P300, A New Player in Mechanosensitivity and Activation of Cancer-Associated Fibroblasts

Török, Natalie J.

doi:10.1053/j.gastro.2018.05.002

Cited by 9 publications

(22 citation statements)

References 14 publications

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“…COX‐2 signaling is strongly correlated to collagen synthesis in cancer cells, and this relation is regarded as a driving force for decrease of the time for cancer metastasis . P300 is a coactivator of COX‐2 promoter, and there is evidence for suppression of matrix cross‐linking and rigidity by inhibition of P300 signal transduction …”

Section: Signals Related To Ecm Stiffnessmentioning

confidence: 99%

Extracellular matrix (ECM) stiffness and degradation as cancer drivers

Najafi

Farhood

Mortezaee

2018

J of Cellular Biochemistry

421

278

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Section: Signals Related To Ecm Stiffnessmentioning

confidence: 99%

Extracellular matrix (ECM) stiffness and degradation as cancer drivers

Najafi

Farhood

Mortezaee

2018

J of Cellular Biochemistry

421

278

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show abstract

“…(1) One of the challenges is no definite source for this cells. Fibroblasts although are the main contributors to the CAF population, other cell sources including adipocytes, myeloid cells, epithelial cells, stellate cells, and mesenchymal stem cells (MSCs) are also able to transform into CAFs . CAFs can even be transdifferentiated from cancer cells .…”

Section: Caf Targeting As a Promising Therapeutic Approachmentioning

confidence: 99%

“…57,58 Fibronectin matrix is also important for migration and invasion of cancer cells. 15 The interaction between ECM and integrin is important for migration and invasion of CAFs. 11 High deposition of ECM components like collagen and fibrin forms an ECM tension (or stiffness) within the TME.…”

Section: Ecm and Related Tumor Progressive Modalitiesmentioning

confidence: 99%

“…33 ECM stiffness also causes enhanced ECM migratory activity. 15 Cancer cells can become extensively motile along collagen bundles, and the cells seem to use the bundles as "highways" for facilitation of their effective migration. 31 In addition, collagen laid down by CAFs is also required for cancer cell survival and growth.…”

Section: Ecm and Related Tumor Progressive Modalitiesmentioning

confidence: 99%

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Cancer‐associated fibroblasts: Secretions, interactions, and therapy

Farhood

Najafi

Mortezaee

2018

J of Cellular Biochemistry

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Tumor microenvironment (TME) could impose a great challenge for cancer targeted therapies. Immunosuppression within the TME creates a barrier between cancer cells and therapeutic approaches. A number of cells are hosted within this milieu, among them cancer-associated fibroblasts (CAFs) are the most abundant cell populations playing major roles in mediating an immunosuppressive TME. CAFs have cross-talks with almost all cells within the TME for reprogramming them into being tumorigenic. This reprogramming reduces the pre-existing tumor immunity and dampens the efficacy of chemotherapeutic approaches. CAFs would do this through releasing a myriad of factors to the TME making it an appropriate nest for tumor growth. The cells degrade and deposit extracellular matrix components, both of which are tumorigenic. Therefore, disruption of cross-talks between CAFs with other cells within the TME would be a promising approach in cancer targeted therapies.This approach is applicable through dampening dominant signals mediated by CAFs. Another interesting approach would be reprogramming of CAFs toward their normal counterpart. This would need identification of different subtypes for these cells and their functions. More knowledge is also required about selective markers for each CAF subtype. K E Y W O R D Scancer, cancer-associated fibroblasts, extracellular matrix, therapy, transforming growth factor-β, tumor microenvironment J Cell Biochem. 2019;120:2791-2800.wileyonlinelibrary.com/journal/jcb

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“…ECM stiffness results from complex interactions among stromal cells, including cancer cells, CAFs, and immune cells. CAF‐induced ECM stiffness is a proper feature for the migration and invasion of cancer cells (Paauwe M et al, 2018; Dauer P et al, 2018; Torok, 2018).…”

Section: Tme Classificationmentioning

confidence: 99%

A survey of herbal medicines as tumor microenvironment‐modulating agents

Park

Lee

Son

et al. 2020

Phytotherapy Research

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The tumor microenvironment (TME) is extremely complex, involving extensive interactions among stromal cells, immune cells, and signaling molecules. Therefore, an approach targeting the TME has emerged as a promising therapeutic strategy. Herbal medicines consist of multiple active compounds, which have multi‐target effects. Therefore, they have been regarded as potential anticancer agents; multiple studies have explored their effects on the TME. In this review, we report the effects of 29 single herb medicines or herbal formulas on the TME, based on the findings of 64 published studies. Specifically, we describe the effects of these herbal medicines on cancer‐associated fibroblasts/tumor‐associated fibroblasts, tumor‐associated endothelial cells, myeloid‐derived suppressor cells, and tumor‐associated macrophages. Among the reviewed herbal medicines, the most promising TME‐modulating effects were exhibited by curcumin, DHA, EGCG, resveratrol, and silibinin; these medicines showed the ability to regulate two or more components of the TME. The findings of this review support the notion that the combination of herbal medicines with conventional anticancer therapies are likely to exhibit a clinical benefit, which should be further explored in clinical trials.

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P300, A New Player in Mechanosensitivity and Activation of Cancer-Associated Fibroblasts

Cited by 9 publications

References 14 publications

Extracellular matrix (ECM) stiffness and degradation as cancer drivers

Extracellular matrix (ECM) stiffness and degradation as cancer drivers

Cancer‐associated fibroblasts: Secretions, interactions, and therapy

A survey of herbal medicines as tumor microenvironment‐modulating agents

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