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Article ; Online: Excretion of Amyloid-β in the Gastrointestinal Tract and Regulation by the Gut Microbiota.

Wu, Shijing / Hu, Li / Lin, Jiajing / Li, Kanglan / Ye, Shicai / Zhu, Shaoping / Liu, Zhou

2022 Volume 90, Issue 3, Page(s) 1153–1162

Abstract: Background: Amyloid-β (Aβ) is important in the etiology of Alzheimer's disease (AD). Removal of Aβ from the brain is a major strategy for the prevention and treatment of AD.: Objective: To clarify whether Aβ42 can be cleared by intestinal excretion ... ...

Abstract	Background: Amyloid-β (Aβ) is important in the etiology of Alzheimer's disease (AD). Removal of Aβ from the brain is a major strategy for the prevention and treatment of AD. Objective: To clarify whether Aβ42 can be cleared by intestinal excretion and whether the gut microbiota (GM) can affect the excretory clearance of Aβ42 in the peripheral blood and intestines. Methods: Male 8-month-old C57BL6 mice were maintained on either normal chow or received broad-spectrum antibiotics in their drinking water for one week. Sterile saline, fluorescein isothiocyanate (FITC), or FITC-Aβ42 (fluorescein isothiocyanate-labeled amyloid-β42 peptides) was injected 1 h before sampling. Related changes of Aβ42 before and after injection were evaluated. Results: FITC-Aβ42 was injected into mice through the tail vein and could later be detected in feces. Furthermore, the fecal concentrations of FITC-Aβ42 were higher in mice that had been fed antibiotics to alter their GM than in normal mice. However, the FITC-Aβ42 concentrations in blood showed the opposite pattern. Conclusion: Aβ42 can be excreted into the intestinal lumen and is regulated by the GM.
MeSH term(s)	Animals ; Mice ; Male ; Gastrointestinal Microbiome/physiology ; Fluorescein-5-isothiocyanate ; Mice, Transgenic ; Mice, Inbred C57BL ; Disease Models, Animal ; Amyloid beta-Peptides/metabolism ; Alzheimer Disease/therapy ; Gastrointestinal Tract/metabolism ; Brain/metabolism ; Anti-Bacterial Agents
Chemical Substances	Fluorescein-5-isothiocyanate (I223NX31W9) ; Amyloid beta-Peptides ; Anti-Bacterial Agents
Language	English
Publishing date	2022-10-09
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1440127-7
ISSN	1875-8908 ; 1387-2877
ISSN (online)	1875-8908
ISSN	1387-2877
DOI	10.3233/JAD-220705
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Diosmetin induces apoptosis and protective autophagy in human gastric cancer HGC-27 cells via the PI3K/Akt/FoxO1 and MAPK/JNK pathways.

Pan, Zhaobin / Tan, Zhiming / Li, Hongyan / Wang, Yang / Du, Haiyan / Sun, Jinhui / Li, Chunchao / Ye, Shicai / Li, Xin / Quan, Juanhua

Medical oncology (Northwood, London, England)

2023 Volume 40, Issue 11, Page(s) 319

Abstract: Gastric cancer represents a significant global health concern, necessitating the exploration of novel therapeutic options. Diosmetin, a natural flavonoid derived from citrus and vegetables, has demonstrated promising anti-tumor activity against various ... ...

Abstract	Gastric cancer represents a significant global health concern, necessitating the exploration of novel therapeutic options. Diosmetin, a natural flavonoid derived from citrus and vegetables, has demonstrated promising anti-tumor activity against various tumor cells. However, the potential anticancer effect of diosmetin in gastric cancer and its underlying mechanism have yet to be elucidated. In this study, we aimed to investigate the impact of diosmetin on cell proliferation, migration, cell cycle progression and apoptosis in human gastric cancer HGC-27 cells. Our findings revealed that diosmetin effectively suppressed cell proliferation, induced G2/M phase cell cycle arrest, and triggered cell apoptosis. Mechanistically, diosmetin downregulated the expression of antiapoptotic proteins Bcl-2 and Bcl-xL, while upregulated the level of proapoptotic proteins such as Bax, cleaved PARP and cleaved caspase-3. Additionally, diosmetin inhibited Akt and FoxO1 phosphorylation, while activated the MAPK signaling pathway. Notably, pretreatment of IGF-1, an Akt activator, attenuated the diosmetin-induced apoptosis. Furthermore, pretreatment with SP600125, a JNK inhibitor, significantly reduced the protein level of LC3B, while promoted the expression of cleaved caspase-3 and cleaved PARP. Collectively, our results suggest that diosmetin holds promise as an effective therapeutic agent against gastric cancer by inducing apoptosis through inhibition of the Akt/FoxO1 pathway and promoting protective autophagy via the MAPK/JNK signaling pathway.
MeSH term(s)	Humans ; Apoptosis ; Autophagy ; Caspase 3 ; Flavonoids/pharmacology ; MAP Kinase Signaling System ; Phosphatidylinositol 3-Kinases ; Poly(ADP-ribose) Polymerase Inhibitors ; Proto-Oncogene Proteins c-akt ; Stomach Neoplasms/drug therapy ; Cell Line, Tumor
Chemical Substances	Caspase 3 (EC 3.4.22.-) ; diosmetin (TWZ37241OT) ; Flavonoids ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Poly(ADP-ribose) Polymerase Inhibitors ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2023-10-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	1201189-7
ISSN	1559-131X ; 0736-0118 ; 1357-0560
ISSN (online)	1559-131X
ISSN	0736-0118 ; 1357-0560
DOI	10.1007/s12032-023-02180-w
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Book: Zhong bu di qu jing ji zhu lei bing chong hai tu shuo

Ye, Shicai

(Taizhong Qu nong ye gai liang chang te kan ; di 104 hao)

2010

Institution	Xing zheng yuan nong ye wei yuan hui (China). / Taizhong Qu nong ye gai liang chang
Author's details	Ye Shicai ... [et al.] bian zhu
Series title	Taizhong Qu nong ye gai liang chang te kan ; di 104 hao
Keywords	Bamboo/Diseases and pests ; Bamboo/Diseases and pests.
Language	Chinese
Size	8, 178 p. :, col. ill. ;, 26 cm.
Edition	Chu ban.
Publisher	Xing zheng yuan nong ye wei yuan hui Taizhong Qu nong ye gai liang chang
Publishing place	Zhanghua Xian Dacun Xiang
Document type	Book
ISBN	9789860262988 ; 9860262985
Database	NAL-Catalogue (AGRICOLA)

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Article: Transcription factor forkhead box K1 regulates miR-32 expression and enhances cell proliferation in colorectal cancer.

Wu, Weiyun / Chen, Yongze / Ye, Shicai / Yang, Hui / Yang, Jianyun / Quan, Juanhua

Oncology letters

2021 Volume 21, Issue 5, Page(s) 407

Abstract: Increased microRNA (miR)-32 expression in colorectal cancer (CRC) tissues enhances CRC cell proliferation, migration, invasion and attenuates CRC cell apoptosis by repressing the expression of phosphatase and tensin homolog (PTEN). Forkhead box K1 (FOXK1) ...

Abstract	Increased microRNA (miR)-32 expression in colorectal cancer (CRC) tissues enhances CRC cell proliferation, migration, invasion and attenuates CRC cell apoptosis by repressing the expression of phosphatase and tensin homolog (PTEN). Forkhead box K1 (FOXK1) was identified as a potential interacting transcription factor using DNA pull-down assays and mass spectrometry. The present study aimed to elucidate the role of FOXK1 in regulating miR-32 expression in CRC. The expressions of
Language	English
Publishing date	2021-03-22
Publishing country	Greece
Document type	Journal Article
ZDB-ID	2573196-8
ISSN	1792-1082 ; 1792-1074
ISSN (online)	1792-1082
ISSN	1792-1074
DOI	10.3892/ol.2021.12668
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Book: Zhong bu di qu fan shi liu bing chong ji hai wu tu shuo

Ye, Shicai

2008

Title variant	Fan shi liu bing chong ji hai wu tu shuo
Author's details	Ye Shicai ... [et al.] bian zhu
Keywords	Guava/Diseases and pests ; Tropical fruit/Diseases and pests/Control
Language	Chinese ; Latin
Size	8, 282 p. :, chiefly col. ill. ;, 26 cm.
Publisher	Xing zheng yuan nong ye wei yuan hui tai zhong qu nong ye gai liang chang
Publishing place	Zhanghua Xian Dacun Xiang
Document type	Book
Note	Nomenclature also in Latin.
ISBN	9789860165647 ; 9860165645
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Book: Zhong bu di qu gan ju bing chong hai tu shuo

Ye, Shicai

(Taizhong Qu nong ye gai liang chang te kan ; di 87 hao)

2007

Institution	Xing zheng yuan nong ye wei yuan hui (China) Taizhong Qu nong ye gai liang chang
Author's details	Ye Shicai ... [et al.] bian zhu
Series title	Taizhong Qu nong ye gai liang chang te kan ; di 87 hao
Keywords	Oranges/Diseases and pests ; Oranges/Diseases and pests. ; Agricultural experiment stations/Research
Language	Chinese
Size	2, 6, 308 p. :, chiefly col. ill. ;, 26 cm.
Edition	Chu ban.
Publisher	Xing zheng yuan nong ye wei yuan hui Taizhong Qu nong ye gai liang chang
Publishing place	Zhanghua Xian Dacun Xiang
Document type	Book
ISBN	9789860125078 ; 9860125074
Database	NAL-Catalogue (AGRICOLA)

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Article: Analysis of promoter methylation and epigenetic regulation of miR-32 in colorectal cancer cells.

Wu, Weiyun / Ye, Shicai / Tan, Wenkai / Zhou, Yu / Quan, Juanhua

Experimental and therapeutic medicine

2019 Volume 17, Issue 4, Page(s) 3209–3214

Abstract: MicroRNA-32 (miR-32) is upregulated in colorectal cancer (CRC) tissues; its overexpression leads to increased cell proliferation, migration and invasion, as well as reduced apoptosis of CRC cells, at least partly by inhibiting the target gene phosphatase ...

Abstract	MicroRNA-32 (miR-32) is upregulated in colorectal cancer (CRC) tissues; its overexpression leads to increased cell proliferation, migration and invasion, as well as reduced apoptosis of CRC cells, at least partly by inhibiting the target gene phosphatase and tensin homolog. However, the mechanisms of its upregulation have remained elusive. In the present study, the effects of methylation and acetylation on the expression of miR-32 were investigated. The promoter methylation status of miR-32 in the CRC cell lines HT-29 and HCT-116 and the normal colonic epithelial cell line NCM460 was investigated by bisulfate sequencing polymerase chain reaction (BSP). The potential role of methylation and histone acetylation in the regulation of miR-32 expression in CRC cells was investigated using the demethylation reagent 5-aza-2'-deoxycytidine (5-Aza-dC), the histone deacetylase inhibitor trichostatin A (TSA) and transfection of DNA methyltransferase 1 (DNMT1) overexpression plasmid. BSP revealed that CpG sites in the miR-32 promoter region of CRC and normal colonic epithelial cells were all hypomethylated, with methylation rates of 0.12, 1.14 and 0.64% in HCT-116, HT-29 and NCM460 cells, respectively. Treatment with 5-Aza-dC and/or TSA and transfection with DNMT1 plasmid did not significantly alter the expression of miR-32. Therefore, the present results suggest that methylation and histone acetylation do not affect miR-32 expression in CRC cells.
Language	English
Publishing date	2019-02-28
Publishing country	Greece
Document type	Journal Article
ZDB-ID	2683844-8
ISSN	1792-1015 ; 1792-0981
ISSN (online)	1792-1015
ISSN	1792-0981
DOI	10.3892/etm.2019.7328
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Analysis of the promoter region of the human miR-32 gene in colorectal cancer.

Wu, Weiyun / Tan, Wenkai / Ye, Shicai / Zhou, Yu / Quan, Juanhua

Oncology letters

2019 Volume 17, Issue 4, Page(s) 3743–3750

Abstract: The pathogenesis of colorectal cancer (CRC) is poorly understood. MicroRNA (miR)-32 upregulation in CRC tissues was previously reported, where it increased the proliferation, migration and invasion, and reduced apoptosis of CRC cells by inhibiting the ... ...

Abstract	The pathogenesis of colorectal cancer (CRC) is poorly understood. MicroRNA (miR)-32 upregulation in CRC tissues was previously reported, where it increased the proliferation, migration and invasion, and reduced apoptosis of CRC cells by inhibiting the expression of phosphatase and tensin homolog (PTEN). However, the mechanism underlying miR-32 upregulation remains unknown. miR-32 is an intronic miRNA located within intron 14 of the transmembrane protein 245 gene (TMEM245). The present study aimed to elucidate the biological pathways underlying miR-32 regulation in CRC. A truncated promoter containing the 5'-flanking region of TMEM245/miR-32 gene was constructed. The promoter region was analyzed by dual luciferase reporter assay in CRC cells. DNA pull-down assay and mass spectrometry (MS) were used to identify proteins binding to the core promoter. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) and transcription factor (TF) analyses were used to identify the binding proteins. The -320 to -1 bp fragment of the 5'-flanking region exhibited the highest luciferase activity. The regions spanning -606 to -320 bp exhibited a significant decrease in luciferase activity, compared with the -320 to -1 bp fragment. DNA pull-down assay and MS revealed 403 potential miR-32 promoter binding proteins. GO and KEGG pathway analysis indicated that these proteins were involved in numerous physiological and biochemical processes, including 'structural molecule activity', 'RNA binding', 'small molecule metabolic process' and 'biogenesis'. Furthermore, TF analysis revealed 10 potential interacting TFs, including SMAD family member 1 (SMAD1), signal transducer and activator of transcription 1 (STAT1) and forkhead box K1 (Foxk1). These results suggested that the core promoter region may be located within-320 to -1 bp of the 5'-flanking region of TMEM245/miR-32 gene, while the region from -606 to -320 bp may harbor repressive regulatory elements. The TFs SMAD1, STAT1 and Foxk1 may be involved in the transcriptional regulation of miR-32.
Language	English
Publishing date	2019-02-14
Publishing country	Greece
Document type	Journal Article
ZDB-ID	2573196-8
ISSN	1792-1082 ; 1792-1074
ISSN (online)	1792-1082
ISSN	1792-1074
DOI	10.3892/ol.2019.10042
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Book ; Conference proceedings: Taizhong qu nong ye gai liang chang 103 nian du ke ji ji hua yan jiu cheng guo fa biao hui lun wen ji

Ye, Shicai / Chen, Yuanmin / Yu, Yizhi

Minguo 104 [2015] nian 1 yue 20 ri wu xing zheng yuan nong ye wei yuan hui Taizhong qu nong ye gai liang chang ju xing

(Taizhong qu nong ye gai liang chang te kan ; Di 129 hao)

2015

Title variant	103 nian du Taizhong qu nong ye gai liang chang ke ji ji hua yan jiu cheng guo fa biao hui lun wen ji
Institution	Xing zheng yuan nong ye wei yuan hui. / Taizhong Qu nong ye gai liang chang
Event/congress	Taizhong qu nong ye gai liang chang ke ji ji hua yan jiu cheng guo fa biao hui (103niandu, 2015, XingzhengyuannongyeweiyuanhuiTaizhongqunongyegailiangchang)
Author's details	Ye Shicai, Chen Yuanmin, Yu Yizhi zhu bian ; Xing zheng yuan nong ye wei yuan hui Taizhong Qu nong ye gai liang chang bian yin
Series title	Taizhong qu nong ye gai liang chang te kan ; Di 129 hao
Keywords	Agriculture/Research ; Agricultural innovations ; Agricultural innovations. ; Agriculture/Research. ; Taiwan.
Language	Chinese
Size	IV, 223 pages :, illustrations (chiefly color) ;, 26 cm.
Document type	Book ; Conference proceedings
ISBN	9789860454208 ; 9860454205
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Effects of Pretreatment with Bifidobacterium bifidum Using 16S Ribosomal RNA Gene Sequencing in a Mouse Model of Acute Colitis Induced by Dextran Sulfate Sodium.

Weng, Yi-Jie / Jiang, Dan-Xian / Liang, Jian / Ye, Shi-Cai / Tan, Wen-Kai / Yu, Cai-Yuan / Zhou, Yu

Medical science monitor : international medical journal of experimental and clinical research

2021 Volume 27, Page(s) e928478

Abstract: BACKGROUND Bifidobacterium is a potentially effective and safe treatment for patients with inflammatory bowel disease (IBD), including ulcerative colitis and Crohn's disease. However, information on the influence of B. bifidum on gut microbial diversity ... ...

Abstract	BACKGROUND Bifidobacterium is a potentially effective and safe treatment for patients with inflammatory bowel disease (IBD), including ulcerative colitis and Crohn's disease. However, information on the influence of B. bifidum on gut microbial diversity of treated and pretreated IBD patients is limited. MATERIAL AND METHODS Our study investigated therapeutic and preventive effects of B. bifidum ATCC 29521 on C57BL/6 mice with dextran sulfate sodium (DSS)-induced acute colitis via 16S ribosomal ribonucleic acid (rRNA) gene sequencing. RESULTS Treatment and pretreatment of mice with B. bifidum ATCC 29521 significantly alleviated the severity of acute colitis on the basis of clinical and pathologic indicators. 16S rRNA gene sequencing showed that administration of B. bifidum shifted composition of the gut microbiome in mice with DSS-induced colitis in both treated and pretreated groups. Mice pretreated with B. bifidum ATCC 29521 for 21 days exhibited a significant increase in diversity of the gut microbiome. Principal coordinate analysis showed that gut microbiota structure was shaped by different treatments and time points. On the basis of linear discriminant analysis of effect size, the abundance of the genus Escherichia-Shigella, belonging to the family Enterobacteriaceae, was reduced in the B. bifidum-treated group, indicating that pathogens were inhibited by the B. bifidum treatment. Furthermore, the genera Intestinimonas and Bacteroides were significantly associated with the B. bifidum-pretreated group. CONCLUSIONS 16S rRNA gene sequencing showed that pretreatment with B. bifidum ATCC 29521 reduced intestinal inflammation and altered the gut microbiota to favor the genera Intestinimonas and Bacteroides.
MeSH term(s)	Animals ; Bacteria/genetics ; Bifidobacterium bifidum/metabolism ; Colitis/drug therapy ; Colitis/microbiology ; Colitis, Ulcerative/genetics ; Colon/pathology ; Dextran Sulfate/adverse effects ; Dextran Sulfate/pharmacology ; Disease Models, Animal ; Feces/microbiology ; Female ; Gastrointestinal Microbiome/drug effects ; Gastrointestinal Microbiome/genetics ; Inflammatory Bowel Diseases/pathology ; Mice ; Mice, Inbred C57BL ; Probiotics/therapeutic use ; RNA, Ribosomal, 16S/genetics
Chemical Substances	RNA, Ribosomal, 16S ; Dextran Sulfate (9042-14-2)
Language	English
Publishing date	2021-03-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	1439041-3
ISSN	1643-3750 ; 1234-1010
ISSN (online)	1643-3750
ISSN	1234-1010
DOI	10.12659/MSM.928478
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