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Article ; Online: POU6F1 promotes ferroptosis by increasing lncRNA-CASC2 transcription to regulate SOCS2/SLC7A11 signaling in gastric cancer.

Wang, Jingyun / Jia, Qiaoyu / Jiang, Shuqin / Lu, Wenquan / Ning, Hanbing

2024 Volume 40, Issue 1, Page(s) 3

Abstract: Objective: This study investigated the effect and mechanism of POU6F1 and lncRNA-CASC2 on ferroptosis of gastric cancer (GC) cells.: Methods: GC cells treated with erastin and RSL3 were detected for ferroptosis, reactive oxygen species (ROS) level, ... ...

Abstract	Objective: This study investigated the effect and mechanism of POU6F1 and lncRNA-CASC2 on ferroptosis of gastric cancer (GC) cells. Methods: GC cells treated with erastin and RSL3 were detected for ferroptosis, reactive oxygen species (ROS) level, and cell viability. The expression levels of POU6F1, lncRNA-CASC2, SOCS2, and ferroptosis-related molecules (GPX4 and SLC7A11) were also measured. The regulations among POU6F1, lncRNA-CASC2, FMR1, SOCS2, and SLC7A11 were determined. Subcutaneous tumor models were established, in which the expressions of Ki-67, SOCS2, and GPX4 were detected by immunohistochemistry. Results: GC patients with decreased expressions of POU6F1 and lncRNA-CASC2 had lower survival rate. Overexpression of POU6F1 or lncRNA-CASC2 decreased cell proliferation and GSH levels in GC cells, in addition to increasing total iron, Fe2+, MDA, and ROS levels. POU6F1 directly binds to the lncRNA-CASC2 promoter to promote its transcription. LncRNA-CASC2 can target FMR1 and increase SOCS2 mRNA stability to promote SLC7A11 ubiquitination degradation and activate ferroptosis signaling. Knockdown of SOCS2 inhibited the ferroptosis sensitivity of GC cells and reversed the effects of POU6F1 and lncRNA-CASC2 overexpression on ferroptosis in GC cells. Conclusion: Transcription factor POU6F1 binds directly to the lncRNA-CASC2 promoter to promote its expression, while upregulated lncRNA-CASC2 increases SOCS2 stability and expression by targeting FMR1, thereby inhibiting SLC7A11 signaling to promote ferroptosis in GC cells and inhibit GC progression.
MeSH term(s)	Humans ; Amino Acid Transport System y+/genetics ; Ferroptosis ; Fragile X Mental Retardation Protein ; POU Domain Factors ; Reactive Oxygen Species ; RNA, Long Noncoding/genetics ; Signal Transduction ; Stomach Neoplasms/genetics ; Suppressor of Cytokine Signaling Proteins
Chemical Substances	Amino Acid Transport System y+ ; FMR1 protein, human ; Fragile X Mental Retardation Protein (139135-51-6) ; POU Domain Factors ; POU6F1 protein, human ; Reactive Oxygen Species ; RNA, Long Noncoding ; SLC7A11 protein, human ; SOCS2 protein, human ; Suppressor of Cytokine Signaling Proteins ; long non-coding RNA CASC2, human
Language	English
Publishing date	2024-01-25
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	48824-0
ISSN	1573-6822 ; 0742-2091
ISSN (online)	1573-6822
ISSN	0742-2091
DOI	10.1007/s10565-024-09843-y
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Article ; Online: MicroRNA-340-5p increases telomere length by targeting telomere protein POT1 to improve Alzheimer's disease in mice.

Li, Xin / Zhang, Jiangkuan / Yang, Yuhang / Wu, Qi / Ning, Hanbing

Cell biology international

2021 Volume 45, Issue 6, Page(s) 1306–1315

Abstract: Alzheimer's disease (AD) is a chronic neurodegenerative disorder which is the primary cause of dementia in the elderly. Telomere attrition has been proposed as a hallmark of aging. Our study aimed to explore the mechanism of the protection of telomere 1 ( ...

Abstract	Alzheimer's disease (AD) is a chronic neurodegenerative disorder which is the primary cause of dementia in the elderly. Telomere attrition has been proposed as a hallmark of aging. Our study aimed to explore the mechanism of the protection of telomere 1 (POT1) in regulating telomere length and affecting cellular senescence in AD. The AD mouse model was established by d-galactose and aluminum chloride, and the water maze test and dark avoidance test were used to detect the behaviors of mice and confirm the success of AD mouse model. AD cell model was established with HT22 cells induced by Aβ
MeSH term(s)	Alzheimer Disease/metabolism ; Animals ; Cellular Senescence ; Female ; HEK293 Cells ; HT29 Cells ; Humans ; Male ; Mice ; MicroRNAs/physiology ; Telomere/metabolism ; Telomere-Binding Proteins/metabolism ; Telomere-Binding Proteins/physiology
Chemical Substances	MIRN340 microRNA, human ; MicroRNAs ; POT1 protein, human ; POT1 protein, mouse ; Telomere-Binding Proteins
Language	English
Publishing date	2021-03-19
Publishing country	England
Document type	Journal Article
ZDB-ID	1143453-3
ISSN	1095-8355 ; 1065-6995
ISSN (online)	1095-8355
ISSN	1065-6995
DOI	10.1002/cbin.11576
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Article: Pneumocystis Jirovecii

Lu, Xiaoxiao / Zhang, Jianhui / Ma, Wentao / Xing, Lihua / Ning, Hanbing / Yao, Mengying

Frontiers in medicine

2022 Volume 9, Page(s) 812005

Abstract: The incidence of non-HIV-infected Pneumocystis Jirovecii Pneumonia (PJP) is increasing. The prognosis for non-HIV PJP is poor and diagnostic tests are of lower sensitivity in non-HIV patients. Metagenomic next-generation sequencing (mNGS) was compared ... ...

Abstract	The incidence of non-HIV-infected Pneumocystis Jirovecii Pneumonia (PJP) is increasing. The prognosis for non-HIV PJP is poor and diagnostic tests are of lower sensitivity in non-HIV patients. Metagenomic next-generation sequencing (mNGS) was compared with routine detection assays, including Gomori methenamine silver (GMS) stain and polymerase chain reaction (PCR) technique. Specimens of 4 bronchoalveolar lavages (BAL) and 1 lung tissue samples were obtained from 4 non-HIV patients from our hospitals. Although both GMS and mNGS were positive for
Language	English
Publishing date	2022-03-09
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2775999-4
ISSN	2296-858X
ISSN	2296-858X
DOI	10.3389/fmed.2022.812005
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Article ; Online: CircRNA GFRA1 promotes hepatocellular carcinoma progression by modulating the miR-498/NAP1L3 axis.

Lv, Shuai / Li, Yingxia / Ning, Hanbing / Zhang, Meihui / Jia, Qiaoyu / Wang, Xijuan

Scientific reports

2021 Volume 11, Issue 1, Page(s) 386

Abstract: Circular RNAs (circRNAs) play essential roles in tumorigenesis and tumor progression. CircRNA GFRA1 (circGFRA1) was dysregulated in many cancer samples and acted as an independent marker for prediction of survivals in various cancer patients. However, ... ...

Abstract	Circular RNAs (circRNAs) play essential roles in tumorigenesis and tumor progression. CircRNA GFRA1 (circGFRA1) was dysregulated in many cancer samples and acted as an independent marker for prediction of survivals in various cancer patients. However, the functions and molecular mechanisms of circGFRA1 in hepatocellular carcinoma (HCC) remain unclear. We collected 62 HCC tissues and normal adjacent tissues to evaluate the expression of circGFRA1 and the relationship between circGFRA1 expression and HCC patients' survival. We carried out a list of characterization experiments to investigate the roles and underling mechanisms of circGFRA1 and miR-498 in HCC progressions. CircGFRA1 was greatly increased in HCC tissues and cells, and the over-expression of circGFRA1 was intimately related with the advanced clinical stage and poor survival of HCC patients. The expression of circGFRA1 was negatively correlated with the expression of miR-498, but a positive correlation was found between circGFRA1 and NAP1L3 expression in HCC tissues. Silencing circGFRA1 inhibited the growth and invasion of hepatocellular carcinoma. Moreover, miR-498 over-expression or NAP1L3 inhibition could abrogate the oncogene role of circGFRA1 in HCC in vivo. Our findings indicated that circGFRA1 contributed to HCC progression by modulating the miR-498/NAP1L3 axis in HCC.
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Animals ; Carcinoma, Hepatocellular/genetics ; Carcinoma, Hepatocellular/pathology ; Cell Proliferation/genetics ; Cells, Cultured ; Cohort Studies ; Disease Progression ; Female ; Glial Cell Line-Derived Neurotrophic Factor Receptors/genetics ; Hep G2 Cells ; Humans ; Liver Neoplasms/genetics ; Liver Neoplasms/pathology ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; MicroRNAs/genetics ; Middle Aged ; Nerve Tissue Proteins/genetics ; RNA, Circular/physiology ; Signal Transduction/genetics
Chemical Substances	GFRA1 protein, human ; Glial Cell Line-Derived Neurotrophic Factor Receptors ; MIRN498 microRNA, human ; MicroRNAs ; NAP1L3 protein, human ; Nerve Tissue Proteins ; RNA, Circular
Language	English
Publishing date	2021-01-11
Publishing country	England
Document type	Journal Article
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-020-79321-y
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Article: Inhibition of cyclinB1 Suppressed the Proliferation, Invasion, and Epithelial Mesenchymal Transition of Hepatocellular Carcinoma Cells and Enhanced the Sensitivity to TRAIL-Induced Apoptosis.

Lv, Shuai / Ning, Hanbing / Li, Yingxia / Wang, Jingyun / Jia, Qiaoyu / Wen, Hongtao

OncoTargets and therapy

2020 Volume 13, Page(s) 1119–1128

Abstract: Background: CyclinB1 is highly expressed in various tumor tissues and plays an important role in tumor progression. However, its role in hepatocellular carcinoma (HCC) remains unclear. Therefore, the aim of this study was to explore the role of cyclinB1 ...

Abstract	Background: CyclinB1 is highly expressed in various tumor tissues and plays an important role in tumor progression. However, its role in hepatocellular carcinoma (HCC) remains unclear. Therefore, the aim of this study was to explore the role of cyclinB1 in the development and progression of HCC. Methods: The expression of cyclinB1 was analyzed using the Gene Expression Profiling Interactive Analysis (GEPIA) database, and detected in HCC tissues and HCC cell lines through quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blotting. CyclinB1-short hairpin RNA (Sh-cyclinB1) was transfected into HCC cells to knockdown cyclinB1, and the effect of cyclinB1 knockdown on HCC was examined via the MTT assay, colony formation assay, wound healing assay, scratch assay, cell cycle analysis in vitro, and xenograft model in nude mice. In addition, the role of cyclinB1 on tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis was measured using flow cytometry and Western blotting. Results: The GEPIA database analysis showed that cyclinB1 was highly expressed in HCC tissues. The results of qRT-PCR and Western blotting proved that the expression of cyclinB1 was significantly increased in HCC tissues and cell lines. The data of the MTT assay, colony formation assay, and cell cycle analysis indicated that cyclinB1 knockdown inhibited the proliferation of HCC cells. In addition, cell migration, invasion, and epithelial mesenchymal transition were also impaired by cyclinB1 knockdown. Furthermore, the xenograft model in nude mice demonstrated that inhibition of cyclinB1 suppressed tumor growth and metastasis in vivo. Finally, the results of flow cytometry and Western blotting indicated that inhibition of cyclinB1 enhanced the sensitivity of HCC cells to TRAIL-induced apoptosis. Conclusion: Overall, these data provide reasonable evidence that cyclinB1 may serve as a proto-oncogene during the progression of HCC.
Language	English
Publishing date	2020-02-05
Publishing country	New Zealand
Document type	Journal Article
ZDB-ID	2495130-4
ISSN	1178-6930
ISSN	1178-6930
DOI	10.2147/OTT.S225202
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Article ; Online: Naked mole-rat very-high-molecular-mass hyaluronan exhibits superior cytoprotective properties.

Takasugi, Masaki / Firsanov, Denis / Tombline, Gregory / Ning, Hanbing / Ablaeva, Julia / Seluanov, Andrei / Gorbunova, Vera

Nature communications

2020 Volume 11, Issue 1, Page(s) 2376

Abstract: Naked mole-rat (NMR), the longest-living rodent, produces very-high-molecular-mass hyaluronan (vHMM-HA), compared to other mammalian species. However, it is unclear if exceptional polymer length of vHMM-HA is important for longevity. Here, we show that ... ...

Abstract	Naked mole-rat (NMR), the longest-living rodent, produces very-high-molecular-mass hyaluronan (vHMM-HA), compared to other mammalian species. However, it is unclear if exceptional polymer length of vHMM-HA is important for longevity. Here, we show that vHMM-HA (>6.1 MDa) has superior cytoprotective properties compared to the shorter HMM-HA. It protects not only NMR cells, but also mouse and human cells from stress-induced cell-cycle arrest and cell death in a polymer length-dependent manner. The cytoprotective effect is dependent on the major HA-receptor, CD44. We find that vHMM-HA suppresses CD44 protein-protein interactions, whereas HMM-HA promotes them. As a result, vHMM-HA and HMM-HA induce opposing effects on the expression of CD44-dependent genes, which are associated with the p53 pathway. Concomitantly, vHMM-HA partially attenuates p53 and protects cells from stress in a p53-dependent manner. Our results implicate vHMM-HA in anti-aging mechanisms and suggest the potential applications of vHMM-HA for enhancing cellular stress resistance.
MeSH term(s)	Animals ; Apoptosis/drug effects ; Apoptosis/physiology ; Cell Cycle Checkpoints/drug effects ; Cell Cycle Checkpoints/physiology ; Cell Line ; Cytoprotection/drug effects ; Cytoprotection/physiology ; Gene Expression Regulation/drug effects ; Gene Expression Regulation/physiology ; Gene Knockout Techniques ; Humans ; Hyaluronan Receptors/metabolism ; Hyaluronic Acid/chemistry ; Hyaluronic Acid/isolation & purification ; Hyaluronic Acid/metabolism ; Hyaluronic Acid/pharmacology ; Longevity/physiology ; Mice ; Mole Rats/physiology ; Molecular Weight ; Primary Cell Culture ; Protein Interaction Maps/drug effects ; RNA-Seq ; Signal Transduction/drug effects ; Signal Transduction/physiology ; Species Specificity ; Stress, Physiological ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	Hyaluronan Receptors ; Tumor Suppressor Protein p53 ; Hyaluronic Acid (9004-61-9)
Language	English
Publishing date	2020-05-12
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-020-16050-w
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Article ; Online: Functional delivery of lncRNA TUG1 by endothelial progenitor cells derived extracellular vesicles confers anti-inflammatory macrophage polarization in sepsis via impairing miR-9-5p-targeted SIRT1 inhibition.

Ma, Wentao / Zhang, Weihong / Cui, Bing / Gao, Jing / Liu, Qiuhong / Yao, Mengying / Ning, Hanbing / Xing, Lihua

Cell death & disease

2021 Volume 12, Issue 11, Page(s) 1056

Abstract: The delivery of biomolecules by extracellular vesicles (EVs) derived from endothelial progenitor cells (EPCs) has been proven to ameliorate sepsis, yet the therapeutic mechanism remains to be elucidated. Taurine upregulated gene 1 (TUG1) is a long ... ...

Abstract	The delivery of biomolecules by extracellular vesicles (EVs) derived from endothelial progenitor cells (EPCs) has been proven to ameliorate sepsis, yet the therapeutic mechanism remains to be elucidated. Taurine upregulated gene 1 (TUG1) is a long noncoding RNA (lncRNA) that is downregulated in sepsis. The current study was designed to explore the role of EPCs derived EVs transmitting TUG1 in macrophage polarization and macrophage-mediated inflammation in a cecal ligation and puncture (CLP)-induced sepsis mouse model. TUG1 was underexpressed in CLP-induced sepsis, and its reexpression induced anti-inflammatory macrophage polarization and suppressed macrophage-medicated inflammatory injury to the pulmonary vascular endothelium. EPCs derived EVs transmitted TUG1 to promote M2 macrophage polarization. Luciferase, RIP, and RNA pull-down assays showed that TUG1 could competitively bind to microRNA-9-5p (miR-9-5p) to upregulate the expression of sirtuin 1 (SIRT1). Furthermore, EPCs derived EVs transmitted TUG1 to promote M2 macrophage polarization through the impairment of miR-9-5p-dependent SIRT1 inhibition. Finally, EPCs derived EVs carrying TUG1 were verified to ameliorate sepsis-induced organ damage in the murine model. In summary, EPCs derived EVs transmit TUG1 to attenuate sepsis via macrophage M2 polarization. This study also highlights the proinflammatory mechanism associated with miR-9-5p-mediated inhibition of SIRT1, which contributes to a more comprehensive understanding of the pathogenesis of sepsis.
MeSH term(s)	Animals ; Anti-Inflammatory Agents/metabolism ; Base Sequence ; Cell Polarity/genetics ; Disease Models, Animal ; Endothelial Progenitor Cells/metabolism ; Extracellular Vesicles/metabolism ; Inflammation/genetics ; Inflammation/pathology ; Lung/blood supply ; Macrophages/metabolism ; Macrophages/pathology ; Male ; Mice ; Mice, Inbred C57BL ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Models, Biological ; Particle Size ; Protein Binding ; RAW 264.7 Cells ; RNA, Long Noncoding/genetics ; RNA, Long Noncoding/metabolism ; Sepsis/genetics ; Sepsis/pathology ; Sirtuin 1/metabolism ; Up-Regulation/genetics
Chemical Substances	Anti-Inflammatory Agents ; MIRN9 microRNA, mouse ; MicroRNAs ; RNA, Long Noncoding ; long non-coding RNA TUG1, mouse ; Sirt1 protein, mouse (EC 3.5.1.-) ; Sirtuin 1 (EC 3.5.1.-)
Language	English
Publishing date	2021-11-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-021-04117-5
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Article: Mesenchymal epithelial transition factor regulates tumor necrosis factor-related apoptotic induction ligand resistance in hepatocellular carcinoma cells through down-regulation of cyclin B1

Lv, Shuai / Wang, Xijuan / Bai, Xia / Ning, Hanbing / Li, Yingxia / Wen, Hongtao / Lu, Wenquan / Wang, Jingyun

international journal of biochemistry & cell biology. 2020 Nov., v. 128

2020

Abstract: Tumor necrosis factor-related apoptotic induction ligand can induce cell apoptosis in various tumor cells. However, many cancer cells are resistant to tumor necrosis factor-related apoptotic induction ligand. Therefore, overcoming the tumor necrosis ... ...

Abstract	Tumor necrosis factor-related apoptotic induction ligand can induce cell apoptosis in various tumor cells. However, many cancer cells are resistant to tumor necrosis factor-related apoptotic induction ligand. Therefore, overcoming the tumor necrosis factor-related apoptotic induction ligand resistance makes it possible for tumor necrosis factor-related apoptotic induction ligand-based anti-cancer therapies. In this study, we took mesenchymal epithelial transition factor as the research target to study its role in tumor necrosis factor-related apoptotic induction ligand-resistant hepatocellular carcinoma. Mesenchymal epithelial transition factor gene has been proved to be an effective predictor of recurrence after hepatocellular carcinoma resection. The expression of mesenchymal epithelial transition factor and cyclin B1 were measured in tumor necrosis factor-related apoptotic induction ligand-resistant and non-resistant hepatocellular carcinoma tissues. Cyclin B1-knockdown and cyclin B1-overexpression hepatocellular carcinoma cells were treated with tumor necrosis factor-related apoptotic induction ligand; mesenchymal epithelial transition factor knockout, mesenchymal epithelial transition factor re-introduction and cyclin B1 restored in hepatocellular carcinoma cells treated with tumor necrosis factor-related apoptotic induction ligand were established. And MTT, bromodeoxyuridine, flow cytometry and western blotting were performed to evaluate the effect of mesenchymal epithelial transition factor and cyclin B1 on hepatocellular carcinoma cells treated with tumor necrosis factor-related apoptotic induction ligand. In addition, subcutaneous tumor transplantation in nude mice was conducted to access the effect of mesenchymal epithelial transition factor and cyclin B1 on tumor formation in vivo. In conclusion, cyclin B1 enhanced the cell growth and inhibited apoptosis in tumor necrosis factor-related apoptotic induction ligand-resistant hepatocellular carcinoma cells. And mesenchymal epithelial transition factor promoted the cell growth and apoptosis in tumor necrosis factor-related apoptotic induction ligand-resistant hepatocellular carcinoma cells by regulating cyclin B1. Therefore, mesenchymal epithelial transition factor regulates the cyclin B1 to regulate tumor necrosis factor-related apoptotic induction ligand resistance in hepatocellular carcinoma cells. Our results suggest a novel molecular mechanism for regulating tumor necrosis factor-related apoptotic induction ligand resistance, which might be helpful to select drug targets in the treatment of liver cancer.
Keywords	apoptosis ; cell growth ; cyclins ; drugs ; epithelium ; flow cytometry ; genes ; hepatoma ; ligands ; necrosis ; resection
Language	English
Dates of publication	2020-11
Publishing place	Elsevier Ltd
Document type	Article
Note	NAL-AP-2-clean
ZDB-ID	1228429-4
ISSN	1878-5875 ; 1357-2725
ISSN (online)	1878-5875
ISSN	1357-2725
DOI	10.1016/j.biocel.2020.105844
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Article: Resveratrol inhibits bile acid‐induced gastric intestinal metaplasia via the PI3K/AKT/p‐FoxO4 signalling pathway

Lu, Wenquan / Ni, Zhen / Jiang, Shuqin / Tong, Mingfu / Zhang, Jian / Zhao, Jing / Feng, Chenchen / Jia, Qiaoyu / Wang, Jingyun / Yao, Tingting / Ning, Hanbing / Shi, Yongquan

Phytotherapy research. 2021 Mar., v. 35, no. 3

2021

Abstract: Gastric intestinal metaplasia (GIM) is the essential pre‐malignancy of gastric cancer. Chronic inflammation and bile acid reflux are major contributing factors. As an intestinal development transcription factor, caudal‐related homeobox 2 (CDX2) is key in ...

Abstract	Gastric intestinal metaplasia (GIM) is the essential pre‐malignancy of gastric cancer. Chronic inflammation and bile acid reflux are major contributing factors. As an intestinal development transcription factor, caudal‐related homeobox 2 (CDX2) is key in GIM. Resveratrol has potential chemopreventive and anti‐tumour effects. The aim of the study is to probe the effect of resveratrol in bile acid‐induced GIM. We demonstrated that resveratrol could reduce CDX2 expression in a time‐ and dose‐dependent manner in gastric cell lines. A Cignal Finder 45‐Pathway Reporter Array and TranSignal Protein/DNA Array Kit verified that resveratrol could increase Forkhead box O4 (FoxO4) activity and that Chenodeoxycholic acid (CDCA) could reduce FoxO4 activity. Furthermore, bioinformatics analysis showed that FoxO4 could bind to the CDX2 promoter, and these conjectures were supported by chromatin‐immunoprecipitation (ChIP) assays. Resveratrol can activate FoxO4 and decrease CDX2 expression by increasing phospho‐FoxO4 nucleus trans‐location. Resveratrol could increase FoxO4 phosphorylation through the PI3K/AKT pathway. Ectopic FoxO4 expression can up‐regulate FoxO4 phosphorylation and suppress CDCA‐induced GIM marker expression. Finally, we found a reverse correlation between p‐FoxO4 and CDX2 in tissue arrays. This study validates that resveratrol could reduce bile acid‐induced GIM through the PI3K/AKT/p‐FoxO4 signalling pathway and has a potential reversing effect on GIM, especially that caused by bile acid reflux.
Keywords	DNA ; bile ; bioinformatics ; chemoprevention ; chenodeoxycholic acid ; dose response ; inflammation ; intestines ; metaplasia ; phosphorylation ; phytotherapy ; research ; resveratrol ; stomach neoplasms ; transcription factors
Language	English
Dates of publication	2021-03
Size	p. 1495-1507.
Publishing place	John Wiley & Sons, Ltd.
Document type	Article
Note	NAL-AP-2-clean ; JOURNAL ARTICLE
ZDB-ID	639136-9
ISSN	1099-1573 ; 0951-418X
ISSN (online)	1099-1573
ISSN	0951-418X
DOI	10.1002/ptr.6915
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Article ; Online: Expression and significance of CDX2, FXR, and TGR5 in esophageal cancer.

Zhang, Hongying / Qu, Xiaodong / Wang, Na / Zhang, Lifeng / Yuan, Ting / Shi, Miao / Sun, Nina / Yuan, Donghong / Ning, Hanbing / Zhao, Mengyun / Wang, Yongxi / Ni, Zhen / Han, Chuan / Shi, Yongquan

International journal of clinical and experimental pathology

2022 Volume 15, Issue 9, Page(s) 354–363

Abstract: This study explored the expression and significance of three critical morphogenesis genes in normal esophagus, reflux esophagitis (RE), Barrett's esophagus (BE), esophageal adenocarcinoma (EA), and esophageal squamous cell carcinoma (ESCC). Esophageal ... ...

Abstract	This study explored the expression and significance of three critical morphogenesis genes in normal esophagus, reflux esophagitis (RE), Barrett's esophagus (BE), esophageal adenocarcinoma (EA), and esophageal squamous cell carcinoma (ESCC). Esophageal tissue samples and tissue microarrays were used. CDX2, FXR, and TGR5 protein expression were measured by immunohistochemistry in normal esophageal, RE, BE, EA, and ESCC tissues. All 3 proteins had markedly changed expression during the progression of EA. The expressions of CDX2 and FXR were positively correlated in EA. In addition, TGR5 expression was positively correlated with CDX2 in RE and BE. The expressions of CDX2 and FXR were also positively correlated in ESCC. Although CDX2, FXR, and TGR5 were upregulated in ESCC, these factors might not be markers for the prognosis of ESCC. These results suggested that CDX2, FXR, and TGR5 might play different roles in EA and ESCC. They may represent novel therapeutic targets for patients with these cancers.
Language	English
Publishing date	2022-09-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	2418306-4
ISSN	1936-2625 ; 1936-2625
ISSN (online)	1936-2625
ISSN	1936-2625
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