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  • Response to Letter to the Editor
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Response

Response to Sehgal

Oncogene volume 29, page 2601 (2010)Cite this article

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In his letter to the editors of Oncogene, Dr Sehgal (2010, this issue) states ‘…the recent articles of Walter et al. (2009) and Sullivan et al. (2009) confirm and recapitulate the concepts about the involvement of IL-6 in breast cancer pathobiology already enunciated by the Tamm and Revel laboratories between 15 to 20 years ago, but without acknowledgement of the existence of that extensive prior literature…’. While we apologize for the inadvertent omission of Drs Tamm and Sehgal's earlier work (Sehgal and Tamm, 1991) on interleukin-6 (IL-6), we disagree with Dr Sehgal's suggestion that our reported findings are merely a duplication of the earlier work carried out by him and Dr Tamm.

Our study investigated the impact of adipose stromal cells (ASCs) on the migratory behavior and invasiveness of breast cancer cells, in particular estrogen receptor-negative breast cancer cells. ASCs have only recently been discovered and characterized, and it had not been the subject of any published studies by Drs Tamm and Sehgal. Importantly, we wish to point out two significant aspects of our work. First, we demonstrate that ASCs from cancer-free individuals have an intrinsic capability of promoting tumor cell migration and invasion, which may provide a molecular explanation for the obesity-associated cancer risk. Second, we identify a previously unappreciated link between the cofilin-mediated pathway and interleukin-6 expression in ASCs. Given that the cofilin-mediated pathway in tumor cells is known to have an important role in tumor invasion and metastasis, our work raises the distinct possibility that simultaneous inhibition of the same pathway in tumor and stromal compartments may provide an attractive therapeutic strategy for cancer treatment. The novelty of our findings, which is clearly presented in our publication, sets our work apart from the published studies by Tamm and Sehgal. The fact that our mechanistic investigation ultimately connects the tumor-promoting effects of ASCs and the cofilin pathway with a well-studied cytokine should not serve as the basis for dismissing the overall significance of our work.

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References

  • Sehgal PB . (2010). Interleukin-6 induces increased motility, cell–cell and cell–substrate dyshesion and epithelial-to-mesenchymal transformation in breast cancer cells. Oncogene (e-pub ahead of print 8 February 2010; doi:10.1038/onc.2010.4).

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  • Sehgal PB, Tamm I . (1991). Interleukin-6 enhances motility of breast carcinoma cells. In: Goldberg ID (ed). Cell Motility Factors. Birkhauser Verlag: Basel–Boston–Berlin, pp 178–193.

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  1. Molecular Medicine, Institute of Biotechnology, University of Texas, San Antonio, TX, USA. E-mail: lir3@uthscsa.edu,

    R Li

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Li, R. Response to Sehgal. Oncogene 29, 2601 (2010). https://doi.org/10.1038/onc.2010.44

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