Abstract A64: Brachyury-mediated epithelial-mesenchymal transition of human carcinoma cells is associated with an increased resistance to immune-mediated attack

2011 ◽  
Author(s):  
Duane H. Hamilton ◽  
Romaine Fernando ◽  
Bruce Huang ◽  
Kwong-Yok Tsang ◽  
Jeffrey Schlom ◽  
...  
Keyword(s):  
Epithelial Mesenchymal Transition ◽  
Carcinoma Cells ◽  
Human Carcinoma ◽  
Mesenchymal Transition ◽  
Immune Mediated

scholarly journals Vitamin D Effects on Cell Differentiation and Stemness in Cancer

Cancers ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 2413 ◽  
Author(s):  
Asunción Fernández-Barral ◽  
Pilar Bustamante-Madrid ◽  
Gemma Ferrer-Mayorga ◽  
Antonio Barbáchano ◽  
María Jesús Larriba ◽  
...  
Keyword(s):  
Vitamin D ◽  
Epithelial Mesenchymal Transition ◽  
Current Knowledge ◽  
Cell Types ◽  
Carcinoma Cells ◽  
Dihydroxyvitamin D3 ◽  
Human Carcinoma ◽  
Mesenchymal Transition ◽  
Major Mechanism ◽  
Egf Signaling

Vitamin D3 is the precursor of 1α,25-dihydroxyvitamin D3 (1,25(OH)2D3), a pleiotropic hormone that is a major regulator of the human genome. 1,25(OH)2D3 modulates the phenotype and physiology of many cell types by controlling the expression of hundreds of genes in a tissue- and cell-specific fashion. Vitamin D deficiency is common among cancer patients and numerous studies have reported that 1,25(OH)2D3 promotes the differentiation of a wide panel of cultured carcinoma cells, frequently associated with a reduction in cell proliferation and survival. A major mechanism of this action is inhibition of the epithelial–mesenchymal transition, which in turn is largely based on antagonism of the Wnt/β-catenin, TGF-β and EGF signaling pathways. In addition, 1,25(OH)2D3 controls the gene expression profile and phenotype of cancer-associated fibroblasts (CAFs), which are important players in the tumorigenic process. Moreover, recent data suggest a regulatory role of 1,25(OH)2D3 in the biology of normal and cancer stem cells (CSCs). Here, we revise the current knowledge of the molecular and genetic basis of the regulation by 1,25(OH)2D3 of the differentiation and stemness of human carcinoma cells, CAFs and CSCs. These effects support a homeostatic non-cytotoxic anticancer action of 1,25(OH)2D3 based on reprogramming of the phenotype of several cell types.

scholarly journals Extracellular Hsp70 Reduces the Pro-Tumor Capacity of Monocytes/Macrophages Co-Cultivated with Cancer Cells

2019 ◽  
Vol 21 (1) ◽  
pp. 59 ◽  
Author(s):  
Elena Y. Komarova ◽  
Larisa V. Marchenko ◽  
Alexander V. Zhakhov ◽  
Alina D. Nikotina ◽  
Nikolay D. Aksenov ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Carcinoma Cells ◽  
Lower Amount ◽  
Extracellular Medium ◽  
Monocytic Cells ◽  
Human Carcinoma ◽  
Mesenchymal Transition ◽  
Extracellular Milieu ◽  
Arginase 1

Cancer cells are known to contain high levels of the heat shock protein 70 kDa (Hsp70), which mediates increased cell proliferation, escape from programmed cell death, enhanced invasion, and metastasis. A part of Hsp70 molecules may release from cancer cells and affect the behavior of adjacent stromal cells. To explore the effects of Hsp70 on the status of monocytes/macrophages in the tumor locale, we incubated human carcinoma cells of three distinct lines with normal and reduced content of Hsp70 with THP1 monocytes. Using two methods, we showed that the cells with knock-down of Hsp70 released a lower amount of protein in the extracellular medium. Three cycles of the co-cultivation of cancer and monocytic cells led to the secretion of several cytokines typical of the tumor microenvironment (TME) and to pro-cancer activation of the monocytes/macrophages as established by elevation of F4/80 and arginase-1 markers. Unexpectedly, the efficacy of epithelial–mesenchymal transition and resistance of carcinoma cells to anticancer drugs after incubation with monocytic cells were more pronounced in cells with lower Hsp70, e.g., releasing less Hsp70 into the extracellular milieu. These data suggest that Hsp70 released from tumor cells into the TME is able, together with the development of an anti-cancer immune response, to limit the conversion of a considerable part of monocytic cells to the pro-tumor phenotype.

scholarly journals IL-8 Signaling Plays a Critical Role in the Epithelial–Mesenchymal Transition of Human Carcinoma Cells

2011 ◽  
Vol 71 (15) ◽  
pp. 5296-5306 ◽  
Author(s):  
Romaine I. Fernando ◽  
Marianne D. Castillo ◽  
Mary Litzinger ◽  
Duane H. Hamilton ◽  
Claudia Palena
Keyword(s):  
Epithelial Mesenchymal Transition ◽  
Critical Role ◽  
Carcinoma Cells ◽  
Human Carcinoma ◽  
Mesenchymal Transition

scholarly journals TNF-α Induces Epithelial–Mesenchymal Transition of Renal Cell Carcinoma Cells via a GSK3β-Dependent Mechanism

2012 ◽  
Vol 10 (8) ◽  
pp. 1109-1119 ◽  
Author(s):  
Ming-Yi Ho ◽  
Shye-Jye Tang ◽  
Mei-Jen Chuang ◽  
Tai-Lung Cha ◽  
Jing-Yao Li ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Epithelial Mesenchymal Transition ◽  
Carcinoma Cells ◽  
Mesenchymal Transition ◽  
Tnf Α ◽  
Dependent Mechanism

scholarly journals Long non-coding (lnc)RNA profiling and the role of a key regulator lnc-PNRC2-1 in the transforming growth factor-β1-induced epithelial–mesenchymal transition of CNE1 nasopharyngeal carcinoma cells

2021 ◽  
Vol 49 (3) ◽  
pp. 030006052199651
Author(s):  
Jie Yang ◽  
Enzi Feng ◽  
Yanxin Ren ◽  
Shun Qiu ◽  
Liufang Zhao ◽  
...  
Keyword(s):  
Growth Factor ◽  
Nasopharyngeal Carcinoma ◽  
Rna Sequencing ◽  
Western Blotting ◽  
Transforming Growth Factor ◽  
Epithelial Mesenchymal Transition ◽  
Carcinoma Cells ◽  
Mesenchymal Transition ◽  
Emt Markers ◽  
Tgf Β1

Objectives To identify key long non-coding (lnc)RNAs responsible for the epithelial–mesenchymal transition (EMT) of CNE1 nasopharyngeal carcinoma cells and to investigate possible regulatory mechanisms in EMT. Methods CNE1 cells were divided into transforming growth factor (TGF)-β1-induced EMT and control groups. The mRNA and protein expression of EMT markers was determined by real-time quantitative PCR and western blotting. Differentially expressed genes (DEGs) between the two groups were identified by RNA sequencing analysis, and DEG functions were analyzed by gene ontology and Kyoto Encyclopedia of Genes and Genomes analyses. EMT marker expression was re-evaluated by western blotting after knockdown of a selected lncRNA. Results TGF-β1-induced EMT was characterized by decreased E-cadherin and increased vimentin, N-cadherin, and Twist expression at both mRNA and protein levels. Sixty lncRNA genes were clustered in a heatmap, and mRNA expression of 14 dysregulated lncRNAs was consistent with RNA sequencing. Knockdown of lnc-PNRC2-1 increased expression of its antisense gene MYOM3 and reduced expression of EMT markers, resembling treatment with the TGF-β1 receptor inhibitor LY2109761. Conclusion Various lncRNAs participated indirectly in the TGF-β1-induced EMT of CNE1 cells. Lnc-PNRC2-1 may be a key regulator of this and is a potential target to alleviate CNE1 cell EMT.

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