Publication: SLMO2 inhibits apoptosis in ovarian cancer cells by modulating mitochondrial function via TRIAP1
Authors
Yuesong Wang ; Zixuan Li ; Tianmei Zhang ; Yaqi Wang
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Publisher
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DOI
https://doi.org/10.14670/HH-18-958
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info:eu-repo/semantics/article
Description
Abstract
Objective. This study aimed to investigate
the role of SLMO2 in regulating mitochondrial function
and its interaction with TRIAP1, which inhibited
apoptosis in ovarian cancer cells. The findings provided
valuable insights into potential therapeutic targets for
ovarian cancer.
Methods. Lentiviral infection models were
developed using SKOV3 and OVCAR3 ovarian cancer
cell lines. Techniques such as flow cytometry, western
blotting, immunofluorescence, and transmission electron
microscopy were employed to systematically assess the
regulatory effects of SLMO2 and TRIAP1 on cell
proliferation, apoptosis, mitochondrial function, and
autophagy. Additionally, a subcutaneous mouse tumor
xenograft model was utilized to further investigate the
combined effects of SLMO2 and TRIAP1 on ovarian
cancer cells, with the aim of elucidating the specific
mechanisms underlying tumor growth and apoptosis.
Results. SLMO2 enhanced mitochondrial function
by increasing membrane potential and reducing reactive
oxygen species (ROS) levels. Furthermore, through its
interaction with TRIAP1, SLMO2 inhibited autophagy,
which further suppressed apoptosis in ovarian cancer
cells and regulated mitochondrial function. In vivo
experiments showed decreased ROS levels and reduced
expression of autophagy-related proteins, further
supporting the roles of SLMO2 and TRIAP1 in the
regulation of mitochondrial function.
Conclusions. SLMO2 regulated mitochondrial
function and inhibited apoptosis in ovarian cancer cells
by interacting with TRIAP1. The combination of
SLMO2 and TRIAP1 promoted tumor cell growth and
induced oxidative stress, suggesting potential therapeutic
targets for ovarian cancer.
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