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Involvement of calreticulin in cell proliferation, invasion and differentiation in diallyl disulfide-treated HL-60 cells

  • Authors:
    • Lan Yi
    • Jian Shan
    • Xin Chen
    • Guoqing Li
    • Linwei Li
    • Hui Tan
    • Qi Su
  • View Affiliations / Copyright

    Affiliations: College of Pharmacy and Biological Sciences, University of South China, Hengyang, Hunan 421001, P.R. China, Cancer Research Institute, University of South China, Hengyang, Hunan 421001, P.R. China
    Copyright: © Yi et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 1861-1867
    |
    Published online on: July 13, 2016
       https://doi.org/10.3892/ol.2016.4850
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Abstract

Diallyl disulfide (DADS) has shown potential as a therapeutic agent in various cancers. Previously, calreticulin (CRT) was found to be downregulated in differentiated HL‑60 cells treated with DADS. The present study investigated the role of CRT proteins in DADS‑induced proliferation, invasion and differentiation in HL-60 cells. The present study demonstrated that DADS treatment significantly changed the morphology of HL-60 cells and caused the significant time‑dependent downregulation of CRT. Small interfering RNA (siRNA)-mediated knockdown of CRT expression significantly inhibited proliferation, decreased invasion ability, increased the expression of cluster of differentiation (CD)11b and reduced the expression of CD33 in DADS‑treated HL-60 cells. DADS also significantly affected cell proliferation, invasion and differentiation in CRT-overexpressed HL-60 cells. Nitroblue tetrazolium (NBT) reduction assays showed decreased NBT reduction activity in the CRT overexpression group and increased NBT reduction in the CRT siRNA group. Following treatment with DADS, the NBT reduction abilities in all groups were increased. In conclusion, the present study clearly demonstrates the downregulation of CRT during DADS‑induced differentiation in HL-60 cells and indicates that CRT is involved in cell proliferation, invasion and differentiation in DADS‑treated HL-60 cells.
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Copy and paste a formatted citation
Spandidos Publications style
Yi L, Shan J, Chen X, Li G, Li L, Tan H and Su Q: Involvement of calreticulin in cell proliferation, invasion and differentiation in diallyl disulfide-treated HL-60 cells. Oncol Lett 12: 1861-1867, 2016.
APA
Yi, L., Shan, J., Chen, X., Li, G., Li, L., Tan, H., & Su, Q. (2016). Involvement of calreticulin in cell proliferation, invasion and differentiation in diallyl disulfide-treated HL-60 cells. Oncology Letters, 12, 1861-1867. https://doi.org/10.3892/ol.2016.4850
MLA
Yi, L., Shan, J., Chen, X., Li, G., Li, L., Tan, H., Su, Q."Involvement of calreticulin in cell proliferation, invasion and differentiation in diallyl disulfide-treated HL-60 cells". Oncology Letters 12.3 (2016): 1861-1867.
Chicago
Yi, L., Shan, J., Chen, X., Li, G., Li, L., Tan, H., Su, Q."Involvement of calreticulin in cell proliferation, invasion and differentiation in diallyl disulfide-treated HL-60 cells". Oncology Letters 12, no. 3 (2016): 1861-1867. https://doi.org/10.3892/ol.2016.4850
Copy and paste a formatted citation
x
Spandidos Publications style
Yi L, Shan J, Chen X, Li G, Li L, Tan H and Su Q: Involvement of calreticulin in cell proliferation, invasion and differentiation in diallyl disulfide-treated HL-60 cells. Oncol Lett 12: 1861-1867, 2016.
APA
Yi, L., Shan, J., Chen, X., Li, G., Li, L., Tan, H., & Su, Q. (2016). Involvement of calreticulin in cell proliferation, invasion and differentiation in diallyl disulfide-treated HL-60 cells. Oncology Letters, 12, 1861-1867. https://doi.org/10.3892/ol.2016.4850
MLA
Yi, L., Shan, J., Chen, X., Li, G., Li, L., Tan, H., Su, Q."Involvement of calreticulin in cell proliferation, invasion and differentiation in diallyl disulfide-treated HL-60 cells". Oncology Letters 12.3 (2016): 1861-1867.
Chicago
Yi, L., Shan, J., Chen, X., Li, G., Li, L., Tan, H., Su, Q."Involvement of calreticulin in cell proliferation, invasion and differentiation in diallyl disulfide-treated HL-60 cells". Oncology Letters 12, no. 3 (2016): 1861-1867. https://doi.org/10.3892/ol.2016.4850
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