Breast cancer genes PSMC3IP and EPSTI1 play a role in apoptosis regulation

A key element to delineate the biology of individual tumors is the regulation of apoptosis. In this work, we functionally characterize two breast cancer associated genes, the proteasome 26S subunit ATPase 3 interacting protein (PSMC3IP) and the epithelial-stromal interaction 1 (EPSTI1), to explore t...

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Bibliographic Details
Published in:PloS one 2015-01, Vol.10 (1), p.e0115352-e0115352
Main Authors: Capdevila-Busquets, Eva, Badiola, Nahuai, Arroyo, Rodrigo, Alcalde, Víctor, Soler-López, Montserrat, Aloy, Patrick
Format: Article
Language:English
Subjects:
Adenosine triphosphatase
Apoptosis
Apoptosis - genetics
Biotechnology
Breast cancer
Breast Neoplasms - genetics
Breast Neoplasms - pathology
Cancer
Cancer genetics
Cell Line, Tumor
Estrogens
Female
Gene expression
Gene Expression Regulation, Neoplastic
Genes
Genetic aspects
Health aspects
Humans
Molecular modelling
Neoplasm Proteins - genetics
Nuclear Proteins - genetics
Proteasome 26S
Trans-Activators - genetics
Tumor cell lines
Tumors
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Summary:A key element to delineate the biology of individual tumors is the regulation of apoptosis. In this work, we functionally characterize two breast cancer associated genes, the proteasome 26S subunit ATPase 3 interacting protein (PSMC3IP) and the epithelial-stromal interaction 1 (EPSTI1), to explore their potential apoptotic role in breast cancer. We first explore the existence of direct physical interactions with annotated BC-apoptotic genes. Based on the generated interaction network, we examine several apoptotic markers to determine the effect of PSMC3IP and EPSTI1 gene expression modulation in two different human breast cancer cell lines to suggest potential molecular mechanisms to unveil their role in the disease. Our results show that PSMC3IP and EPSTI1 are able to modulate the extrinsic apoptotic pathway in estrogen receptor positive and triple negative breast cancer cell lines, highlighting them as potential therapeutic targets.
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0115352