@article{TCR34433,
author = {Junjiang Wang and Xiaowu Li and Yong Li and Xueqing Yao},
title = {Girdin knockdown promotes apoptosis in colorectal cancer via miR-29c-3p/Girdin axis},
journal = {Translational Cancer Research},
volume = {8},
number = {8},
year = {2019},
keywords = {},
abstract = {Background: In recent years, the incidence and mortality of colorectal cancer (CRC) have increased year by year among young people. Increased levels of Girdin expression predict a poor prognosis of CRC, which presents a serious threat to human health globally. Herein, we investigated the role of Girdin in CRC and explored the underlying mechanisms in CRC.
Methods: The expression of Girdin was detected in human specimens. HCT116 cells with stably expressing or knock-out Girdin protein were successfully constructed to observe the biological function of gene. Protein expression was determined by immunohistochemistry, immunofluorescence and western blot.
Results: Clinically, overexpression of Girdin was observed in the tumor tissue and poor prognosis of CRC patients. Gain-of-function and loss-of-function assays showed that Girdin promoted CRC cell proliferation in vitro. Mechanistically, Girdin knock-down significantly enhanced apoptosis, the mitochondrial membrane potential dropped, and the reactive oxygen species increased greatly. Last but not least, we analyzed the TargetScan dataset and found that Girdin was a regulated target of hsa-miR-29c-3p in CRC. Luciferase reporter assay was used to verify the interaction between hsa-miR-29c-3p and the 3’UTR of Girdin.
Conclusions: Our findings suggest that Girdin has a crucial role in CRC progression via miR-29c-3p/ Girdin axis, highlighting Girdin as a therapeutic target for CRC.},
issn = {2219-6803}, url = {https://tcr.amegroups.org/article/view/34433}
}