Investigations on the clinical significance of FOXP3 protein expression in cervical oesophageal cancer and the number of FOXP3+ tumour-infiltrating lymphocytes

Xia, Ming; Zhao, Mingqiu; Wu, Kai; Lin, Xinhua; Li, Ying; Qin, Yejun

doi:10.1177/0300060513488504

Cited by 17 publications

(12 citation statements)

References 22 publications

(23 reference statements)

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“…Other investigators found Foxp3 expressed by human melanoma cells from fresh tissue and suggested that malignant transformation of healthy cells could induce Foxp3 expression [55]. More recently, Foxp3 protein expression was detected by immunohistochemistry and Western Blot in human parenchymal cells from cervical oesophageal cancer [56], gastric tumor cells [57] [58] and invasive ductal breast carcinoma [59]. Furthermore, expression of Foxp3 mRNA has been observed in several human cancer cell lines [60] and recently in the mouse B16F10 melanoma cell line [61].…”

Section: ) Foxp3 In Normal and Malignant Epithelial Cellsmentioning

confidence: 96%

Foxp3 expression in T regulatory cells and other cell lineages

Devaud

Darcy

Kershaw

2014

Cancer Immunol Immunother

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Forkhead box P3 (Foxp3) is an important transcription factor that belongs to the forkhead/winged-helix family of transcriptional regulators. Foxp3 has been extensively studied over the past 13 years as a master regulator of transcription in a specific T-cell type, CD4(+) regulatory T cells (Treg), both in humans and in mice. Compelling data characterize Foxp3 as critically important and necessary for the development and the differentiation of Treg. It has been considered initially as the only specific marker for Treg. However, recent work has proposed that Foxp3 can be expressed by other types of lymphoid cells or myeloid cells and also by some non-hematopoietic cells such as epithelial cells. It remains controversial about the expression of Foxp3 in cells other than Treg, but understanding the potential expression and function of this master regulator in different cell subsets could have a wide range of implications for immune tolerance and several pathologies including autoimmune disorders and immune responses to cancer.

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Section: ) Foxp3 In Normal and Malignant Epithelial Cellsmentioning

confidence: 96%

Foxp3 expression in T regulatory cells and other cell lineages

Devaud

Darcy

Kershaw

2014

Cancer Immunol Immunother

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“…Increased recruitment of Tregs in esophageal cancer, particularly ESCC, is at least partially mediated by the chemokines CCL17 and CCL22, which are secreted by tumor cells and macrophages to recruit Tregs via the CCR4 receptor 114 . Furthermore, Treg infiltration was found to have prognostic significance, with higher amounts of Tregs associated with deeper tumor invasion 115 , metastasis 116 , overall disease severity 117 , and decreased survival post-chemotherapy 118 . In addition, a recent report on esophageal cancer patients receiving neoadjuvant chemoradiation showed that the density of Tregs in the residual tumor (post-treatment) was correlated not only with pathological response but also with cancer-specific survival 119 .…”

Section: Immune Modulation Promotes Tumor Evasion and Survivalmentioning

confidence: 99%

The tumor microenvironment in esophageal cancer

et al. 2016

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Esophageal cancer is a deadly disease, ranking sixth among all cancers in mortality. Despite incremental advances in diagnostics and therapeutics, esophageal cancer still carries a poor prognosis, and thus there remains a need to elucidate the molecular mechanisms underlying this disease. There is accumulating evidence that a comprehensive understanding of the molecular composition of esophageal cancer requires attention to not only tumor cells but also the tumor microenvironment, which contains diverse cell populations, signaling factors, and structural molecules that interact with tumor cells and support all stages of tumorigenesis. In esophageal cancer, environmental exposures can trigger chronic inflammation, which leads to constitutive activation of pro-inflammatory signaling pathways that promote survival and proliferation. Anti-tumor immunity is attenuated by cell populations such as myeloid-derived suppressor cells (MDSCs) and regulatory T cells (Tregs), as well as immune checkpoints like programmed death-1 (PD-1). Other immune cells such as tumor-associated macrophages can have other pro-tumorigenic functions, including the induction of angiogenesis and tumor cell invasion. Cancer-associated fibroblasts secrete growth factors and alter the extracellular matrix (ECM) to create a tumor niche and enhance tumor cell migration and metastasis. Further study of how these TME components relate to the different stages of tumor progression in each esophageal cancer subtype will lead to development of novel and specific TME-targeting therapeutic strategies, which offer considerable potential especially in the setting of combination therapy.

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“…T regs are often found at high frequencies in the peripheral blood and tumors of human patients compared with those in healthy donors and normal mucosa or tissue [93], and in many cancers, a high density of T regs correlates with poor disease outcomes [94]. In adoptive cellular immunotherapy in cancer, the functions of immune cells are always inhibited.…”

Section: Clinical Implications In Cancer Therapymentioning

confidence: 99%

IL-17+Foxp3+ T cells: an intermediate differentiation stage between Th17 cells and regulatory T cells

Zhao

Fan

et al. 2014

Journal of Leukocyte Biology

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Foxp3(+) Tregs have been known as a major regulator of immune homeostasis through their immunosuppressive function. Th17 lineage is a CD4(+) T cell subset that exerts its function by secreting proinflammatory cytokines and protecting host against microbial infections. The altered ratio between Foxp3(+) Tregs and Th17 cells plays an important role in the pathogenesis of immune-related diseases. Recent mice and human studies have demonstrated that Tregs can be reprogrammed into a novel population, IL-17(+)Foxp3(+) T cells, phenotypically and functionally resembling Th17 cells under the complicated cytokine stimulation. The identification of IL-17(+)Foxp3(+) T cells may provide a new understanding of therapy targeting Tregs and Th17 cells in autoimmune diseases and cancer. Here, we highlight significant data regarding the phenotype profile, origination, differentiation, and the pleiotropic functions of IL-17(+)Foxp3(+) T cells and the reciprocal relationships of these cells to Tregs and Th17 cells. Furthermore, the role of IL-17(+)Foxp3(+) T cells in tumorigenesis and clinical implications in cancer therapy are discussed in this review.

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Investigations on the clinical significance of FOXP3 protein expression in cervical oesophageal cancer and the number of FOXP3+ tumour-infiltrating lymphocytes

Cited by 17 publications

References 22 publications

Foxp3 expression in T regulatory cells and other cell lineages

Foxp3 expression in T regulatory cells and other cell lineages

The tumor microenvironment in esophageal cancer

IL-17+Foxp3+ T cells: an intermediate differentiation stage between Th17 cells and regulatory T cells

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