Abstract

Our current investigation attempts to study the role of the fascin1 gene in growth and metastasis of gastric cancer cell line MKN45. Small interfering RNA (siRNA) was used to inhibit fascin1 expression in the human gastric cancer cell line MKN45. Expression of fascin1 in fascin1 siRNA transfected cells (sifascin1), non-transfected cells (NT) and non-specific fascin1 siRNA cells (CON) were examined by Western blotting and reverse transcription polymerase chain reaction (RT-PCR). Cell growth ability in vitro was evaluated by MTT and clone formation assays. Cell mobility in vitro was examined by the Boyden chamber assay. Nude mice metastasis models were established by abdominal cavity transfer method. Tumour growth was evaluated by immunohistochemistry with proliferating cell nuclear antigen (PCNA). Knockdown of fascin1 expression in MKN45 cells resulted in decreased cellular proliferative and migratory abilities. In vitro, the cloning efficiency of siFascin1 cells (34.2%) was significantly lower compared to that in NT (78.5%) (p < 0.05). The migration rate in siFascin1 cells was significantly decreased (33.7%) compared with NT cells (89.4%) (p < 0.05). In vivo, the cell proliferation rate was lower in siFascin1 cells (25.8%) compared to that in NT (75.0%) (p < 0.05). The number of tumour clones in the liver was significantly lower in siFascin1 cells (2.0 +/- 1.1) compared to that in NT (5.1 +/- 1.6) (p < 0.05). Our study demonstrates that down-regulation of fascin1 suppresses the proliferation and migration of gastric cancer cells MKN45, suggesting that fascin1 siRNA may offer a novel potential gene therapy approach for human gastric cancer with fascin1 over-expression.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.