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Fig. 3 | BMC Cancer

Fig. 3

From: RNF43 ubiquitinates and degrades phosphorylated E-cadherin by c-Src to facilitate epithelial-mesenchymal transition in lung adenocarcinoma

Fig. 3

Activated c-Src mediated the ubiquitination and degradation of E-cadherin in lung adenocarcinoma cells. a, Immunoblot analysis of c-Src, pY416-Src (p-Src), E-cadherin (E-cad), RNF43, Hakai and β-actin in the human lung adenocarcinoma cell lines A549, NCI-H522, NCI-H1975, NCI-H1623 and NCI-H2073. b, A549 cells were stably transfected with lentivirus containing control or Caspase-8 shRNA (Cap8 KD). Caspase-8, p-Src, c-Src, E-cad and β-actin in total cell lysates (TCLs) were detected by western blot. c, Caspase-8-deficient H522 cells were stably transfected with a control vector or wild-type Caspase-8 via adenovirus. Caspase-8, p-Src, c-Src, E-cad and β-actin in TCLs were detected by western blot. d, The TCLs of A549 and H522 cells in which c-Src was activated were subjected to immunoprecipitation (IP) using an anti-E-cadherin antibody. Ubiquitinated (Ubi-) E-cadherin was detected by western blot (upper blot). The blot was then stripped and reprobed for RNF43 (second from upper panel). RNF43, E-cadherin and β-actin were in TCLs detected by western blot (lower blot). e, A549 cells were allowed to attach to dishes for 12 h and then assessed by confocal microscopy using antibodies against E-cadherin and RNF43. Scale bars, 10 μm. f, E-cadherin mRNA was examined in A549 + control/Caspase-8 shRNA cells (Casp8 KD) and in H522 + control vector/wild-type Caspase-8 cells

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