Title : Proliferation and survival molecules implicated in the inhibition of BRAF pathway in thyroid cancer cells harbouring different genetic mutations.

Pub. Date : 2009 Oct 31

PMID : 19878585






6 Functional Relationships(s)
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1 METHODS: Suppression of BRAF pathway in thyroid cancer cell lines (8505C, TPC1 and C643) was achieved using RNA interference (RNAi) for BRAF and the kinase inhibitor, sorafenib. Sorafenib B-Raf proto-oncogene, serine/threonine kinase Homo sapiens
2 RESULTS: Both BRAF RNAi and sorafenib inhibited proliferation in all the cell lines independently of the genetic background, mostly in cells with BRAF(V600E) mutation. Sorafenib B-Raf proto-oncogene, serine/threonine kinase Homo sapiens
3 In the case of sorafenib treatment, cells harbouring BRAF(V600E) mutation showed increase levels of apoptosis due to a balance of the anti-apoptotic proteins Mcl-1 and Bcl-2. Sorafenib B-Raf proto-oncogene, serine/threonine kinase Homo sapiens
4 We have shown that in thyroid cancer cells sorafenib induces apoptosis by affecting Mcl-1 and Bcl-2 in BRAF(V600E) mutated cells which was independent of BRAF. Sorafenib B-Raf proto-oncogene, serine/threonine kinase Homo sapiens
5 We have shown that in thyroid cancer cells sorafenib induces apoptosis by affecting Mcl-1 and Bcl-2 in BRAF(V600E) mutated cells which was independent of BRAF. Sorafenib B-Raf proto-oncogene, serine/threonine kinase Homo sapiens
6 These results suggest that sorafenib may prove useful in the treatment of thyroid carcinomas, particularly those refractory to conventional treatment and harbouring BRAF mutations. Sorafenib B-Raf proto-oncogene, serine/threonine kinase Homo sapiens