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Article

Annexin A1 is involved in resistance to 5-FU in colon cancer cells

  • Authors:
    • Hisashi Onozawa
    • Motonobu Saito
    • Katsuharu Saito
    • Yasuyuki Kanke
    • Yohei Watanabe
    • Suguru Hayase
    • Wataru Sakamoto
    • Teruhide Ishigame
    • Tomoyuki Momma
    • Shinji Ohki
    • Seiichi Takenoshita
  • View Affiliations / Copyright

    Affiliations: Department of Organ Regulatory Surgery, Fukushima Medical University School of Medicine, Fukushima 960-1295, Japan
  • Pages: 235-240
    |
    Published online on: November 8, 2016
       https://doi.org/10.3892/or.2016.5234
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Abstract

Resistance to 5-fluorouracil (5‑FU), a key drug in the treatment of colorectal cancer, is one of the major reasons for poor patient prognosis during cancer treatment. Annexin A1 (ANXA1) is a calcium‑dependent phospholipid‑linked protein that is associated with drug resistance, anti‑inflammatory effects, regulation of cellular differentiation, proliferation and apoptosis. Although there have been several studies investigating ANXA1 expression in drug resistant cells, the role of ANXA1 is yet to be fully understood. We therefore, in this study, generated SW480 cells resistant to 5‑FU (SW480/5‑FU) to evaluate ANXA1 expression. When compared to the control cells, ANXA1 expression was significantly induced in the SW480/5‑FU cells. We then revealed the role of ANXA1 expression in 5‑FU resistance by using overexpression and knockdown methods in colon cancer cells. Overexpression of ANXA1 induced a significant increase of cell viability to 5‑FU, whereas ANXA1 knockdown induced a significant decrease of cell viability to 5‑FU. Further experiments revealed that ANXA1 expression was induced by hypoxia in colon cancer cells. These results suggest that ANXA1 expression may play a critical role in 5‑FU resistance and may be induced by hypoxia during cancer progression. Our results provide a possible strategy to overcome 5‑FU resistance by modulating ANXA1 expression.
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Copy and paste a formatted citation
Spandidos Publications style
Onozawa H, Saito M, Saito K, Kanke Y, Watanabe Y, Hayase S, Sakamoto W, Ishigame T, Momma T, Ohki S, Ohki S, et al: Annexin A1 is involved in resistance to 5-FU in colon cancer cells. Oncol Rep 37: 235-240, 2017.
APA
Onozawa, H., Saito, M., Saito, K., Kanke, Y., Watanabe, Y., Hayase, S. ... Takenoshita, S. (2017). Annexin A1 is involved in resistance to 5-FU in colon cancer cells. Oncology Reports, 37, 235-240. https://doi.org/10.3892/or.2016.5234
MLA
Onozawa, H., Saito, M., Saito, K., Kanke, Y., Watanabe, Y., Hayase, S., Sakamoto, W., Ishigame, T., Momma, T., Ohki, S., Takenoshita, S."Annexin A1 is involved in resistance to 5-FU in colon cancer cells". Oncology Reports 37.1 (2017): 235-240.
Chicago
Onozawa, H., Saito, M., Saito, K., Kanke, Y., Watanabe, Y., Hayase, S., Sakamoto, W., Ishigame, T., Momma, T., Ohki, S., Takenoshita, S."Annexin A1 is involved in resistance to 5-FU in colon cancer cells". Oncology Reports 37, no. 1 (2017): 235-240. https://doi.org/10.3892/or.2016.5234
Copy and paste a formatted citation
x
Spandidos Publications style
Onozawa H, Saito M, Saito K, Kanke Y, Watanabe Y, Hayase S, Sakamoto W, Ishigame T, Momma T, Ohki S, Ohki S, et al: Annexin A1 is involved in resistance to 5-FU in colon cancer cells. Oncol Rep 37: 235-240, 2017.
APA
Onozawa, H., Saito, M., Saito, K., Kanke, Y., Watanabe, Y., Hayase, S. ... Takenoshita, S. (2017). Annexin A1 is involved in resistance to 5-FU in colon cancer cells. Oncology Reports, 37, 235-240. https://doi.org/10.3892/or.2016.5234
MLA
Onozawa, H., Saito, M., Saito, K., Kanke, Y., Watanabe, Y., Hayase, S., Sakamoto, W., Ishigame, T., Momma, T., Ohki, S., Takenoshita, S."Annexin A1 is involved in resistance to 5-FU in colon cancer cells". Oncology Reports 37.1 (2017): 235-240.
Chicago
Onozawa, H., Saito, M., Saito, K., Kanke, Y., Watanabe, Y., Hayase, S., Sakamoto, W., Ishigame, T., Momma, T., Ohki, S., Takenoshita, S."Annexin A1 is involved in resistance to 5-FU in colon cancer cells". Oncology Reports 37, no. 1 (2017): 235-240. https://doi.org/10.3892/or.2016.5234
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