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Proteomic analysis of inhibitor of apoptosis protein-like protein-2 on breast cancer cell proliferation

Although inhibitor of apoptosis protein-like protein-2 (ILP-2) is considered to be a novel enhancer of breast cancer proliferation, its underlying mechanism of action remains unknown. Therefore, the present study aimed to investigate the expression profile of ILP-2-related proteins in MCF-7 cells to...

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Detalles Bibliográficos
Autores principales: Xiang, Siqi, Zhu, Lin, Zhang, Zhiliang, Wang, Siyuan, Cui, Ruxia, Xiang, Mingjun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8809121/
https://www.ncbi.nlm.nih.gov/pubmed/35039877
http://dx.doi.org/10.3892/mmr.2022.12605
Descripción
Sumario:Although inhibitor of apoptosis protein-like protein-2 (ILP-2) is considered to be a novel enhancer of breast cancer proliferation, its underlying mechanism of action remains unknown. Therefore, the present study aimed to investigate the expression profile of ILP-2-related proteins in MCF-7 cells to reveal their effect on promoting breast cancer cell proliferation. The isobaric tags for relative and absolute quantification (iTRAQ) method was used to analyse the expression profile of ILP-2-related proteins in MCF-7 breast cancer cells transfected with small interfering (si)RNA against ILP-2 (siRNA-5 group) and the negative control (NC) siRNA. The analysis of the iTRAQ data was carried out using western blotting and reverse transcription-quantitative PCR. A total of 4,065 proteins were identified in MCF-7 cells, including 241 differentially expressed proteins (DEPs; fold change ≥1.20 or ≤0.83; P<0.05). Among them, 156 proteins were upregulated and 85 were downregulated in the siRNA-5 group compared with in the NC group. The aforementioned DEPs were mainly enriched in ‘ECM-receptor interaction’. In addition, the top 10 biological processes related to these proteins were associated with signal transduction, cell proliferation and immune system processes. Furthermore, ILP-2 silencing upregulated N(4)-(β-N-acetylglucosaminyl)-L-asparaginase, metallothionein-1E and tryptophan 2,3-dioxygenase, whereas ILP-2 overexpression exerted the opposite effect. The results of the present study suggested that ILP-2 could promote breast cancer growth via regulating cell proliferation, signal transduction, immune system processes and other cellular physiological activities.