Open Access

HSP60 participates in the anti‑glioma effects of curcumin

  • Authors:
    • Fengchen Bi
    • Junyan Wang
    • Xiaomin Zheng
    • Jingjing Xiao
    • Chai Zhi
    • Jinhai Gu
    • Yumei Zhang
    • Juan Li
    • Zhenhua Miao
    • Yin Wang
    • Yunhong Li
  • View Affiliations

  • Published online on: January 11, 2021     https://doi.org/10.3892/etm.2021.9637
  • Article Number: 204
  • Copyright: © Bi et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

The chaperone protein heat shock protein 60 (HSP60) is considered a tumor promoter in several types of primary human tumors, where it orchestrates a broad range of survival programs. Curcumin (CCM) is well‑established to exhibit several anticancer properties with an excellent safety profile. Our previous study showed that CCM suppresses extracellular HSP60 expression, which is typically released by activated microglia, and acts as an inflammatory factor by binding to Toll‑like receptor 4 (TLR‑4) on the cell membrane. The present study assessed whether CCM exerted its anti‑neuroglioma effects on U87 cells via inhibition of HSP60/TLR‑4 signaling, similar to that in microglia. The results demonstrated that CCM significantly inhibited the viability and invasive capacity of neuroglioma U87 cells as evidenced by a Cell Counting Kit‑8 assay. Western blotting and ELISA results showed that CCM decreased the expression of HSP60 and its transcriptional factor, heat shock factor 1, and reduced HSP60 release. Accordingly, TLR‑4, as the target of HSP60, and its downstream signaling proteins myeloid differentiation primary response 88 (MYD88), NF‑κB, inducible nitric oxide synthase and cytokines IL‑1β and IL‑6 were downregulated by CCM. The expression levels of apoptotic factors associated with NF‑κB activation, including TNF‑α and caspase‑3 were increased in U87 cells by CCM treatment, while p53 expression, a tumor suppressor, was shown to be decreased. Based on the results of the present study, CCM may exert its anti‑tumor effects in U87 cells by inhibiting the HSP60/TLR‑4/MYD88/NF‑κB pathway and inducing tumor cell apoptosis. Thus, CCM may be used as a potential therapy for the clinical treatment of neuroglioma.
View Figures
View References

Related Articles

Journal Cover

March-2021
Volume 21 Issue 3

Print ISSN: 1792-0981
Online ISSN:1792-1015

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Bi F, Wang J, Zheng X, Xiao J, Zhi C, Gu J, Zhang Y, Li J, Miao Z, Wang Y, Wang Y, et al: HSP60 participates in the anti‑glioma effects of curcumin. Exp Ther Med 21: 204, 2021
APA
Bi, F., Wang, J., Zheng, X., Xiao, J., Zhi, C., Gu, J. ... Li, Y. (2021). HSP60 participates in the anti‑glioma effects of curcumin. Experimental and Therapeutic Medicine, 21, 204. https://doi.org/10.3892/etm.2021.9637
MLA
Bi, F., Wang, J., Zheng, X., Xiao, J., Zhi, C., Gu, J., Zhang, Y., Li, J., Miao, Z., Wang, Y., Li, Y."HSP60 participates in the anti‑glioma effects of curcumin". Experimental and Therapeutic Medicine 21.3 (2021): 204.
Chicago
Bi, F., Wang, J., Zheng, X., Xiao, J., Zhi, C., Gu, J., Zhang, Y., Li, J., Miao, Z., Wang, Y., Li, Y."HSP60 participates in the anti‑glioma effects of curcumin". Experimental and Therapeutic Medicine 21, no. 3 (2021): 204. https://doi.org/10.3892/etm.2021.9637