Publication: Down-regulated REIC expression in lung carcinogenesis: a molecular target for gene therapy
Authors
Yang, Lei ; Zhao, Shuang ; Xia, Pu ; Zheng, Hua Chuan
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Publisher
Universidad de Murcia. Departamento de BiologĂa Celular e HistologĂa
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DOI
DOI: 10.14670/HH-11-964
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info:eu-repo/semantics/article
Description
Abstract
REIC (Reduced Expression in Immortalized
Cells) gene is down-regulated in immortalized cells,
compared with the normal parental counterparts. Its
encoding protein could inhibit colony formation, tumor
growth, and induce apoptosis. To investigate the roles of
REIC expression in lung cancer, we examined REIC
expression in lung cancer cells and tissues by RT-PCR or
Western blot, and observed the effects of both
recombinant REIC exposure and REIC overexpression
on the aggressive phenotypes of lung cancer cells. It was
found that the demethylation of REIC promoter by 5-
Aza-dC could reserve its mRNA expression in lung
cancer cells (P<0.05). There was a lower REIC mRNA
expression in lung cancer than that in matched normal
tissue (P<0.05). Recombinant REIC treatment enhanced
the proliferation of lung cancer cells (P<0.05), but versa
for REIC overexpression (P<0.05). Both recombinant
REIC treatment and REIC overexpression induced
apoptosis, and inhibited the migration and invasion of
SQ-5 and KJ cells (P<0.05). Immunohistochemically,
there was a positive correlation between REIC and
Caspase-3 expression in lung cancer (P<0.05).
According to Kaplan-Meier plotter, REIC mRNA
overexpression was found to positively correlate with
overall, progression-free and post- progression survival
rates of lung cancer patients (P<0.05), even stratified by
sex, histological subtyping, grading, TNM staging,
chemotherapy, radiotherapy, or smoking. These findings
suggested that down-regulated REIC expression might
be involved in lung carcinogenesis due to its promoter
methylation. Both recombinant REIC exposure and
REIC overexpression might reverse the aggressive
phenotypes of lung cancer cells. REIC may be employed
as a potential target of gene therapy for lung cancer.
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Citation
Histology and Histopathology, Vol.33, nÂş7, (2018)
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