Journal of Molecular Medicine

, Volume 91, Issue 3, pp 407–408

Erratum to: Celastrol suppresses invasion of colon and pancreatic cancer cells through the downregulation of expression of CXCR4 chemokine receptor

Authors

  • Vivek R. Yadav
    • Cytokine Research Laboratory, Department of Experimental TherapeuticsThe University of Texas MD Anderson Cancer Center
  • Bokyung Sung
    • Cytokine Research Laboratory, Department of Experimental TherapeuticsThe University of Texas MD Anderson Cancer Center
  • Sahdeo Prasad
    • Cytokine Research Laboratory, Department of Experimental TherapeuticsThe University of Texas MD Anderson Cancer Center
  • Ramaswamy Kannappan
    • Cytokine Research Laboratory, Department of Experimental TherapeuticsThe University of Texas MD Anderson Cancer Center
  • Sung-Gook Cho
    • Institute of Biosciences and Technology, Department of Molecular and Cellular MedicineTexas A&M University Health Science Center
  • Mingyao Liu
    • Institute of Biosciences and Technology, Department of Molecular and Cellular MedicineTexas A&M University Health Science Center
  • Madan M. Chaturvedi
    • Cytokine Research Laboratory, Department of Experimental TherapeuticsThe University of Texas MD Anderson Cancer Center
    • Department of ZoologyUniversity of Delhi
    • Cytokine Research Laboratory, Department of Experimental TherapeuticsThe University of Texas MD Anderson Cancer Center
Erratum

DOI: 10.1007/s00109-012-0987-8

Cite this article as:
Yadav, V.R., Sung, B., Prasad, S. et al. J Mol Med (2013) 91: 407. doi:10.1007/s00109-012-0987-8
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Erratum to: J Mol Med. 2010 Dec;88(12):1243-53

DOI 10.1007/s00109-010-0669-3

The authors claim that Figs. 5a and b, and 6a and d, reporting data from in vitro invasion assays were published incorrectly. Specifically, two images of invaded cells were by mistake duplicated. The authors performed 2 additional experiments to confirm their data. The results from these experiments are reported in the corrected versions of the figures and legends, as well as the corresponding results section that are shown below. The authors claim that this correction does not influence the conclusion of the study and would like to apologize for this oversight.
https://static-content.springer.com/image/art%3A10.1007%2Fs00109-012-0987-8/MediaObjects/109_2012_987_Fig1_HTML.gif
Fig. 5

Celastrol suppresses invasion in colon cancer cells. a HCT116 cells (0.25 × 106 cells per well) were transfected with siRNAs and the transfected cells were collected after 48 h. After transfection, cells were seeded in the top chamber of Matrigel. Transwell chambers were then placed into 24-well plates in which either the basal medium was added or 100 ng/mL CXCL12 in the basal medium. After the incubation, invasion assay was done as described in the “Materials and methods” section. The results shown are representative of two independent experiments. b Histogram of data obtained from invasion assay in Fig. 5a. …, bars SE. *P < 0.05

https://static-content.springer.com/image/art%3A10.1007%2Fs00109-012-0987-8/MediaObjects/109_2012_987_Fig2_HTML.gif
Fig. 6

Celastrol suppresses CXCR4 and invasion in pancreatic cancer cells. aLeft panel AsPC-1 cells (2 × 105; 2 % FBS–DMEM) were seeded in the top chamber of Matrigel. After preincubation with or without celastrol (3 μmol/ L) for 6 h, Transwell chambers were then placed into 24-well plates in which either the basal medium was added or 100 ng/mL CXCL12 in basal medium. After incubation, invasion assay was done as described in the “Materials and methods” section. The results shown are representative of two independent experiments. Right panel histogram of data obtained from invasion assay in Fig. 6a, left panel, SE. *P < 0.05. …dLeft panel MIA PaCa-2 cells (2 × 105; 2 % FBS–DMEM) were seeded in the top chamber of Matrigel and invasion assay was done as describe above. The results shown are representative of two independent experiments. Right panel histogram of data obtained from invasion assay in Fig. 6d, left panel

Results

CXCR4 is essential for CXCL12-induced invasion

Disruption of CXCR4 and CXCL12 interaction by selective antagonists or anti-CXCR4 antibody blocks cancer metastasis, suggesting an essential role for CXCR4. Therefore, when HCT116 cells were transfected with siRNA specific for CXCR4, it efficiently inhibited CXCL12-mediated invasion to about 31 % compared to the control condition. (Fig. 5a, b). Indeed, the CXCR4-specific siRNA reduced CXCR4 protein expression (Fig. 5c).

Copyright information

© Springer-Verlag Berlin Heidelberg 2013