Somatic nuclear auto-antigenic sperm protein sensitizes human breast cancer cells to 5-Fluorouracil

Purpose To assess the potential role of nuclear auto-antigenic sperm protein (NASP) in the cellular sensitivity to 5-Fluorouracil (5-FU) in breast cancer cells. Methods The expression of two NASP isotypes, namely somatic NASP (sNASP) and testis NASP (tNASP) in breast cancer lines were detected under...

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Bibliographic Details
Published in:Cancer chemotherapy and pharmacology 2022-04, Vol.89 (4), p.559-564
Main Authors: Huang, Yanjing, Yang, Shenghui, Yu, Weiling, Gui, Ling
Format: Article
Language:English
Subjects:
5-Fluorouracil
Antigens
Antigens, Nuclear
Apoptosis
Breast cancer
Breast Neoplasms - drug therapy
Cancer Research
Cell Line, Tumor
Cell Survival
Cell viability
Drug Resistance, Neoplasm
Evaluation
Fluorouracil - pharmacology
Gene expression
Humans
Immunoprecipitation
Isotypes
Male
Medicine
Medicine & Public Health
mRNA
Oncology
Overexpression
Pharmacology/Toxicology
Polymerase chain reaction
Proteins
Sensitivity
Short Communication
Sperm
Spermatozoa
TRAF6 protein
Tumor necrosis factor
Tumor necrosis factor receptors
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Summary:Purpose To assess the potential role of nuclear auto-antigenic sperm protein (NASP) in the cellular sensitivity to 5-Fluorouracil (5-FU) in breast cancer cells. Methods The expression of two NASP isotypes, namely somatic NASP (sNASP) and testis NASP (tNASP) in breast cancer lines were detected under 5-FU treatment using real-time polymerase chain reaction and western blot assays. NASP effect on cellular viability and apoptosis under 5-FU treatment were evaluated. The interaction between NASP and its downstream proteins were evaluated using the co-immunoprecipitation (Co-IP) assays. Results 5-FU significantly decreased the mRNA and protein expression levels of sNASP. Inhibition of sNASP increased cellular viability, colony formation ability, but reduced apoptosis in tested cell lines in response to 5-FU, which were reversed by sNASP over-expression. Further study reveals 5-FU disrupts sNASP/TNF receptor-associated factor 6 (TRAF6) complex, potentiates cellular sensitivity to 5-FU via NK-kB. Conclusion Our findings suggest sNASP is a novel molecular target having potential to overcome the resistance to 5-FU in breast cancer cells.
ISSN:0344-5704
1432-0843
DOI:10.1007/s00280-021-04391-2