A positive feedback loop between Wnt/β‐catenin signaling and hTERT regulates the cancer stem cell‐like traits in radioresistant nasopharyngeal carcinoma cells

2020 ◽  
Vol 121 (11) ◽  
pp. 4612-4622 ◽  
Author(s):  
Kaihua Chen ◽  
Li Chen ◽  
Ling Li ◽  
Song Qu ◽  
Binbin Yu ◽  
...  
Keyword(s):  
Stem Cell ◽  
Nasopharyngeal Carcinoma ◽  
Cancer Stem Cell ◽  
Positive Feedback ◽  
Feedback Loop ◽  
Carcinoma Cells ◽  
Positive Feedback Loop

scholarly journals A Positive Feedback Loop Between c-Myc Upregulation, Glycolytic Shift, and Histone Acetylation Enhances Cancer Stem Cell-like Property and Tumorigenicity of Cr(VI)-transformed Cells

2020 ◽  
Vol 177 (1) ◽  
pp. 71-83
Author(s):  
Marco Clementino ◽  
Jie Xie ◽  
Ping Yang ◽  
Yunfei Li ◽  
Hsuan-Pei Lin ◽  
...  
Keyword(s):  
Stem Cell ◽  
Cancer Stem Cell ◽  
Histone Acetylation ◽  
Positive Feedback ◽  
Feedback Loop ◽  
Cell Transformation ◽  
Transformed Cells ◽  
Atp Citrate Lyase ◽  
Acetyl Coa ◽  
Positive Feedback Loop

Abstract Chronic hexavalent chromium [Cr(VI)] exposure causes lung cancer and other types of cancer; however, the mechanism of Cr(VI) carcinogenesis remains to be clearly defined. Our recent study showed that chronic Cr(VI) exposure upregulates the proto oncogene c-Myc expression, which contributes significantly to Cr(VI)-induced cell transformation, cancer stem cell (CSC)-like property and tumorigenesis. c-Myc is a master regulator of cancer cell abnormal metabolism and accumulating evidence suggests that metabolism dysregulation plays an important role in both cancer development and progression. However, little is known about the role of metabolism dysregulation in Cr(VI) carcinogenesis. This study was performed to investigate the potential role and mechanism of metabolism dysregulation in Cr(VI) carcinogenesis. It was found that Cr(VI)-transformed cells display glycolytic shift, which depends on the upregulation of c-Myc. The glycolytic shift in Cr(VI)-transformed cells led to increased production of acetyl coenzyme A (acetyl-CoA) and elevation of histone acetylation. This, in turn, upregulated the expression of an acetyl-CoA producing key enzyme ATP citrate lyase and c-Myc, forming a positive feedback loop between the upregulation of c-Myc expression, glycolytic shift and increased histone acetylation. It was further determined that glucose depletion not only reverses the glycolytic shift in Cr(VI)-transformed cells, but also significantly reduces their growth, CSC-like property and tumorigenicity. These findings indicate that glycolytic shift plays an important role in maintaining malignant phenotypes of Cr(VI)-transformed cells, suggesting that metabolism dysregulation is critically involved in Cr(VI) carcinogenesis.

The positive feedback loop of RNASEH1-AS1/has-miR-218-5p/NET1 mediated by POU2F1 contributes to the development and progression of human lung squamous carcinoma

2020 ◽  
Author(s):  
Jing-hao Jia ◽  
Jing Wang ◽  
Jia-rui Yu ◽  
Peng Gao ◽  
Yan-kun Liu ◽  
...  
Keyword(s):  
Positive Feedback ◽  
Feedback Loop ◽  
Human Lung ◽  
Squamous Carcinoma ◽  
Carcinoma Cells ◽  
Human Lung Cancer ◽  
Migration And Invasion ◽  
Positive Feedback Loop ◽  
Squamous Carcinoma Cells ◽  
Lung Squamous Carcinoma

Abstract Background In molecular level, competing endogenous RNAs (ceRNAs) regulates other RNA transcripts through competing for shared microRNAs (miRNA). miRNA negatively regulate gene expression at the levels of mRNAs stability and translation suppression. Methods We tested the mRNA level of miR-218-5p and RNASEH1-AS1 in clinical lung squamous cell carcinoma tissues by qRT-PCR. In the exploring of the role of miR-218-5p and RNASEH1-AS1 in the malignant phenotype of NCI-H520 cells, colony formation and MTT assay were used to test the cell viability and proliferation capability, trans-well invasion and wound healing assay were performed to examine the cell migration and invasion. ChIP assay was conducted to confirm the direct interact of POU2F1 and RNASEH1-AS1 promoter. Results In this investigation, we found that LncRNA RNASEH1-AS1 is up-regulated in human lung cancer, and serves as a miRNA sponge for hsa-miR-218-5p in human lung squamous carcinoma cells. lncRNA RNASEH1-AS1 facilitates growth and motility of lung squamous carcinoma cells, while miR-218-5p does the opposite. NET1 and POU2F1 are validated as direct and functional targets of miR-218-5p. The downregulation of miR-218-5p releases the suppression of NET1 and POU2F1. POU2F1 binds directly to the lncRNA-RNASEH1-AS1 promoter and acts as transcription factor to enhance the promoter activity of RNASEH1-AS1. Conclusion Above all, the positive feedback loop of RNASEH1-AS1/ hsa-miR-218-5p/ NET1/ POU2F1 can help us to understand the regulatory mechanism behind genesis and progression of human lung squamous carcinoma, possibly providing new biomarkers for its diagnosis and treatment.

APOBEC3B and IL-6 form a positive feedback loop in hepatocellular carcinoma cells

2017 ◽  
Vol 60 (6) ◽  
pp. 617-626 ◽  
Author(s):  
Shuran Li ◽  
Xueyang Bao ◽  
Duowei Wang ◽  
Linjun You ◽  
Xianjing Li ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Positive Feedback ◽  
Feedback Loop ◽  
Carcinoma Cells ◽  
Positive Feedback Loop ◽  
Hepatocellular Carcinoma Cells

scholarly journals CD44 and CD24 coordinate the reprogramming of nasopharyngeal carcinoma cells towards a cancer stem cell phenotype through STAT3 activation

Oncotarget ◽  
2016 ◽  
Vol 7 (36) ◽  
pp. 58351-58366 ◽  
Author(s):  
Yao-An Shen ◽  
Chia-Yu Wang ◽  
Hui-Yen Chuang ◽  
John Jeng-Jong Hwang ◽  
Wei-Hsin Chi ◽  
...  
Keyword(s):  
Stem Cell ◽  
Nasopharyngeal Carcinoma ◽  
Cancer Stem Cell ◽  
Carcinoma Cells ◽  
Cell Phenotype ◽  
Cancer Stem Cell Phenotype ◽  
Stem Cell Phenotype
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