Publication: Downregulation of PDCD10 mitigates the malignant biological behavior and increases the sensitivity of esophageal squamous cell carcinoma cells to radiotherapy by inhibiting the PI3K/AKT pathway
Authors
Qisong Chen ; Qing Gao ; Junkai Xu
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Publisher
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Universidad de Murcia, Departamento de Biologia Celular e Histiologia
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DOI
https://doi.org/10.14670/HH-25-010
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info:eu-repo/semantics/article
Description
Abstract
The intensification of radiotherapy is an
effective way to improve the therapeutic efficacy of
radiation-sensitive malignancies such as esophageal
cancer (EC). Esophageal squamous cell carcinoma
(ESCC) accounts for 85% of all EC cases worldwide,
with a relatively higher incidence and mortality in East
Asia. In this study, we explored the functions and
mechanisms of programmed cell death 10 (PDCD10) in
the malignancy and radiotherapy sensitivity of ESCC
cells. We observed that PDCD10 is highly expressed in
ESCC tissues and is correlated with a poor prognosis in
patients with ESCC. PDCD10 downregulation
suppressed ESCC cell proliferation, migration, and
invasion but promoted apoptosis. In addition, it
enhanced ionizing radiation (IR)-induced ESCC cell
damage, whereas PDCD10 overexpression had the
opposite effect. Mechanistically, PDCD10 increased the
phosphorylation of phosphatidylinositol 3-kinase (PI3K)
and protein kinase B (AKT) in ESCC cell lines. The
administration of LY294002, a PI3K inhibitor,
significantly inhibited the oncogenic functions of
PDCD10, leading to an increase in IR-induced cell
damage. These findings establish PDCD10 as a critical
intrinsic regulator of the sensitivity of ESCC cells to IR
through the modulation of the PI3K/AKT pathway.
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