Mesenchymal Stem Cells in the Tumor Microenvironment

Atiya, Huda I.; Frisbie, Leonard; Pressimone, Catherine A.; Coffman, Lan

doi:10.1007/978-3-030-37184-5_3

Cited by 91 publications

(91 citation statements)

References 82 publications

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“…TME is made up of a network of stromal cells, immune cells, cancer-associated fibroblasts (CAFs), vascular endothelial cells, and a series of secreted molecules that assemble the extracellular matrix (ECM) [ 61 , 100 ]. Some immune cells and CAFs produce factors such as growth factors, cytokines, and chemokines that regulate the phenotype and function of tumor-resident cells.…”

Section: Cscs and Microenvironmentmentioning

confidence: 99%

CSC Radioresistance: A Therapeutic Challenge to Improve Radiotherapy Effectiveness in Cancer

Olivares-Urbano

Griñán‐Lisón

Marchal

et al. 2020

Cells

146

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Radiotherapy (RT) is a modality of oncologic treatment that can be used to treat approximately 50% of all cancer patients either alone or in combination with other treatment modalities such as surgery, chemotherapy, immunotherapy, and therapeutic targeting. Despite the technological advances in RT, which allow a more precise delivery of radiation while progressively minimizing the impact on normal tissues, issues like radioresistance and tumor recurrence remain important challenges. Tumor heterogeneity is responsible for the variation in the radiation response of the different tumor subpopulations. A main factor related to radioresistance is the presence of cancer stem cells (CSC) inside tumors, which are responsible for metastases, relapses, RT failure, and a poor prognosis in cancer patients. The plasticity of CSCs, a process highly dependent on the epithelial–mesenchymal transition (EMT) and associated to cell dedifferentiation, complicates the identification and eradication of CSCs and it might be involved in disease relapse and progression after irradiation. The tumor microenvironment and the interactions of CSCs with their niches also play an important role in the response to RT. This review provides a deep insight into the characteristics and radioresistance mechanisms of CSCs and into the role of CSCs and tumor microenvironment in both the primary tumor and metastasis in response to radiation, and the radiobiological principles related to the CSC response to RT. Finally, we summarize the major advances and clinical trials on the development of CSC-based therapies combined with RT to overcome radioresistance. A better understanding of the potential therapeutic targets for CSC radiosensitization will provide safer and more efficient combination strategies, which in turn will improve the live expectancy and curability of cancer patients.

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Section: Cscs and Microenvironmentmentioning

confidence: 99%

CSC Radioresistance: A Therapeutic Challenge to Improve Radiotherapy Effectiveness in Cancer

Olivares-Urbano

Griñán‐Lisón

Marchal

et al. 2020

Cells

146

View full text Add to dashboard Cite

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“…Occurrence of BC metastases in lungs and bones is also supported by the induction of TWIST transcription by BM-MSC production of lysil oxidase enzyme (59) and by the production of exosomes containing miRNA-222/223 (60). Finally, it has been shown that, in contact with BC cells, BM-MSCs are able to transdifferentiate into cancer associated fibroblasts (CAFs), the best companions for BC cells (50,51,61).…”

Section: Bc-associated Adipose Cellsmentioning

confidence: 99%

Mammary Adipose Tissue Control of Breast Cancer Progression: Impact of Obesity and Diabetes

et al. 2020

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Mammary adipose tissue (AT) is necessary for breast epithelium. However, in breast cancer (BC), cell-cell interactions are deregulated as the tumor chronically modifies AT microenvironment. In turn, breast AT evolves to accommodate the tumor, and to participate to its dissemination. Among AT cells, adipocytes and their precursor mesenchymal stem cells (MSCs) play a major role in supporting tumor growth and dissemination. They provide energy supplies and release a plethora of factors involved in cancer aggressiveness. Here, we discuss the main molecular mechanisms underlining the interplay between adipose (adipocytes and MSCs) and BC cells. Following close interactions with BC cells, adipocytes lose lipids and change morphology and secretory patterns. MSCs also play a major role in cancer progression. While bone marrow MSCs are recruited by BC cells and participate in metastatic process, mammary AT-MSCs exert a local action by increasing the release of cytokines, growth factors and extracellular matrix components and become principal actors in cancer progression. Common systemic metabolic diseases, including obesity and diabetes, further modify the interplay between AT and BC. Indeed, metabolic perturbations are accompanied by well-known alterations of AT functions, which might contribute to worsen cancer phenotype. Here, we highlight how metabolic alterations locally affect mammary AT and interfere with the molecular mechanisms of bidirectional communication between adipose and cancer cells.

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“…During the progression of carcinogenesis, MSCs are recruited to the TME by growth factors, cytokines and chemokines, such as IL‐6, IL‐1β, TGF‐β1, EGF, PDGF, TNF‐α and SDF‐1α, secreted by cancer cells and stomal cells 63 . Upon entry into the tumour microenvironment niche, MSCs promote or inhibit tumour progression by various mechanisms.…”

Section: Composition and Function Of The Tmementioning

confidence: 99%

Modifying the tumour microenvironment and reverting tumour cells: New strategies for treating malignant tumours

et al. 2020

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The tumour microenvironment (TME) plays a pivotal role in tumour fate determination. The TME acts together with the genetic material of tumour cells to determine their initiation, metastasis and drug resistance. Stromal cells in the TME promote the growth and metastasis of tumour cells by secreting soluble molecules or exosomes. The abnormal microenvironment reduces immune surveillance and tumour killing. The TME causes low anti‐tumour drug penetration and reactivity and high drug resistance. Tumour angiogenesis and microenvironmental hypoxia limit the drug concentration within the TME and enhance the stemness of tumour cells. Therefore, modifying the TME to effectively attack tumour cells could represent a comprehensive and effective anti‐tumour strategy. Normal cells, such as stem cells and immune cells, can penetrate and disrupt the abnormal TME. Reconstruction of the TME with healthy cells is an exciting new direction for tumour treatment. We will elaborate on the mechanism of the TME to support tumours and the current cell therapies for targeting tumours and the TME—such as immune cell therapies, haematopoietic stem cell (HSC) transplantation therapies, mesenchymal stem cell (MSC) transfer and embryonic stem cell‐based microenvironment therapies—to provide novel ideas for producing breakthroughs in tumour therapy strategies.

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Mesenchymal Stem Cells in the Tumor Microenvironment

Cited by 91 publications

References 82 publications

CSC Radioresistance: A Therapeutic Challenge to Improve Radiotherapy Effectiveness in Cancer

CSC Radioresistance: A Therapeutic Challenge to Improve Radiotherapy Effectiveness in Cancer

Mammary Adipose Tissue Control of Breast Cancer Progression: Impact of Obesity and Diabetes

Modifying the tumour microenvironment and reverting tumour cells: New strategies for treating malignant tumours

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