BACKGROUND/AIMS: A wide variety of evidence has pointed to a critical role of transcriptional nuclear factor Kappa B (NF-kappaB) in tumour migration and invasion,but the mechanisms involved are not clear.In the present study, we reported that activation of NF-kappaB promotes migration and invasion in cholangiocarcinoma cell through upregulating Snail and consequent repression of E-cadherin. METHODOLOGY: We examined the expression of the NF-kappaB subunit P65 (NF-kappaBP65) after being treated by tumour necrosis factor (TNF)-a, a strong NF-kappaB activator or PDTC, a specific NF-kappaB inhibitor. Snail and E-cadherin in cholangiocarcinoma cell lines QBC939 and FRH 0201 was examined by Western blotting and RT-PCR. To confirm the involvement of NF-kappaB in snail activation, small interfering RNA (siRNA) specific for snail was used to suppress the expression of Snail, then the Snail siRNA- transfected cells were treated by TNF-a,and the migration and invasion was assayed. RESULTS: The results showed that Snail activation and consequent repression of E-cadherin may depend on NF-kappaB activation, and NF-KB promotes migration and invasion by upregulating Snail and consequent repression of E-cadherin in cholangiocarcinoma cell. CONCLUSIONS: NF-kappaB-Snail-E-cadherin signal is a potential target for antimetastatic therapeutics in cholangiocarcinoma.
BACKGROUND/AIMS: A wide variety of evidence has pointed to a critical role of transcriptional nuclear factor Kappa B (NF-kappaB) in tumour migration and invasion,but the mechanisms involved are not clear.In the present study, we reported that activation of NF-kappaB promotes migration and invasion in cholangiocarcinoma cell through upregulating Snail and consequent repression of E-cadherin. METHODOLOGY: We examined the expression of the NF-kappaB subunit P65 (NF-kappaBP65) after being treated by tumour necrosis factor (TNF)-a, a strong NF-kappaB activator or PDTC, a specific NF-kappaB inhibitor. Snail and E-cadherin in cholangiocarcinoma cell lines QBC939 and FRH 0201 was examined by Western blotting and RT-PCR. To confirm the involvement of NF-kappaB in snail activation, small interfering RNA (siRNA) specific for snail was used to suppress the expression of Snail, then the Snail siRNA- transfected cells were treated by TNF-a,and the migration and invasion was assayed. RESULTS: The results showed that Snail activation and consequent repression of E-cadherin may depend on NF-kappaB activation, and NF-KB promotes migration and invasion by upregulating Snail and consequent repression of E-cadherin in cholangiocarcinoma cell. CONCLUSIONS:NF-kappaB-Snail-E-cadherin signal is a potential target for antimetastatic therapeutics in cholangiocarcinoma.