All of this changes of biological behavior suggest that LRIG1 is a tumor suppressor gene on ag gressive bladder cancer cells. However, the change of biological behavior is not exclusively attributed to the restriction of one molecule, as the signal transduction is a complicated matter in cells. In our study, we examined the effect of LRIG1 gene transfection on the expression of several key regulators involved in the EGFR signaling pathway, including MAPK and AKT. We found that p MAPK and p AKT in T24 and 5637 cells were significantly reduced following LRIG1 cDNA transfection which also inhibited phosphorylation of EGFR. Because of the above results we can conclude that LRIG1 indeed affects the biology behaviors of bald der cancer cells in vitro by inhibiting phosphorylation of EGFR and the downstream signaling pathway.
And we found that EGFR expression is critical for the effect of LRIG1 on bladder cancer cells in vitro. Taken together, these results could offer a novel therapeutic strategy for suppression of bladder cancer by restoration of LRIG1. Background Ovarian cancer is characterized {find more information| selleck chemicals|selleck inhibitor|selleckchem|LDC000067 ic50 by a high rate of mortal ity among gynecologic oncology patients. To date, al though the exact cause of ovarian cancer remains largely unknown, BRCA mutations are known hereditary fac tors, and the risk of ovarian cancer conferred by BRCA mutations can be regulated by both genetic and environ mental components. The epidermal growth factor receptor is a member of the ErbB family of re ceptor tyrosine kinases that exert a direct effect on ovar ian cell proliferation, migration, and invasion, as well as angiogenesis.
The overexpression of EGFR frequently occurs in ovarian cancer tissues and correlates with poor prognosis of the patients. Notably, emerging evidence has established that, EGFR is a potential link between genetic and environmental interactions, EGFR and BRCA1 purchase Etizolam can be found in the same protein complex, and convergence exists between EGFR and BRCA1 related signaling pathways, and BRCA1 mutations are vulnerable to the development of EGFR positive cancers. Therefore, insights into the com plex interrelationship between BRCA and EGFR might improve our understanding of the basic molecular mech anism of ovarian cancer. For this reason, the present study was undertaken to investigate EGFR expression after BRCA inactivation events, and to provide novel insights into the regulatory mechanism of EGFR.
Methods Patients and tissue collection This study was approved by the Institutional Review Board at China Medical University. Serous ovarian can cer patients were enrolled between 2010 and 2012, and all patients gave informed consent. Fresh tumor samples, adjacent normal ovarian tissues, ascites, and blood samples were obtained at the time of primary surgery before any chemotherapy or radio therapy.