metastasis-associated in colon cancer 1 (MACC1) is an oncogene associated with the progression and prognosis of gastric cancer (GC). Bioinformatic analysis revealed that MACC1 is positively associated with fatty acid synthase (FASN), a major enzyme of lipogenesis, and drives chemoresistance to oxaliplatin in GC. Similar findings were demonstrated in two GC cell lines (BGC-823 and MKN-28) with MACC1 ectopic expression. We next employed FASN inhibitor C75 or siFASN (small interfering RNA targeted to FASN) to block endogenous fatty acid metabolism and it was revealed that cell proliferation and chemoresistance to oxaliplatin induced by MACC1 upregulation were attenuated by FASN blockade to various extents. Conclusively, these outcomes highlight a novel role of MACC1 in GC cell lipogenesis, and suggest that MACC1 may be an attractive target to decrease oxaliplatin resistance in GC.
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Copy and paste a formatted citation
Spandidos Publications style
Duan J, Chen L, Zhou M, Zhang J, Sun L, Huang N, Bin J, Liao Y and Liao W: MACC1 decreases the chemosensitivity of gastric cancer cells to oxaliplatin by regulating FASN expression. Oncol Rep 37: 2583-2592, 2017.
APA
Duan, J., Chen, L., Zhou, M., Zhang, J., Sun, L., Huang, N. ... Liao, W. (2017). MACC1 decreases the chemosensitivity of gastric cancer cells to oxaliplatin by regulating FASN expression. Oncology Reports, 37, 2583-2592. https://doi.org/10.3892/or.2017.5519
MLA
Duan, J., Chen, L., Zhou, M., Zhang, J., Sun, L., Huang, N., Bin, J., Liao, Y., Liao, W."MACC1 decreases the chemosensitivity of gastric cancer cells to oxaliplatin by regulating FASN expression". Oncology Reports 37.5 (2017): 2583-2592.
Chicago
Duan, J., Chen, L., Zhou, M., Zhang, J., Sun, L., Huang, N., Bin, J., Liao, Y., Liao, W."MACC1 decreases the chemosensitivity of gastric cancer cells to oxaliplatin by regulating FASN expression". Oncology Reports 37, no. 5 (2017): 2583-2592. https://doi.org/10.3892/or.2017.5519
Copy and paste a formatted citation
x
Spandidos Publications style
Duan J, Chen L, Zhou M, Zhang J, Sun L, Huang N, Bin J, Liao Y and Liao W: MACC1 decreases the chemosensitivity of gastric cancer cells to oxaliplatin by regulating FASN expression. Oncol Rep 37: 2583-2592, 2017.
APA
Duan, J., Chen, L., Zhou, M., Zhang, J., Sun, L., Huang, N. ... Liao, W. (2017). MACC1 decreases the chemosensitivity of gastric cancer cells to oxaliplatin by regulating FASN expression. Oncology Reports, 37, 2583-2592. https://doi.org/10.3892/or.2017.5519
MLA
Duan, J., Chen, L., Zhou, M., Zhang, J., Sun, L., Huang, N., Bin, J., Liao, Y., Liao, W."MACC1 decreases the chemosensitivity of gastric cancer cells to oxaliplatin by regulating FASN expression". Oncology Reports 37.5 (2017): 2583-2592.
Chicago
Duan, J., Chen, L., Zhou, M., Zhang, J., Sun, L., Huang, N., Bin, J., Liao, Y., Liao, W."MACC1 decreases the chemosensitivity of gastric cancer cells to oxaliplatin by regulating FASN expression". Oncology Reports 37, no. 5 (2017): 2583-2592. https://doi.org/10.3892/or.2017.5519
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