scholarly journals Naringenin Regulates FKBP4/NR3C1/NRF2 Axis in Autophagy and Proliferation of Breast Cancer and Differentiation and Maturation of Dendritic Cell

2022 ◽  
Vol 12 ◽  
Author(s):  
Hanchu Xiong ◽  
Zihan Chen ◽  
Baihua Lin ◽  
Bojian Xie ◽  
Xiaozhen Liu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Dendritic Cell ◽  
Signaling Pathway ◽  
Nuclear Translocation ◽  
Mrna Level ◽  
Negative Regulator ◽  
Human Breast ◽  
Nrf2 Signaling Pathway

NRF2 is an important regulatory transcription factor involved in tumor immunity and tumorigenesis. In this study, we firstly identified that FKBP4/NR3C1 axis was a novel negative regulator of NRF2 in human breast cancer (BC) cells. The effect of FKBP4 appeared to be at protein level of NRF2 since it could not suppress the expression of NRF2 at mRNA level. Bioinformatics analysis and in vitro experiments further demonstrated that FKBP4 regulated NRF2 via regulating nuclear translocation of NR3C1. We then reported that naringenin, a flavonoid, widely distributed in citrus and tomato, could suppress autophagy and proliferation of BC cells through FKBP4/NR3C1/NRF2 signaling pathway in vitro and in vivo. Naringenin was also found to promote dendritic cell (DC) differentiation and maturation through FKBP4/NR3C1/NRF2 axis. Therefore, our study found that naringenin could induce inhibition of autophagy and cell proliferation in BC cells and enhance DC differentiation and maturation, at least in part, though regulation of FKBP4/NR3C1/NRF2 signaling pathway. Identification of FKBP4/NR3C1/NRF2 axis would provide insights for novel anti-tumor strategy against BC among tumor microenvironment.

scholarly journals Naringenin Regulates FKBP4/NR3C1/TMEM173 Signaling Pathway in Autophagy and Proliferation of Breast Cancer and Tumor-Infiltrating Dendritic Cell Maturation

2021 ◽  
Author(s):  
Hanchu Xiong ◽  
Zihan Chen ◽  
Baihua Lin ◽  
Cong Chen ◽  
Zhaoqing Li ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Dendritic Cell ◽  
Signaling Pathway ◽  
Nuclear Translocation ◽  
Negative Regulator ◽  
Luciferase Reporter ◽  
Transcriptional Level ◽  
Isolation And Identification ◽  
Cell Proliferation Inhibition

Abstract Background TMEM173 is a pattern recognition receptor detecting cytoplasmic nucleic acids and transmits cGAS related signals that activate host innate immune responses. It has also been found to be involved in tumor immunity and tumorigenesis. Methods Bc-GenExMiner, PROMO and STRING database were used for analyzing clinical features and interplays of FKBP4, TMEM173 and NR3C1. Transient transfection, western blotting, quantitative real-time PCR, luciferase reporter assay, immunofluorescence and nuclear and cytoplasmic fractionation were used for regulation of FKBP4, TMEM173 and NR3C1. Both knockdown and overexpression of FKBP4, TMEM173 and NR3C1 were used to analyze effects on autophagy and proliferation of breast cancer (BC) cells. Flow cytometry analysis, cytokine analysis and exosome isolation and identification were utilized to test tumor-infiltrating dendritic cell (TIDC) maturation. Results In this study, we firstly identified that FKBP4/NR3C1 axis was a novel negative regulator of TMEM173 in BC cells. The effect of FKBP4 appeared to be at the transcriptional level of TMEM173 since it could suppress the promoter activity of TMEM173, thereby affecting TMEM173 at mRNA and protein levels. Bioinformatics and in vitro experiments further demonstrated that FKBP4 regulated TMEM173 via regulating nuclear translocation of NR3C1. We then reported that naringenin, a flavonoid, could enhance autophagy and suppress proliferation of BC cells through the induction of TMEM173 in vitro and in vivo. Naringenin was also found to promote TIDC maturation through FKBP4/NR3C1/TMEM173 axis of both BC cells exosome and DC itself. Conclusion We demonstrated that naringenin could induce cell proliferation inhibition and cytoprotective autophagy of BC cells and enhance TIDC maturation, at least in part, though regulation of FKBP4/NR3C1/TMEM173 signaling pathway. Identification of FKBP4/NR3C1 axis as a novel TMEM173 regulator would provide insights for novel anti-tumor strategy against BC among tumor microenvironment.

Clomiphene Analogs with Activity In Vitro and In Vivo against Human Breast Cancer Cells

1998 ◽  
Vol 55 (6) ◽  
pp. 841-851 ◽  
Author(s):  
R.Jeffrey Baumann ◽  
Tammy L. Bush ◽  
Doreen E. Cross-Doersen ◽  
Elizabeth A. Cashman ◽  
Paul S. Wright ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Human Breast Cancer Cells ◽  
Human Breast

scholarly journals Mead acid inhibits the growth of KPL-1 human breast cancer cells in vitro and in vivo

2014 ◽  
Vol 32 (4) ◽  
pp. 1385-1394 ◽  
Author(s):  
YUICHI KINOSHITA ◽  
KATSUHIKO YOSHIZAWA ◽  
KEI HAMAZAKI ◽  
YUKO EMOTO ◽  
TAKASHI YURI ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Mead Acid

Ginsenoside Rg1 protects against acetaminophen-induced liver injury via activating Nrf2 signaling pathway in vivo and in vitro

2018 ◽  
Vol 98 ◽  
pp. 58-68 ◽  
Author(s):  
Chenqing Ning ◽  
Xiaoguang Gao ◽  
Changyuan Wang ◽  
Yulong Kong ◽  
Zhihao Liu ◽  
...  
Keyword(s):  
Liver Injury ◽  
Signaling Pathway ◽  
Ginsenoside Rg1 ◽  
Nrf2 Signaling Pathway

scholarly journals LncRNA GHET1 Promotes Hypoxia-Induced Glycolysis, Proliferation, and Invasion in Triple-Negative Breast Cancer Through the Hippo/YAP Signaling Pathway

2021 ◽  
Vol 9 ◽  
Author(s):  
Yu Wang ◽  
Shuwei Liu
Keyword(s):  
Breast Cancer ◽  
Signaling Pathway ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Nuclear Translocation ◽  
Lactate Production ◽  
Glucose Consumption ◽  
Breast Epithelial Cell ◽  
Epithelial Cell Line

ObjectiveThis study was to assess the specific impacts and mechanism of lncRNA GHET1 in the development of triple-negative breast cancer (TNBC).MethodsThe lncRNA GHET1 expression in TNBC tissues and adjacent healthy tissues was detected by qRT-PCR, and its expression was then measured at the cellular level, including TNBC cells and human normal breast epithelial cell line MCF10A. On the completion of transfection of negative shRNA or lncRNA GHET1 shRNA, the TNBC cells, HCC1937 and MDA-MB-468, were then cultured in a normoxia or hypoxia environment, respectively. 5-Ethynyl-2′-deoxyuridine (EdU) assay, colony formation assay, and transwell assay were applicable to the determination of cell proliferation, cell viability, and invasion in each group, respectively. Reagent kits were used for testing glucose consumption and lactate production levels. HCC1937 cells with knockdown or overexpression of lncRNA GHET1 were injected into the nude mice, followed by the examination of resulting tumor volume and weight. The distribution and expression of Hippo/YAP signaling pathway-related proteins were probed using western blotting.ResultsHighly expressed lncRNA GHET1 in TNBC tissues and cells and induction of lncRNA GHET1 by hypoxia were proved. Knockdown of lncRNA GHET1 significantly reduced proliferation, viability, and invasion of TNBC cells, and decreased glucose consumption and lactate production levels under the hypoxia condition. Furthermore, lncRNA GHET1 knockdown decreased HIF-1α expression in hypoxia and significantly inhibited tumor development in vivo. Knockdown of lncRNA GHET1 increased the phosphorylation levels of LATS1 and Yes-associated protein (YAP) to retain YAP within the cytoplasm, while the overexpression of lncRNA GHET1 or hypoxia promoted nuclear translocation of YAP and TNBC development.ConclusionLncRNA GHET1 expression can be induced by hypoxia, which leads to excessive activation of the Hippo/YAP signaling pathway, thus promoting TNBC progression.

scholarly journals α-Tocopherol succinate enhances pterostilbene anti-tumor activity in human breast cancer cells in vivo and in vitro

Oncotarget ◽  
2017 ◽  
Vol 9 (4) ◽  
pp. 4593-4606 ◽  
Author(s):  
Ka-Wai Tam ◽  
Chi-Tang Ho ◽  
Shih-Hsin Tu ◽  
Wen-Jui Lee ◽  
Ching-Shui Huang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Anti Tumor Activity
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