Talen-mediated girdin knockout downregulates cell proliferation, migration and invasion in human esophageal carcinoma ECA109 cells

Abstract

Girdin is an actin-binding Akt substrate that is involved in the regulation of cell migration. Accumulating evidence has revealed that girdin has regulatory effects on invasion and metastasis in several types of cancer. However, the role of girdin in esophageal squamous cell carcinomas (ESCCs) is yet to be investigated. In the present study, tissue microarray data revealed that among 95 cases of ESCC, 27 cases (28.7%) exhibited a low expression of girdin, while 67 cases (71.3%) had an enhanced expression of girdin. However, among 78 cases of adjacent tissues, 64 cases (82.1%) did not express girdin and 14 cases (17.9%) exhibited a low expression of girdin. Furthermore, the expression of girdin was significantly associated with the tumor stage, lymph node metastasis stage, and tumor, lymph node and metastasis stage. Of note, the mean survival time of girdin-positive cases was only 30.62±2.99 months, while it was 53.37±5.02 months in girdin-negative cases, indicating that girdin protein expression is an independent prognostic factor of poor survival. Talen-mediated girdin knockout (KO) significantly suppressed cellular proliferation, migration and invasion in ESCC ECA109 cells. In conclusion, the present study suggested that girdin protein expression was significantly correlated with cancer progression and poor prognosis in ESCCs, and that girdin had a positive role in the regulation of cell proliferation, migration and invasion in ESCC cells. Therefore, girdin may be a potential candidate for the development of novel prognostic tools and therapeutic strategies for ESCCs.

Girdin regulates the migration and invasion of glioma cells via the PI3K-Akt signaling pathway

“…Consistent with these findings, Natsume et al ( 16 ) reported that genetic girdin knockout promoted glioma stem cell differentiation, but inhibited cell motility, invasion, metastasis and proliferation in vivo . Cao et al ( 17 ) demonstrated that girdin knockout reduced esophageal cancer cell proliferation, migration and invasion, which was also similar to the findings of the present study. Girdin deprivation has also been observed to inhibit vascular smooth muscle cell (VSMC) proliferation and to affect actin cytoskeletal rearrangement, resulting the in impaired migration of VSMCs and altered neointimal formation following vascular injury ( 10 ).…”

Girdin regulates the proliferation and apoptosis of pancreatic cancer cells via the PI3K/Akt signalling pathway

“…The current study also has implications for our understanding of the role of Girdin as an oncogene in cancer cells, as Girdin knockdown impaired pancreatic cancer cell proliferation and induced apoptosis. Consistent with these findings, scientists have suggested that Girdin knockout inhibits cell proliferation ( 20 ). Girdin has also been shown to directly interact with Par-3, a cell polarity protein, to regulate cell polarity during cell migration ( 21 ).…”

miR-101 Inhibiting Cell Proliferation, Migration and Invasion in Hepatocellular Carcinoma through Downregulating Girdin

“…When the cells reached 80% confluence, Lipofectamin2000 (Invitrogen) was used to transfect miR-101 mimics, miR-101 inhibitor and miRNA NC mimics into HepG2 cells according to the instructions, respectively. According to the method reported by literatures, plasmids were transfected into HepG2 cells in order to perform the knockout of the Girdin gene ( Cao et al, 2014 ). 48h after transfection, the fluorescence microscopy and the qRT-PCR were used to detect whether the cell cloning process was successful.…”