Reduced CX3CL1 Secretion Contributes to the Susceptibility of Oral Leukoplakia-Associated Fibroblasts to Candida albicans

Cheng, Ran; Li, Duo; Shi, Xueke; Gao, Qiong; Wei, Changlei; Li, Xiaoyü; Li, Yan; Zhou, Hongmei

doi:10.3389/fcimb.2016.00150

Cited by 13 publications

(10 citation statements)

References 34 publications

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“… 69 , 70 Indeed, we extended the two-dimensional (2D) culture of fibroblasts from oral precancerous lesions with the addition of Candida. 71 Furthermore, techniques differ for cell culture in 2D and 3D, with the latter allowing patterns of growth in vitro to better mimic that of the tissue architecture in vivo. 72 One type of 3D coculture is implemented through the use of reconstituted matrices.…”

Section: From Fibroblasts To Cafs In Tmementioning

confidence: 99%

Signaling pathways in cancer-associated fibroblasts and targeted therapy for cancer

Yang

Liu

et al. 2021

Sig Transduct Target Ther

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To flourish, cancers greatly depend on their surrounding tumor microenvironment (TME), and cancer-associated fibroblasts (CAFs) in TME are critical for cancer occurrence and progression because of their versatile roles in extracellular matrix remodeling, maintenance of stemness, blood vessel formation, modulation of tumor metabolism, immune response, and promotion of cancer cell proliferation, migration, invasion, and therapeutic resistance. CAFs are highly heterogeneous stromal cells and their crosstalk with cancer cells is mediated by a complex and intricate signaling network consisting of transforming growth factor-beta, phosphoinositide 3-kinase/AKT/mammalian target of rapamycin, mitogen-activated protein kinase, Wnt, Janus kinase/signal transducers and activators of transcription, epidermal growth factor receptor, Hippo, and nuclear factor kappa-light-chain-enhancer of activated B cells, etc., signaling pathways. These signals in CAFs exhibit their own special characteristics during the cancer progression and have the potential to be targeted for anticancer therapy. Therefore, a comprehensive understanding of these signaling cascades in interactions between cancer cells and CAFs is necessary to fully realize the pivotal roles of CAFs in cancers. Herein, in this review, we will summarize the enormous amounts of findings on the signals mediating crosstalk of CAFs with cancer cells and its related targets or trials. Further, we hypothesize three potential targeting strategies, including, namely, epithelial–mesenchymal common targets, sequential target perturbation, and crosstalk-directed signaling targets, paving the way for CAF-directed or host cell-directed antitumor therapy.

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Section: From Fibroblasts To Cafs In Tmementioning

confidence: 99%

Signaling pathways in cancer-associated fibroblasts and targeted therapy for cancer

Yang

Liu

et al. 2021

Sig Transduct Target Ther

Self Cite

345

249

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“…Cheng et al observed that epithelial barrier disorder and the altered biological characteristics of the adjacent stroma (fibroblasts) were conducive to C. albicans infection in OLK, which, in turn, promoted disease progression. 136 Intercellular junctions are important structures for the physiological functions of cells. 137 TJs play a main role in signaling cascades that control cell growth and differentiation.…”

Section: Interaction Between the Oral Microbiota And Epithelial Malignancymentioning

confidence: 99%

Crosstalk between the oral microbiota, mucosal immunity, and the epithelial barrier regulates oral mucosal disease pathogenesis

et al. 2021

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Oral mucosal disease (OMD), which is also called soft tissue oral disease, is described as a series of disorders or conditions affecting the mucosa and soft tissue in the oral cavity. Its etiology is unclear, but emerging evidence has implicated the influence of the composition of the oral mucosa and saliva-resident microbiota. In turn, this dysbiosis effects the immune response balance and epithelial barrier function, followed by the occurrence and progression of OMD. In addition, oral microbial dysbiosis is diverse in different types of diseases and different disease progressions, suggesting that key causal pathogens may exist in various oral pathologies. This narrative literature review primarily discusses the most recent findings focusing on how microbial dysbiosis communicates with mucosal adaptive immune cells and the epithelial barrier in the context of five representative OMDs, including oral candidiasis (OC), oral lichen planus (OLP), recurrent aphthous ulcer (RAU), oral leukoplakia (OLK), and oral squamous cell carcinoma (OSCC), to provide new insight into the pathogenetic mechanisms of OMDs.

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“…They recruit MDSCs and Tregs, inhibit the function of T cells, and secrete TGF-β [ 17 ]. In addition, the fibroblasts increase the risk of OPMDs carcinogenesis, by enhancing the chance of infection by exogenous pathogenic microorganisms [ 51 ]. Previous research of our group proved that oral leukoplakia-associated fibroblasts reduce CX3CL1 secretion by inhibiting the ERK signaling pathway, thus, resulting in reduced resistance of OLK to candida albicans [ 51 ].…”

Section: Immune Microenvironmentmentioning

confidence: 99%

Microenvironment in Oral Potentially Malignant Disorders: Multi-Dimensional Characteristics and Mechanisms of Carcinogenesis

Deng

Wang

Shi

et al. 2022

IJMS

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Oral potentially malignant disorders (OPMDs) are a group of diseases involving the oral mucosa and that have a risk of carcinogenesis. The microenvironment is closely related to carcinogenesis and cancer progression by regulating the immune response, cell metabolic activities, and mechanical characteristics. Meanwhile, there are extensive interactions between the microenvironments that remodel and provide favorable conditions for cancer initiation. However, the changes, exact roles, and interactions of microenvironments during the carcinogenesis of OPMDs have not been fully elucidated. Here, we present an updated landscape of the microenvironments in OPMDs, emphasizing the changes in the immune microenvironment, metabolic microenvironment, mechanical microenvironment, and neural microenvironment during carcinogenesis and their carcinogenic mechanisms. We then propose an immuno–metabolic–mechanical–neural interaction network to describe their close relationships. Lastly, we summarize the therapeutic strategies for targeting microenvironments, and provide an outlook on future research directions and clinical applications. This review depicts a vivid microenvironment landscape and sheds light on new strategies to prevent the carcinogenesis of OPMDs.

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Reduced CX3CL1 Secretion Contributes to the Susceptibility of Oral Leukoplakia-Associated Fibroblasts to Candida albicans

Cited by 13 publications

References 34 publications

Signaling pathways in cancer-associated fibroblasts and targeted therapy for cancer

Signaling pathways in cancer-associated fibroblasts and targeted therapy for cancer

Crosstalk between the oral microbiota, mucosal immunity, and the epithelial barrier regulates oral mucosal disease pathogenesis

Microenvironment in Oral Potentially Malignant Disorders: Multi-Dimensional Characteristics and Mechanisms of Carcinogenesis

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