Background:
Esophageal carcinoma is one of the common malignant tumors in digestive
tract. BECLIN-1 is a key gene that regulates autophagy, and its abnormal expression may be related
with many human tumors. However, the mechanism of BECLIN-1 in esophageal carcinoma remains
unknown.
Objective:
In this study, we explored the effect of BECLIN-1 overexpression on tumor growth in mice
with esophageal carcinoma and its mechanism.
Methods:
Recombined lentiviral vector containing BECLIN-1 was used to transfect human esophageal
carcinoma Eca109 cells and establish stable cell line. qRT-PCR was used to detect BECLIN-1 mRNA
level in the transfected Eca109 cells, CCK-8 assay was used to detect cell proliferation. Beclin-1, P62
and LC3-II protein expression levels in Eca109 cells were detected using Western blot analysis. Subcutaneous
xenograft nude mice model of human esophageal carcinoma was established, and the tumor
growths in Beclin-1 group, control group and empty vector group were monitored. Beclin-1 protein
expression in vivo was detected by immunohistochemistry.
Results:
Beclin-1 mRNA and protein were overexpressed in Eca109 cells. Compared with empty vector
group, the growth rate of cells transfected with BECLIN-1 decreased significantly. Compared with
the control group and empty vector group, the expression level of P62 protein in beclin-1 group was
significantly decreased, while the expression level of LC3-II protein was significantly increased. The
tumor growth rate in nude mice of Beclin-1 group was significantly lower than that of the control
group and empty vector group, and Beclin-1 protein was mainly expressed in Beclin-1 group in vivo.
Conclusion:
BECLIN-1 can induce autophagy in esophageal carcinoma Eca109 cells, and it can significantly
inhibit the growth of esophageal carcinoma.
A nanoemulsion of an anti‐oxidant synergy formulation reduces tumor growth rate in neuroblastoma‐bearing nude mice.
