MiR-206 suppresses the deterioration of intrahepatic cholangiocarcinoma and promotes sensitivity to chemotherapy by inhibiting interactions with stromal CAFs

Yang, Renjie; Wang, Dong; Han, Shen; Gu, Yun; Li, Zhi; Deng, Lei; Yin, Aihong; Gao, Yun; Li, Xiangcheng; Yu, Yue; Wang, Xuehao

doi:10.7150/ijbs.62602

Cited by 17 publications

(15 citation statements)

References 58 publications

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“…For instance, Takahiro et al suggested that nintedanib is capable of treating refractory ICC by inhibiting the activation of CAFs after the use of nintedanib [23]. It has also been confirmed that MiR-206 inhibits the deterioration of ICC and increases chemosensitivity by inhibiting the interaction with interstitial CAFs [24]. Table 1 lists the promoting and inhibiting effects of CAFs on CCA.…”

Section: Cafs In Ccamentioning

confidence: 99%

Tumor Microenvironment and its Implications for Antitumor Immunity in Cholangiocarcinoma: Future Perspectives for Novel Therapies

Cao¹,

Huang²,

Dai³

et al. 2022

Int. J. Biol. Sci.

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The incidence of cholangiocarcinoma (CCA) has been increasing over the past few years. Although there are surgery, chemotherapy and other conventional treatment methods, the effect is not as expected. At present, immunotherapy has become the research frontier of cancer treatment, and CCA tumor microenvironment (TME) is becoming a hot exploration direction of immunobiology. TME can affect tumor progression through changes in metabolism, secretion and immunity. Accordingly, understanding the role played by immune cells and stromal cells in TME is important for the study of CCA immunotherapy. This review will discuss the interactions between immune cells (including CD8 + T cells, CD4 + T cells, macrophages, natural killer cells, dendritic cells, myeloid suppressor cells, mast cells, and neutrophils) and stromal cells (including cancer-associated fibroblasts, endothelial cells) in the TME of CCA. In addition, we will also discuss current research results on TME of CCA and recent advances in immunotherapy.

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Section: Cafs In Ccamentioning

confidence: 99%

Tumor Microenvironment and its Implications for Antitumor Immunity in Cholangiocarcinoma: Future Perspectives for Novel Therapies

Cao¹,

Huang²,

Dai³

et al. 2022

Int. J. Biol. Sci.

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“…Lung cancer cells transform NFs into CAFs by causing an increase in CAF miR-31 and a decrease in their miR-1 and miR-206 content, effects which induce the expression of VEGFA/CCL2 and FOXO3a and promote tumor angiogenesis, accumulation of tumor-associated macrophages, tumor growth, and lung metastasis [ 143 ]. Similarly, intrahepatic cholangiocarcinoma cells downregulate miR-206 in NFs and convert them to CAFs [ 272 ]. miR-206 suppresses tumorigenesis of intrahepatic cholangiocarcinoma by inhibiting cell proliferation, migration, and invasion [ 272 ].…”

Section: Cancer-associated Fibroblastsmentioning

confidence: 99%

Fibroblasts as Turned Agents in Cancer Progression

Wieder

2023

Cancers

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Differentiated epithelial cells reside in the homeostatic microenvironment of the native organ stroma. The stroma supports their normal function, their G0 differentiated state, and their expansion/contraction through the various stages of the life cycle and physiologic functions of the host. When malignant transformation begins, the microenvironment tries to suppress and eliminate the transformed cells, while cancer cells, in turn, try to resist these suppressive efforts. The tumor microenvironment encompasses a large variety of cell types recruited by the tumor to perform different functions, among which fibroblasts are the most abundant. The dynamics of the mutual relationship change as the sides undertake an epic battle for control of the other. In the process, the cancer “wounds” the microenvironment through a variety of mechanisms and attracts distant mesenchymal stem cells to change their function from one attempting to suppress the cancer, to one that supports its growth, survival, and metastasis. Analogous reciprocal interactions occur as well between disseminated cancer cells and the metastatic microenvironment, where the microenvironment attempts to eliminate cancer cells or suppress their proliferation. However, the altered microenvironmental cells acquire novel characteristics that support malignant progression. Investigations have attempted to use these traits as targets of novel therapeutic approaches.

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“… 71 The investigation of Exos-miR-206 function in GC and HCC revealed that miR-206 has a key suppressor role in the TME of these tumors. 112 , 113 Interestingly, overexpression of miR-206 promoted the recruitment of CD8 + T cells to the TME by inducing M1 polarization through increasing CCL2. 114 In nasopharyngeal carcinoma (NPC), there was a significant upregulation of miR-24-3p in the serum that inhibited proliferation of Th1 and Th17 but induced differentiation of Tregs by inhibiting fibroblast growth factor 11 (FGF11) gene in T cells.…”

Section: Role Of Exos-ncrnas In T Cell Recruitment and Function In Th...mentioning

confidence: 99%

Role of exosomal ncRNAs released by M2 macrophages in tumor progression of gastrointestinal cancers

Meyiah¹,

Alahdal²,

Elkord³

2023

iScience

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MiR-206 suppresses the deterioration of intrahepatic cholangiocarcinoma and promotes sensitivity to chemotherapy by inhibiting interactions with stromal CAFs

Cited by 17 publications

References 58 publications

Tumor Microenvironment and its Implications for Antitumor Immunity in Cholangiocarcinoma: Future Perspectives for Novel Therapies

Tumor Microenvironment and its Implications for Antitumor Immunity in Cholangiocarcinoma: Future Perspectives for Novel Therapies

Fibroblasts as Turned Agents in Cancer Progression

Role of exosomal ncRNAs released by M2 macrophages in tumor progression of gastrointestinal cancers

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