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Chinese Journal of Clinicians(Electronic Edition) ›› 2021, Vol. 15 ›› Issue (10): 779-784. doi: 10.3877/cma.j.issn.1674-0785.2021.10.011

• Basic Science Research • Previous Articles     Next Articles

Mechanism of bortezomib resistance induced by HSP27 in multiple myeloma cells

Jie Su1,(), Xiaojing Yang1, Xue Zhou1   

  1. 1. Department of Hematology, Nanjing Jiangbei People's Hospital, Nanjing 210048, China
  • Received:2021-06-07 Online:2021-10-15 Published:2022-01-29
  • Contact: Jie Su

Abstract:

Objective

To investigate the mechanism of heat shock proteins 27 (HSP27) induced bortezomib (BTZ) resistance in multiple myeloma (MM) cell line U266.

Methods

Drug-resistant cell strain U266/BTZ was induced by treatment with increasing concentrations of BTZ, and drug resistance was detected by CCK8 method. The expression of HSP27 in U266 and U266/BTZ cells before and post BTZ treatment was detected by real-time fluorescence quantitative PCR (RT-PCR) and Western blot. Hsp27-siRNA was used to interfere with the expression of HSP27 in U266/BTZ cells, and then RT-PCR and Western blot were used to identify the effects of HSP27-siRNA interference on apoptosis and endoplasmic reticulum stress, as well as the expression of cl-Caspase-3, cl-Caspase-8, and cl-Caspase-9.

Results

CCK8 assay showed that U266/BTZ cells had reduced drug resistance to many drugs. BTZ exposure significantly upregulated the expression of HSP27 mRNA and protein in U266 and U266/BTZ cells (P<0.01). Hsp27-siRNA interference significantly down-regulated the expression of HSP27. Hsp27-siRNA interference could enhance the apoptosis of U266/BTZ cells and increase the activation of Caspase-3, Caspase-8 and Caspase-9 (P<0.01).

Conclusion

HSP27-mediated MM resistance is caused by inhibition of endoplasmic network stress to reduce myeloma cell apoptosis.

Key words: Multiple myeloma, U266 cell line, Heat shock proteins 27, Bortezomib, Drug resistance

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