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Article

ANP32A modulates cell growth by regulating p38 and Akt activity in colorectal cancer

  • Authors:
    • Wei Yan
    • Zhun Bai
    • Juan Wang
    • Xumei Li
    • Bixia Chi
    • Xu Chen
  • View Affiliations / Copyright

    Affiliations: College of Pharmacy, Guilin Medical University, Guilin 541004, P.R. China, Intensive Care Unit, The Affiliated Zhuzhou Hospital XiangYa Medical College CSU, Zhuzhou, Hunan 412007, P.R. China, Department of Gastroenterology, The First People's Hospital of Yueyang, Yueyang, Hunan 414000, P.R. China
  • Pages: 1605-1612
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    Published online on: July 21, 2017
       https://doi.org/10.3892/or.2017.5845
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Abstract

Acidic leucine-rich nuclear phosphoprotein-32A (ANP32A) possesses multiple biochemical activities, has been found to be decreased or absent in malignant tumors. However, new findings have shown that it is expressed in greater amounts in advanced cancers than in early-stage tumors. The role and clinical significance of ANP32A in colorectal cancer (CRC) is still unknown. In the present study, the expression of ANP32A was assessed in 68 CRC patients by IHC, and then the correlation of its expression with clinicopathological factors was investigated using the Allred, Klein and immune response scoring system analysis. Western blot and real-time PCR analyses were used to assess ANP32A expression and the activity of Akt and p38 in cancer and normal tissues. These data indicated a significant association between ANP32A expression and the activity of Akt and p38, besides the tumor differentiation status in CRC patients. IHC and western blotting data revealed that ANP32A was overexpressed in CRC patients, and ANP32A levels were higher in poorly differentiated tumors. Protein and mRNA analysis revealed that with a high expression of ANP32A, the activation of Akt was enhanced, while the p-38 phosphorylation level was decreased in CRC tissues. MTT assay and functional studies revealed that knockdown of ANP32A inhibited cell growth and induced p38 phosphorylation and Akt dephosphorylation. The present study indicated that ANP32A promoted CRC proliferation by inhibition of p38 and activation of Akt signaling pathways and suggested that ANP32A may play a potential role in CRC diagnosis and therapy.
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Copy and paste a formatted citation
Spandidos Publications style
Yan W, Bai Z, Wang J, Li X, Chi B and Chen X: ANP32A modulates cell growth by regulating p38 and Akt activity in colorectal cancer. Oncol Rep 38: 1605-1612, 2017.
APA
Yan, W., Bai, Z., Wang, J., Li, X., Chi, B., & Chen, X. (2017). ANP32A modulates cell growth by regulating p38 and Akt activity in colorectal cancer. Oncology Reports, 38, 1605-1612. https://doi.org/10.3892/or.2017.5845
MLA
Yan, W., Bai, Z., Wang, J., Li, X., Chi, B., Chen, X."ANP32A modulates cell growth by regulating p38 and Akt activity in colorectal cancer". Oncology Reports 38.3 (2017): 1605-1612.
Chicago
Yan, W., Bai, Z., Wang, J., Li, X., Chi, B., Chen, X."ANP32A modulates cell growth by regulating p38 and Akt activity in colorectal cancer". Oncology Reports 38, no. 3 (2017): 1605-1612. https://doi.org/10.3892/or.2017.5845
Copy and paste a formatted citation
x
Spandidos Publications style
Yan W, Bai Z, Wang J, Li X, Chi B and Chen X: ANP32A modulates cell growth by regulating p38 and Akt activity in colorectal cancer. Oncol Rep 38: 1605-1612, 2017.
APA
Yan, W., Bai, Z., Wang, J., Li, X., Chi, B., & Chen, X. (2017). ANP32A modulates cell growth by regulating p38 and Akt activity in colorectal cancer. Oncology Reports, 38, 1605-1612. https://doi.org/10.3892/or.2017.5845
MLA
Yan, W., Bai, Z., Wang, J., Li, X., Chi, B., Chen, X."ANP32A modulates cell growth by regulating p38 and Akt activity in colorectal cancer". Oncology Reports 38.3 (2017): 1605-1612.
Chicago
Yan, W., Bai, Z., Wang, J., Li, X., Chi, B., Chen, X."ANP32A modulates cell growth by regulating p38 and Akt activity in colorectal cancer". Oncology Reports 38, no. 3 (2017): 1605-1612. https://doi.org/10.3892/or.2017.5845
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