CORRIGENDUM: GPER1 is regulated by insulin in cancer cells and cancer-associated fibroblasts

in Endocrine-Related Cancer
Authors:
Paola De Marco Department of Pharmacy, Health and Nutritional Sciences, University of Calabria, Rende (CS), Italy

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Enrica Romeo Department of Pharmacy, Health and Nutritional Sciences, University of Calabria, Rende (CS), Italy

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Adele Vivacqua Department of Pharmacy, Health and Nutritional Sciences, University of Calabria, Rende (CS), Italy

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Roberta Malaguarnera Endocrinology, Department of Health, University Magna Graecia of Catanzaro, Catanzaro, Italy

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Sergio Abonante Regional Hospital, Cosenza, Italy

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Francesco Romeo Regional Hospital, Cosenza, Italy

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Vincenzo Pezzi Department of Pharmacy, Health and Nutritional Sciences, University of Calabria, Rende (CS), Italy

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Antonino Belfiore Endocrinology, Department of Health, University Magna Graecia of Catanzaro, Catanzaro, Italy

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Marcello Maggiolini Department of Pharmacy, Health and Nutritional Sciences, University of Calabria, Rende (CS), Italy

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Correspondence should be addressed to M Maggiolini: marcellomaggiolini@yahoo.it
DOI:
https://doi.org/10.1530/ERC-14-0245e
Volume/Issue:
Volume 30: Issue 12
Article Type:
Correction
Article ID:
e140245e
Online Publication Date:
18 Oct 2023
Copyright:
© the author(s) 2023
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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.

Figure 6
Figure 6

(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

Figure 7
Figure 7

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

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Print ISSN:
1351-0088
Online ISSN:
1479-6821
Copyright:
© the author(s) 2023
Article ID:
e140245e
Print Publication Date:
01 Dec 2023
Online Publication Date:
18 Oct 2023
  • Figure 6
    View in gallery
    Figure 6

    (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.

  • Figure 7
    View in gallery
    Figure 7

    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.

Figure 6

(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.
Figure 7

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.