The authors and journal apologise for errors in the above paper, which appeared in volume 21 part 5, pages 739–753 (October 2014). The error relates to Figs. 6 and 7 given on page 747, in which control blot images were unintentionally duplicated. The authors repeated the experiments, supplied uncropped full blots, and supplied corrected figure artwork which is given in full belowa.
(A, B, C, and D) CTGF protein expression is upregulated by 10 nM insulin in R−/INSR-A (R−/IR-A) and R−/INSR-B (R−/IR-B), CAFs, and SKUT-1 cells. The charts show the results from densitometric analysis of the blots normalized to β-tubulin or β-actin. Each column represents the mean±S.D. of three independent experiments (closed square) Indicates P<0.05 for cells receiving vehicle (−) vs treatments.
Citation: Endocrine-Related Cancer 30, 12; 10.1530/ERC-14-0245e
(A, B, C, and D) CTGF protein expression is upregulated by 10 nM insulin in R−/INSR-A (R−/IR-A) and R−/INSR-B (R−/IR-B), CAFs, and SKUT-1 cells. The charts show the results from densitometric analysis of the blots normalized to β-tubulin or β-actin. Each column represents the mean±S.D. of three independent experiments (closed square) Indicates P<0.05 for cells receiving vehicle (−) vs treatments.
Citation: Endocrine-Related Cancer 30, 12; 10.1530/ERC-14-0245e
(A, B, C, and D) CTGF protein expression is upregulated by 10 nM insulin in R−/INSR-A (R−/IR-A) and R−/INSR-B (R−/IR-B), CAFs, and SKUT-1 cells. The charts show the results from densitometric analysis of the blots normalized to β-tubulin or β-actin. Each column represents the mean±S.D. of three independent experiments (closed square) Indicates P<0.05 for cells receiving vehicle (−) vs treatments.
Citation: Endocrine-Related Cancer 30, 12; 10.1530/ERC-14-0245e
The upregulation of CTGF protein levels induced by a 4 h treatment with 10 nM insulin was abolished by transfecting CAFs and SKUT-1 cells with shINSR (A, B, C, and D), shGPER1 (E, F, G, and H), or a dominant negative form of c-Fos (DN/c-Fos) (I and J). The migration of CAFs and SKUT-1 cells after a 6 h treatment with 10 nM insulin was prevented by silencing GPER1 and CTGF expression (K, L, M, N, O, and P). Results shown are representative of three independent experiments. The charts show the results from densitometric analysis of the blots normalized to β-actin. (closed square) P<0.05 for cells receiving vehicle (−) vs treatments.
Citation: Endocrine-Related Cancer 30, 12; 10.1530/ERC-14-0245e
The upregulation of CTGF protein levels induced by a 4 h treatment with 10 nM insulin was abolished by transfecting CAFs and SKUT-1 cells with shINSR (A, B, C, and D), shGPER1 (E, F, G, and H), or a dominant negative form of c-Fos (DN/c-Fos) (I and J). The migration of CAFs and SKUT-1 cells after a 6 h treatment with 10 nM insulin was prevented by silencing GPER1 and CTGF expression (K, L, M, N, O, and P). Results shown are representative of three independent experiments. The charts show the results from densitometric analysis of the blots normalized to β-actin. (closed square) P<0.05 for cells receiving vehicle (−) vs treatments.
Citation: Endocrine-Related Cancer 30, 12; 10.1530/ERC-14-0245e
The upregulation of CTGF protein levels induced by a 4 h treatment with 10 nM insulin was abolished by transfecting CAFs and SKUT-1 cells with shINSR (A, B, C, and D), shGPER1 (E, F, G, and H), or a dominant negative form of c-Fos (DN/c-Fos) (I and J). The migration of CAFs and SKUT-1 cells after a 6 h treatment with 10 nM insulin was prevented by silencing GPER1 and CTGF expression (K, L, M, N, O, and P). Results shown are representative of three independent experiments. The charts show the results from densitometric analysis of the blots normalized to β-actin. (closed square) P<0.05 for cells receiving vehicle (−) vs treatments.
Citation: Endocrine-Related Cancer 30, 12; 10.1530/ERC-14-0245e
