Heterogeneity of stromal fibroblasts in tumor

Orimo, Akira; Weinberg, Robert A.

doi:10.4161/cbt.6.4.4255

Cited by 132 publications

(116 citation statements)

References 20 publications

(23 reference statements)

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“…This communication results in a tumor microenvironment replete with inflammatory mediators, growth factors, matrix remodeling enzymes, and angiogenic factors (Tlsty and Coussens 2006). Growth factors produced by many kinds of cancer cells including breast and ovarian carcinomas attract fibroblasts and stimulate their proliferation (Orimo and Weinberg 2007). Differentiation of fibroblasts in the vicinity of cancer cells to myofibroblasts (i.e., activated fibroblasts) is important for tumor growth and has been observed in several in vitro studies using ovarian cells (Schauer et al 2011).…”

Section: Regulation Of Alternative Splicing In the Tumor Microenvironmentioning

confidence: 98%

Tumor microenvironment–associated modifications of alternative splicing

Brosseau

Lucier

Nwilati

et al. 2013

RNA

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Pre-mRNA alternative splicing is modified in cancer, but the origin and specificity of these changes remain unclear. Here, we probed ovarian tumors to identify cancer-associated splicing isoforms and define the mechanism by which splicing is modified in cancer cells. Using high-throughput quantitative PCR, we monitored the expression of splice variants in laser-dissected tissues from ovarian tumors. Surprisingly, changes in alternative splicing were not limited to the tumor tissues but were also found in the tumor microenvironment. Changes in the tumor-associated splicing events were found to be regulated by splicing factors that are differentially expressed in cancer tissues. Overall, ∼20% of the alternative splicing events affected by the down-regulation of the splicing factors QKI and RBFOX2 were altered in the microenvironment of ovarian tumors. Together, our results indicate that the tumor microenvironment undergoes specific changes in alternative splicing orchestrated by a limited number of splicing factors.

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Section: Regulation Of Alternative Splicing In the Tumor Microenvironmentioning

confidence: 98%

Tumor microenvironment–associated modifications of alternative splicing

Brosseau

Lucier

Nwilati

et al. 2013

RNA

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“…Direct targeting of CAFs, and targeting of CAF-derived factors, is attracting increasing attention as a novel strategy for cancer treatment (5,6). It is becoming recognized that CAFs are heterogeneous and are likely to be composed of subsets, still remaining to be better defined (7)(8)(9).…”

Section: Introductionmentioning

confidence: 99%

Forkhead Box F1 Regulates Tumor-Promoting Properties of Cancer-Associated Fibroblasts in Lung Cancer

et al. 2010

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Cancer-associated fibroblasts (CAF) attract increasing attention as potential cancer drug targets due to their ability to stimulate, for example, tumor growth, invasion, angiogenesis, and metastasis. However, the molecular mechanisms causing the tumor-promoting properties of CAFs remain poorly understood. Forkhead box F1 (FoxF1) is a mesenchymal target of hedgehog signaling, known to regulate mesenchymalepithelial interactions during lung development. Studies with FoxF1 gain-and loss-of-function fibroblasts revealed that FoxF1 regulates the contractility of fibroblasts, their production of hepatocyte growth factor and fibroblast growth factor-2, and their stimulation of lung cancer cell migration. FoxF1 status of fibroblasts was also shown to control the ability of fibroblasts to stimulate xenografted tumor growth. FoxF1 was expressed in CAFs of human lung cancer and associated with activation of hedgehog signaling. These observations suggest that hedgehog-dependent FoxF1 is a clinically relevant lung CAF-inducing factor, and support experimentally the general concept that CAF properties can be induced by activation of developmentally important transcription factors. Cancer Res; 70(7); 2644-54. ©2010 AACR.

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“…97 Finally, a field worth investigation in regard to NME1 tumoral expression is the potential role of the tumoral stroma, in particular, cancer-associated fibroblasts (CAF), which have been shown to promote cancer invasion and migration, and metastasis in many different models. 98 Taken together, these data strongly suggest that re-expression of NME1 in invasive cancer cells could constitute a promising strategy for anti-metastatic therapy. 99,100 NME IN MEMBRANE REMODELING AND NUCLEOTIDE CHANNELING Studies using several model systems, including Drosophila melanogaster, Caenorhabditis elegans, and mouse, as well as human, have demonstrated a fundamental role of the NME/NDPK family in endocytosis, intracellular trafficking, and nucleotide channeling (Figure 1).…”

Section: Nme In Metastasismentioning

confidence: 83%

The NDPK/NME superfamily: state of the art

Boissan

Schlattner

Lacombe

2018

Laboratory Investigation

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Nucleoside diphosphate kinases (NDPK) are nucleotide metabolism enzymes encoded by NME genes (also called NM23). Given the fact that not all NME-encoded proteins are catalytically active NDPKs and that NM23 generally refers to clinical studies on metastasis, we use here NME/NDPK to denote the proteins. Since their discovery in the 1950's, NMEs/NDPKs have been shown to be involved in multiple physiological and pathological cellular processes, but the molecular mechanisms have not been fully determined. Recent progress in elucidating these underlying mechanisms has been presented by experts in the field at the 10th International Congress on the NDPK/NME/AWD protein family in October 2016 in Dubrovnik, Croatia, and is summarized in review articles or original research in this and an upcoming issue of Laboratory Investigation. Within this editorial, we discuss three major cellular processes that involve members of the multi-functional NME/NDPK family: (i) cancer and metastasis dissemination, (ii) membrane remodeling and nucleotide channeling, and iii) protein histidine phosphorylation.

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Heterogeneity of stromal fibroblasts in tumor

Cited by 132 publications

References 20 publications

Tumor microenvironment–associated modifications of alternative splicing

Tumor microenvironment–associated modifications of alternative splicing

Forkhead Box F1 Regulates Tumor-Promoting Properties of Cancer-Associated Fibroblasts in Lung Cancer

The NDPK/NME superfamily: state of the art

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