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. Author manuscript; available in PMC: 2016 Jul 8.
Published in final edited form as: Oncogene. 2015 Oct 19;35(25):3293–3302. doi: 10.1038/onc.2015.390

Fig. 3. E-cadherin regulates CPD repair through increasing the levels of both XPC and DDB1.

Fig. 3

(A) Immunoblot analysis of E-cadherin, XPC, Ub-XPC, DDB1 and GAPDH in HaCaT cells transfected with shCon, shE-cadherin, or the combination of shE-cadherin with vector (Con), XPC, DDB1, or the combination of XPC and DDB1 plasmids at 0, 1.5, 6 and 24 h post-UVB (20 mJ/cm2). The results were obtained from three independent experiments. XPC protein levels in A were quantified using ImageJ software (below each band in arbitrary units). (B) Slot blot analysis of 6-4PP in HaCaT cells transfected with shCon, shE-cadherin, or the combination of shE-cadherin with vector (Con), XPC, or DDB1 plasmids at 0, 1.5 and 6 h post-UVB (20 mJ/cm2). (C) Quantification of percentage (%) of 6-4PP repair from B. *, P < 0.05, compared with shCon group; #, P < 0.05, compared with shE-cadherin/Con groups. (D) Slot blot analysis of CPD in HaCaT cells treated as in B at 0, 6, or 24 h post-UVB. (E) Quantification of percentage (%) of CPD repair from D. *, P < 0.05, compared with shCon group; #, P < 0.05, compared with shE-cadherin/Con groups. (F) Immunofluorescence assay of the colocalization of XPC and subnuclear CPD in HaCaT cells transfected as in B at 0.5 h post-UVC (10 mJ/cm2) through a 5 μm micropore filter. Scale bar, 10 μm. (G) The relative intensity of XPC focus was calculated by analyzing 100 foci and normalized to that of CPD (n= 100, error bar: SD).