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Article

OCT4B1 promotes cell growth, migration and invasion suppressing sensitivity to οxaliplatin in colon cancer

  • Authors:
    • Kun-Ming Wen
    • Gui-Hai Zhang
    • Jiang Li
    • Zheng-Quan Chen
    • Yi-Lin Cheng
    • Xuan Su
    • Qing-Liang Zeng
  • View Affiliations / Copyright

    Affiliations: Department of Gastrointestinal Surgery, The Affiliated Hospital of Zunyi Medical College, Zunyi, Guizhou 563000, P.R. China, Department of Abdominal Oncology, The Affiliated Hospital of Zunyi Medical College, Zunyi, Guizhou 563000, P.R. China
  • Pages: 2943-2952
    |
    Published online on: September 17, 2015
       https://doi.org/10.3892/or.2015.4286
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Abstract

OCT4B1, a splice variant of OCT4, is a key regulator in maintaining the properties of pluripotency and self-renewal in embryonic stem (ES) cells. Recent results have shown that OCT4B1 is involved in tumorigenesis. However, the contribution of OCT4B1 in the tumorigenesis and drug resistance of colon cancer remains to be determined. The aim of the present study was to determine whether OCT4B1, which maintains the stemness of ES cells, promoted cell growth by facilitating transition of the cell cycle and reduced apoptosis in colon cancer and drug‑resistant cells using flow cytometry and western blotting. The results showed that, OCT4B1 promoted the growth of colon cancer and drug‑resistant cancer cells by maintaining the activity of ES cells and by facilitating the transition of the cell cycle and reducing apoptosis. Additionally, OCT4B1 was able to reduce sensitivity to oxaliplatin by altering the expression of two important mediators in drug resistance, P-gp and ABCG2 [ATP-binding cassette, sub‑family G (WHITE), member 2]. Furthermore, OCT4B1 enhanced the ability of migration and invasion through alteration of the epithelial-to-mesenchymal transition (EMT) in colon cancer. In conclusion, to the best of our knowledge, the results demonstrated for the first time that OCT4B1 functions as an oncogene in colon cancer and provides the development of novel therapeutic strategies to treat colon cancer, particularly drug resistance.
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Copy and paste a formatted citation
Spandidos Publications style
Wen K, Zhang G, Li J, Chen Z, Cheng Y, Su X and Zeng Q: OCT4B1 promotes cell growth, migration and invasion suppressing sensitivity to οxaliplatin in colon cancer. Oncol Rep 34: 2943-2952, 2015.
APA
Wen, K., Zhang, G., Li, J., Chen, Z., Cheng, Y., Su, X., & Zeng, Q. (2015). OCT4B1 promotes cell growth, migration and invasion suppressing sensitivity to οxaliplatin in colon cancer. Oncology Reports, 34, 2943-2952. https://doi.org/10.3892/or.2015.4286
MLA
Wen, K., Zhang, G., Li, J., Chen, Z., Cheng, Y., Su, X., Zeng, Q."OCT4B1 promotes cell growth, migration and invasion suppressing sensitivity to οxaliplatin in colon cancer". Oncology Reports 34.6 (2015): 2943-2952.
Chicago
Wen, K., Zhang, G., Li, J., Chen, Z., Cheng, Y., Su, X., Zeng, Q."OCT4B1 promotes cell growth, migration and invasion suppressing sensitivity to οxaliplatin in colon cancer". Oncology Reports 34, no. 6 (2015): 2943-2952. https://doi.org/10.3892/or.2015.4286
Copy and paste a formatted citation
x
Spandidos Publications style
Wen K, Zhang G, Li J, Chen Z, Cheng Y, Su X and Zeng Q: OCT4B1 promotes cell growth, migration and invasion suppressing sensitivity to οxaliplatin in colon cancer. Oncol Rep 34: 2943-2952, 2015.
APA
Wen, K., Zhang, G., Li, J., Chen, Z., Cheng, Y., Su, X., & Zeng, Q. (2015). OCT4B1 promotes cell growth, migration and invasion suppressing sensitivity to οxaliplatin in colon cancer. Oncology Reports, 34, 2943-2952. https://doi.org/10.3892/or.2015.4286
MLA
Wen, K., Zhang, G., Li, J., Chen, Z., Cheng, Y., Su, X., Zeng, Q."OCT4B1 promotes cell growth, migration and invasion suppressing sensitivity to οxaliplatin in colon cancer". Oncology Reports 34.6 (2015): 2943-2952.
Chicago
Wen, K., Zhang, G., Li, J., Chen, Z., Cheng, Y., Su, X., Zeng, Q."OCT4B1 promotes cell growth, migration and invasion suppressing sensitivity to οxaliplatin in colon cancer". Oncology Reports 34, no. 6 (2015): 2943-2952. https://doi.org/10.3892/or.2015.4286
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