Cytokine-mediated crosstalk between cancer stem cells and their inflammatory niche from the colorectal precancerous adenoma stage to the cancerous stage: Mechanisms and clinical implications

Cui, Guanglin; Wang, Ziqi; Liu, Hanzhe; Pang, Zhigang

doi:10.3389/fimmu.2022.1057181

Cited by 5 publications

(3 citation statements)

References 189 publications

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“…Eliminating cancer stem cells, which are at the apex of a hierarchy prevalent in numerous cancer types, is regarded as a crucial aspect of effective antitumor treatment [126]. Precancerous stem cells (pCSCs) undergo complicated genetic and molecular alterations when exposed to diverse microenvironmental variables, leading to the slow transformation of precancerous stem cells into colon cancer stem cells, which is assumed to be the origin of most colorectal malignancies [127].…”

Section: The Role Of Emt In Tumor Stroma and Crc Stem Cellsmentioning

confidence: 99%

Role of Epithelial to Mesenchymal Transition in Colorectal Cancer

Lu,

Kornmann,

Traub

2023

IJMS

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The epithelial–mesenchymal transition (EMT) is a cellular reprogramming process that occurs during embryonic development and adult tissue homeostasis. This process involves epithelial cells acquiring a mesenchymal phenotype. Through EMT, cancer cells acquire properties associated with a more aggressive phenotype. EMT and its opposite, mesenchymal–epithelial transition (MET), have been described in more tumors over the past ten years, including colorectal cancer (CRC). When EMT is activated, the expression of the epithelial marker E-cadherin is decreased and the expression of the mesenchymal marker vimentin is raised. As a result, cells temporarily take on a mesenchymal phenotype, becoming motile and promoting the spread of tumor cells. Epithelial–mesenchymal plasticity (EMP) has become a hot issue in CRC because strong inducers of EMT (such as transforming growth factor β, TGF-β) can initiate EMT and regulate metastasis, microenvironment, and immune system resistance in CRC. In this review, we take into account the significance of EMT-MET in CRC and the impact of the epithelial cells’ plasticity on the prognosis of CRC. The analysis of connection between EMT and colorectal cancer stem cells (CCSCs) will help to further clarify the current meager understandings of EMT. Recent advances affecting important EMT transcription factors and EMT and CCSCs are highlighted. We come to the conclusion that the regulatory network for EMT in CRC is complicated, with a great deal of crosstalk and alternate paths. More thorough research is required to more effectively connect the clinical management of CRC with biomarkers and targeted treatments associated with EMT.

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Section: The Role Of Emt In Tumor Stroma and Crc Stem Cellsmentioning

confidence: 99%

Role of Epithelial to Mesenchymal Transition in Colorectal Cancer

Lu,

Kornmann,

Traub

2023

IJMS

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“…Extracellular vesicles, including exosomes, as well as soluble factors such as interleukins, cytokines, and other metabolites are found in the tumor microenvironment (TME) [21][22][23]. These factors contribute to the establishment of a specialized tumor niche by attracting stromal cells, modulating angiogenesis, promoting metastasis, conferring resistance to anti-tumor treatments, and maintaining CSCs themselves through the secretion of specific molecules like IL-6, VEGF, and TGF-ß [24][25][26].…”

Section: Cancer Stem Cellsmentioning

confidence: 99%

Cancer Stem Cells and Glioblastoma: Time for Innovative Biomarkers of Radio-Resistance?

Pasqualetti,

Miniati,

Gonnelli

et al. 2023

Biology

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Despite countless papers in the field of radioresistance, researchers are still far from clearly understanding the mechanisms triggered in glioblastoma. Cancer stem cells (CSC) are important to the growth and spread of cancer, according to many studies. In addition, more recently, it has been suggested that CSCs have an impact on glioblastoma patients’ prognosis, tumor aggressiveness, and treatment outcomes. In reviewing this new area of biology, we will provide a summary of the most recent research on CSCs and their role in the response to radio-chemotherapy in GB. In this review, we will examine the radiosensitivity of stem cells. Moreover, we summarize the current knowledge of the biomarkers of stemness and evaluate their potential function in the study of radiosensitivity.

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“…STAT6, a signal transducer and activator of transcription 6, has shown promise as a powerful target for anti-cancer medications [ 15 , 16 ]. Clinical evidence reveals a positive correlation between high levels of STAT6 expression and poor clinical outcomes in colorectal cancer patients [ 17 ]. A previous study demonstrated that STAT6-deficient mice displayed fewer and smaller colorectal tumors compared to wild-type mice [ 18 ].…”

Section: Introductionmentioning

confidence: 99%

23-Hydroxybetulinic acid attenuates 5-fluorouracil resistance of colorectal cancer by modulating M2 macrophage polarization via STAT6 signaling

Fan,

Cui,

Chen

et al. 2024

Cancer Immunol Immunother

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Macrophage polarization is closely associated with the inflammatory processes involved in the development and chemoresistance of colorectal cancer (CRC). M2 macrophages, the predominant subtype of tumor-associated macrophages (TAMs) in a wide variety of malignancies, have been demonstrated to promote the resistance of CRC to multiple chemotherapeutic drugs, such as 5-fluorouracil (5-FU). In our study, we investigated the potential of 23-Hydroxybetulinic Acid (23-HBA), a significant active component of Pulsatilla chinensis (P. chinensis), to inhibit the polarization of M2 macrophages induced by IL-4. Our results showed that 23-HBA reduced the expression of M2 specific marker CD206, while downregulating the mRNA levels of M2 related genes (CD206, Arg1, IL-10, and CCL2). Additionally, 23-HBA effectively attenuated the inhibitory effects of the conditioned medium from M2 macrophages on apoptosis in colorectal cancer SW480 cells. Mechanistically, 23-HBA prevented the phosphorylation and nuclear translocation of the STAT6 protein, resulting in the inhibition of IL-10 release in M2 macrophages. Moreover, it interfered with the activation of the IL-10/STAT3/Bcl-2 signaling pathway in SW480 cells, ultimately reducing M2 macrophage-induced resistance to 5-FU. Importantly, depleting STAT6 expression in macrophages abolished the suppressive effect of 23-HBA on M2 macrophage polarization, while also eliminating its ability to decrease M2 macrophage-induced 5-FU resistance in cancer cells. Furthermore, 23-HBA significantly diminished the proportion of M2 macrophages in the tumor tissues of colorectal cancer mice, simultaneously enhancing the anti-cancer efficacy of 5-FU. The findings presented in this study highlight the capacity of 23-HBA to inhibit M2 macrophage polarization, a process that contributes to reduced 5-FU resistance in colorectal cancer.

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Cytokine-mediated crosstalk between cancer stem cells and their inflammatory niche from the colorectal precancerous adenoma stage to the cancerous stage: Mechanisms and clinical implications

Cited by 5 publications

References 189 publications

Role of Epithelial to Mesenchymal Transition in Colorectal Cancer

Role of Epithelial to Mesenchymal Transition in Colorectal Cancer

Cancer Stem Cells and Glioblastoma: Time for Innovative Biomarkers of Radio-Resistance?

23-Hydroxybetulinic acid attenuates 5-fluorouracil resistance of colorectal cancer by modulating M2 macrophage polarization via STAT6 signaling

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