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同时照射成纤维细胞和癌细胞会抑制能够刺激癌细胞迁移的可溶性因子的分泌。

Simultaneous irradiation of fibroblasts and carcinoma cells repress the secretion of soluble factors able to stimulate carcinoma cell migration.

作者信息

Arshad Adnan, Deutsch Eric, Vozenin Marie-Catherine

机构信息

INSERM U1030, LabEx LERMIT, Villejuif, France; Université Paris Sud, Kremlin-Bicêtre, France; Institut Gustave Roussy, Villejuif, France.

INSERM U1030, LabEx LERMIT, Villejuif, France; Université Paris Sud, Kremlin-Bicêtre, France; Institut Gustave Roussy, Villejuif, France; Laboratoire de recherche en Radio-Oncologie, Service de Radio-Oncologie/département d'Oncologie/CHUV, Lausanne, Switzerland.

出版信息

PLoS One. 2015 Jan 30;10(1):e0115447. doi: 10.1371/journal.pone.0115447. eCollection 2015.

DOI:10.1371/journal.pone.0115447
PMID:25635683
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4312053/
Abstract

Stroma mediated wound healing signals may share similarities with the ones produced by tumor's microenvironment and their modulation may impact tumor response to the various anti-cancer treatments including radiation therapy. Therefore we conducted this study, to assess the crosstalk between stromal and carcinoma cells in response to radiotherapy by genetic modulation of the stroma and irradiation. We found that fibroblasts irrespective of their RhoB status do not modulate intrinsic radiosensitivity of TC-1 but produce diffusible factors able to modify tumor cell fate. Then we found that Wt and RhoB deficient fibroblasts stimulated TC-1 migration through distinct mechanisms which are TGF-β1 and MMP-mediated respectively. Lastly, we found that simultaneous irradiation of fibroblasts and TC-1 abrogated the pro-migratory phenotype by repression of TGF-β and MMP secretion. This last result is highly relevant to the clinical situation and suggests that conversely to, the current view; irradiated stroma would not enhance carcinoma migration and could be manipulated to promote anti-tumor immune response.

摘要

基质介导的伤口愈合信号可能与肿瘤微环境产生的信号具有相似性，对其进行调节可能会影响肿瘤对包括放射治疗在内的各种抗癌治疗的反应。因此，我们开展了这项研究，通过对基质进行基因调节和照射来评估基质细胞与癌细胞之间对放疗的相互作用。我们发现，无论RhoB状态如何，成纤维细胞都不会调节TC-1的内在放射敏感性，但会产生能够改变肿瘤细胞命运的可扩散因子。然后我们发现，野生型和RhoB缺陷型成纤维细胞分别通过TGF-β1和MMP介导的不同机制刺激TC-1迁移。最后，我们发现同时照射成纤维细胞和TC-1可通过抑制TGF-β和MMP分泌消除促迁移表型。这一最新结果与临床情况高度相关，表明与当前观点相反；照射后的基质不会增强癌细胞迁移，并且可以通过调控来促进抗肿瘤免疫反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab7b/4312053/e4b19b8468d4/pone.0115447.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab7b/4312053/45290c56d10e/pone.0115447.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab7b/4312053/1d0c5af5bfb7/pone.0115447.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab7b/4312053/d508d7ffd225/pone.0115447.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab7b/4312053/738a1b7f1af7/pone.0115447.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab7b/4312053/48cf0cc611ed/pone.0115447.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab7b/4312053/006c4928ec37/pone.0115447.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab7b/4312053/e4b19b8468d4/pone.0115447.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab7b/4312053/45290c56d10e/pone.0115447.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab7b/4312053/1d0c5af5bfb7/pone.0115447.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab7b/4312053/d508d7ffd225/pone.0115447.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab7b/4312053/738a1b7f1af7/pone.0115447.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab7b/4312053/48cf0cc611ed/pone.0115447.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab7b/4312053/006c4928ec37/pone.0115447.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab7b/4312053/e4b19b8468d4/pone.0115447.g007.jpg

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