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Article ; Online: Liver injury in coronavirus disease 2019

LAI Shujie

Linchuang Gandanbing Zazhi, Vol 36, Iss 5, Pp 1004-

2020 Volume 1007

Abstract: At present, coronavirus disease 2019 (COVID-19) caused by 2019 novel coronavirus (2019-nCoV) infection has spread rapidly in China and more than 70 countries around the world and thus become a public health event of international concern. In addition to ... ...

Abstract	At present, coronavirus disease 2019 (COVID-19) caused by 2019 novel coronavirus (2019-nCoV) infection has spread rapidly in China and more than 70 countries around the world and thus become a public health event of international concern. In addition to fever and respiratory symptoms, varying degrees of liver injury is also observed after 2019-nCoV infection. This article reviews the clinical features, pathology, pathogenic mechanism, and therapeutic strategies of liver injury associated with COVID-19, hoping to provide a reference for clinical decision-making on the prevention and treatment of COVID-19.
Keywords	Diseases of the digestive system. Gastroenterology ; RC799-869 ; covid19
Language	Chinese
Publishing date	2020-05-01T00:00:00Z
Publisher	Editorial Department of Journal of Clinical Hepatology
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Hypoxia derived exosomes promote the proliferation and metastasis of colorectal cancer through the regulation of HIF-1α/miR-4299/ZBTB4.

Wu, Lunpo / Xue, Meng / Lai, Sanchuan / Chen, Jingyu / Lin, Yifeng / Ding, Ning / Zhong, Jing / Chen, Shujie / Wang, Liangjing

Life sciences

2023 Volume 329, Page(s) 121872

Abstract: Aims: The biological functions of colorectal cancer (CRC) cell derived exosomes responding to hypoxic microenvironment and its underlying mechanisms remain unclear.: Main methods: Extracted exosomes were confirmed. CRC cells were incubated with ... ...

Abstract	Aims: The biological functions of colorectal cancer (CRC) cell derived exosomes responding to hypoxic microenvironment and its underlying mechanisms remain unclear. Main methods: Extracted exosomes were confirmed. CRC cells were incubated with hypoxic and normoxic exosomes and its biological behavior were analyzed. miRNA microarray were conducted. Cells were incubated with miRNAs mimics, inhibitors, or small interfering RNAs; expression of reporter constructs was measured in luciferase assays. Cells were transfected with Lentivirus vectors containing eGFP-miR-4299 overexpression (or ZBTB4 siRNA expression plasmid) and they were injected into BALB/C nude mice subcutaneously or by tail vein and the growth of xenograft tumors or lung metastasis were measured. The clinical significance of ZBTB4 was measured in tumor tissues and adjacent non-tumor tissues. Key findings: Hypoxic exosomes could tranfer to the recipient normoxic cells and promote the cell proliferation and migration. We found several miRNAs were significantly up-regulated in hypoxic exosomes and the expression levels of miR-4299 increased in both hypoxic cells and hypoxic exosomes. We observed that miR-4299 was upregulated in a HIF-1α dependent way. In addition, ectopic expression of miR-4299 promoted the tumor growth and metastasis in vitro and in vivo. ZBTB4, an identified direct target of miR-4299, could abrogate the effect on tumor growth and distant metastasis. The expression of ZBTB4 were decreased in tumor tissues compared with non-tumor colon tissues from patients. Significance: We demonstrated that in response to hypoxia, CRC cells had an increased production of exosomes. The hypoxia derived exosomes promote the proliferation and metastasis of colorectal cancer by exporting miR-4299 and modulating its target gene ZBTB4.
MeSH term(s)	Animals ; Mice ; Humans ; Exosomes/metabolism ; Mice, Nude ; Mice, Inbred BALB C ; MicroRNAs/metabolism ; RNA, Small Interfering/metabolism ; Hypoxia/metabolism ; Colorectal Neoplasms/pathology ; Cell Proliferation/genetics ; Gene Expression Regulation, Neoplastic ; Cell Line, Tumor ; Cell Movement ; Tumor Microenvironment ; Repressor Proteins/genetics
Chemical Substances	MicroRNAs ; RNA, Small Interfering ; ZBTB4 protein, human ; Repressor Proteins ; MIR4299 microRNA, human
Language	English
Publishing date	2023-06-22
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	3378-9
ISSN	1879-0631 ; 0024-3205
ISSN (online)	1879-0631
ISSN	0024-3205
DOI	10.1016/j.lfs.2023.121872
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Article ; Online: Hypoxia derived exosomes promote the proliferation and metastasis of colorectal cancer through the regulation of HIF-1α/miR-4299/ZBTB4

Wu, Lunpo / Xue, Meng / Lai, Sanchuan / Chen, Jingyu / Lin, Yifeng / Ding, Ning / Zhong, Jing / Chen, Shujie / Wang, Liangjing

Life Sciences. 2023 Sept., v. 329 p.121872-

2023

Abstract: The biological functions of colorectal cancer (CRC) cell derived exosomes responding to hypoxic microenvironment and its underlying mechanisms remain unclear. Extracted exosomes were confirmed. CRC cells were incubated with hypoxic and normoxic exosomes ... ...

Abstract	The biological functions of colorectal cancer (CRC) cell derived exosomes responding to hypoxic microenvironment and its underlying mechanisms remain unclear. Extracted exosomes were confirmed. CRC cells were incubated with hypoxic and normoxic exosomes and its biological behavior were analyzed. miRNA microarray were conducted. Cells were incubated with miRNAs mimics, inhibitors, or small interfering RNAs; expression of reporter constructs was measured in luciferase assays. Cells were transfected with Lentivirus vectors containing eGFP-miR-4299 overexpression (or ZBTB4 siRNA expression plasmid) and they were injected into BALB/C nude mice subcutaneously or by tail vein and the growth of xenograft tumors or lung metastasis were measured. The clinical significance of ZBTB4 was measured in tumor tissues and adjacent non-tumor tissues. Hypoxic exosomes could tranfer to the recipient normoxic cells and promote the cell proliferation and migration. We found several miRNAs were significantly up-regulated in hypoxic exosomes and the expression levels of miR-4299 increased in both hypoxic cells and hypoxic exosomes. We observed that miR-4299 was upregulated in a HIF-1α dependent way. In addition, ectopic expression of miR-4299 promoted the tumor growth and metastasis in vitro and in vivo. ZBTB4, an identified direct target of miR-4299, could abrogate the effect on tumor growth and distant metastasis. The expression of ZBTB4 were decreased in tumor tissues compared with non-tumor colon tissues from patients. We demonstrated that in response to hypoxia, CRC cells had an increased production of exosomes. The hypoxia derived exosomes promote the proliferation and metastasis of colorectal cancer by exporting miR-4299 and modulating its target gene ZBTB4.
Keywords	Lentivirus ; caudal vein ; cell proliferation ; colon ; colorectal neoplasms ; exosomes ; genes ; hypoxia ; luciferase ; lungs ; metastasis ; microRNA ; microarray technology ; plasmids ; xenotransplantation ; Colorectal cancer ; miRNAs
Language	English
Dates of publication	2023-09
Publishing place	Elsevier Inc.
Document type	Article ; Online
ZDB-ID	3378-9
ISSN	1879-0631 ; 0024-3205
ISSN (online)	1879-0631
ISSN	0024-3205
DOI	10.1016/j.lfs.2023.121872
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: A Shortage of FTH Induces ROS and Sensitizes RAS-Proficient Neuroblastoma N2A Cells to Ferroptosis.

Lu, Ruiqing / Jiang, Yinan / Lai, Xianxin / Liu, Shujie / Sun, Litao / Zhou, Zhong-Wei

International journal of molecular sciences

2021 Volume 22, Issue 16

Abstract: Ferroptosis, an iron-dependent form of programmed cell death, has excellent potential as an anti-cancer therapeutic strategy in different types of tumors, especially in RAS-mutated ones. However, the function of ferroptosis for inhibiting neuroblastoma, ... ...

Abstract	Ferroptosis, an iron-dependent form of programmed cell death, has excellent potential as an anti-cancer therapeutic strategy in different types of tumors, especially in RAS-mutated ones. However, the function of ferroptosis for inhibiting neuroblastoma, a common child malignant tumor with minimal treatment, is unclear. This study investigated the anti-cancer function of ferroptosis inducer Erastin or RSL3 in neuroblastoma N2A cells. Our results show that Erastin or RSL3 induces ROS level and cell death and, therefore, reduces the viability of RAS-proficient N2A cells. Importantly, inhibitors to ferroptosis, but not apoptosis, ameliorate the high ROS level and viability defect in Erastin- or RSL3-treated cells. In addition, our data also show that N2A cells are much more sensitive to ferroptosis inducers than primary mouse cortical neural stem cells (NSCs) or neurons. Moreover, a higher level of ROS and PARylation is evidenced in N2A, but not NSCs. Mechanically, ferritin heavy chain 1 (
Language	English
Publishing date	2021-08-18
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms22168898
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Oridonin Inhibits SARS-CoV-2 by Targeting Its 3C-Like Protease.

Zhong, Baisen / Peng, Weiyu / Du, Shan / Chen, Bingyi / Feng, Yajuan / Hu, Xinfeng / Lai, Qi / Liu, Shujie / Zhou, Zhong-Wei / Fang, Pengfei / Wu, Yan / Gao, Feng / Zhou, Huihao / Sun, Litao

Small science

2022 Volume 2, Issue 6, Page(s) 2270012

Abstract: Oridonin Inhibits SARS-CoV-2 Oridonin, a natural product extracted ... ...

Abstract	Oridonin Inhibits SARS-CoV-2 Oridonin, a natural product extracted from
Language	English
Publishing date	2022-06-12
Publishing country	Germany
Document type	Journal Article
ZDB-ID	3042766-6
ISSN	2688-4046 ; 2688-4046
ISSN (online)	2688-4046
ISSN	2688-4046
DOI	10.1002/smsc.202270012
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Article ; Online: A Shortage of FTH Induces ROS and Sensitizes RAS-Proficient Neuroblastoma N2A Cells to Ferroptosis

Ruiqing Lu / Yinan Jiang / Xianxin Lai / Shujie Liu / Litao Sun / Zhong-Wei Zhou

International Journal of Molecular Sciences, Vol 22, Iss 8898, p

2021 Volume 8898

Abstract	Ferroptosis, an iron-dependent form of programmed cell death, has excellent potential as an anti-cancer therapeutic strategy in different types of tumors, especially in RAS-mutated ones. However, the function of ferroptosis for inhibiting neuroblastoma, a common child malignant tumor with minimal treatment, is unclear. This study investigated the anti-cancer function of ferroptosis inducer Erastin or RSL3 in neuroblastoma N2A cells. Our results show that Erastin or RSL3 induces ROS level and cell death and, therefore, reduces the viability of RAS-proficient N2A cells. Importantly, inhibitors to ferroptosis, but not apoptosis, ameliorate the high ROS level and viability defect in Erastin- or RSL3-treated cells. In addition, our data also show that N2A cells are much more sensitive to ferroptosis inducers than primary mouse cortical neural stem cells (NSCs) or neurons. Moreover, a higher level of ROS and PARylation is evidenced in N2A, but not NSCs. Mechanically, ferritin heavy chain 1 ( Fth ), the ferroxidase function to oxidate redox-active Fe 2+ to redox-inactive Fe 3+ , is likely responsible for the hypersensitivity of N2A to ferroptosis induction since its expression is lower in N2A compared to NSCs; ectopic expression of Fth reduces ROS levels and cell death, and induces expression of GPX4 and cell viability in N2A cells. Most importantly, neuroblastoma cell lines express a significantly low level of Fth than almost all other types of cancer cell lines. All these data suggest that Erastin or RSL3 induce ferroptosis cell death in neuroblastoma N2A cells, but not normal neural cells, regardless of RAS mutations, due to inadequate FTH. This study, therefore, provides new evidence that ferroptosis could be a promising therapeutic target for neuroblastoma.
Keywords	FTH ; ROS ; ferroptosis ; neuroblastoma ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	616
Language	English
Publishing date	2021-08-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: ELOVLs Predict Distinct Prognosis Value and Immunotherapy Efficacy In Patients With Hepatocellular Carcinoma.

Zhang, Yu / Pang, Shujie / Sun, Bo / Zhang, Minbo / Jiao, Xiaoxiao / Lai, Linying / Qian, Yiting / Yang, Ning / Yang, Wenzhuo

Frontiers in oncology

2022 Volume 12, Page(s) 884066

Abstract: Background: Hepatocellular carcinoma (HCC) is a primary malignancy of the liver with high prevalence worldwide and poor prognosis. It has been verified that elongation of very-long-chain fatty acids gene family (ELOVLs), a group of genes that ... ...

Abstract	Background: Hepatocellular carcinoma (HCC) is a primary malignancy of the liver with high prevalence worldwide and poor prognosis. It has been verified that elongation of very-long-chain fatty acids gene family (ELOVLs), a group of genes that responsible for elongation of saturated and polyunsaturated fatty acids, participate in the pathogenesis and development of multiplex disease including cancers. However, the functions and prognosis of ELOVLs in HCC are still indistinguishable. Methods: First, we searched the mRNA expression and survival data of ELOVLs in patients with HCC Results: Significant expression alteration was observed in ELOVLs family at the pan-cancer level. In liver cancer, ELOVL1 and ELOVL3 were strongly associated with poor prognosis of HCC by survival analysis and differential expression analysis. Immunohistochemistry microarray, WB, and RT-qPCR confirmed that ELOVL1 but not ELOVL3 played an important role in HCC. Mechanistically, functional network analysis revealed that ELOVL1 might be involved in the immune response. ELOVL1 could affect immune cell infiltration and immune checkpoint markers such as PD-1 and CTLA4 in HCC. Meanwhile, high expression of ELOVL1 would be insensitive to immunotherapy. Correlation analysis of immunotherapy markers showed that ELOVL1 has been associated with MSI, TMB, and oncogene mutations such as TP53. Conclusion: ELOVLs play distinct prognostic value in HCC. ELOVL1 could predict the poor prognosis and might be a potential indicator of immunotherapy efficacy in HCC patients.
Language	English
Publishing date	2022-07-15
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2022.884066
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Cholecystokinin B receptor antagonists for the treatment of depression via blocking long-term potentiation in the basolateral amygdala.

Zhang, Xu / Asim, Muhammad / Fang, Wei / Md Monir, Hossain / Wang, Huajie / Kim, Kyuhee / Feng, Hemin / Wang, Shujie / Gao, Qianqian / Lai, Yuanying / He, Jufang

Molecular psychiatry

2023 Volume 28, Issue 8, Page(s) 3459–3474

Abstract: Depression is a common and severe mental disorder. Evidence suggested a substantial causal relationship between stressful life events and the onset of episodes of major depression. However, the stress-induced pathogenesis of depression and the related ... ...

Abstract	Depression is a common and severe mental disorder. Evidence suggested a substantial causal relationship between stressful life events and the onset of episodes of major depression. However, the stress-induced pathogenesis of depression and the related neural circuitry is poorly understood. Here, we investigated how cholecystokinin (CCK) and CCKBR in the basolateral amygdala (BLA) are implicated in stress-mediated depressive-like behavior. The BLA mediates emotional memories, and long-term potentiation (LTP) is widely considered a trace of memory. We identified that the cholecystokinin knockout (CCK-KO) mice impaired LTP in the BLA, while the application of CCK4 induced LTP after low-frequency stimulation (LFS). The entorhinal cortex (EC) CCK neurons project to the BLA and optogenetic activation of EC CCK afferents to BLA-promoted stress susceptibility through the release of CCK. We demonstrated that EC CCK neurons innervate CCKBR cells in the BLA and CCK-B receptor knockout (CCKBR-KO) mice impaired LTP in the BLA. Moreover, the CCKBR antagonists also blocked high-frequency stimulation (HFS) induced LTP formation in the BLA. Notably, CCKBR antagonists infusion into the BLA displayed an antidepressant-like effect in the chronic social defeat stress model. Together, these results indicate that CCKBR could be a potential target to treat depression.
MeSH term(s)	Humans ; Mice ; Animals ; Basolateral Nuclear Complex ; Long-Term Potentiation/physiology ; Receptor, Cholecystokinin B/physiology ; Depression/drug therapy ; Cholecystokinin/pharmacology ; Cholecystokinin/physiology
Chemical Substances	Receptor, Cholecystokinin B ; Cholecystokinin (9011-97-6)
Language	English
Publishing date	2023-06-26
Publishing country	England
Document type	Journal Article
ZDB-ID	1330655-8
ISSN	1476-5578 ; 1359-4184
ISSN (online)	1476-5578
ISSN	1359-4184
DOI	10.1038/s41380-023-02127-7
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Liver injury in coronavirus disease 2019

Lai, ShuJie / Cui, HongLi / Chen, DongFeng

Journal of Clinical Hepatology

Abstract: At present, coronavirus disease 2019 (COVID - 19) caused by 2019 novel coronavirus (2019 - nCoV) infection has spread rapidly in China and more than 70 countries around the world and thus become a public health event of international concern In addition ... ...

Abstract	At present, coronavirus disease 2019 (COVID - 19) caused by 2019 novel coronavirus (2019 - nCoV) infection has spread rapidly in China and more than 70 countries around the world and thus become a public health event of international concern In addition to fever and respiratory symptoms, varying degrees of liver injury is also observed after 2019 - nCoV infection This article reviews the clinical features, pathology, pathogenic mechanism, and therapeutic strategies of liver injury associated with COVID - 19, hoping to provide a reference for clinical decision - making on the prevention and treatment of COVID - 19
Keywords	covid19
Publisher	WHO
Document type	Article
Note	WHO #Covidence: #827442
Database	COVID19

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Article ; Online: Angiogenic Factor with G Patch and FHA Domains 1 (AGGF1) Acts as Diagnostic Biomarker and Adverse Prognostic Factor of Hepatocellular Carcinoma (HCC): Evidence from Bioinformatic Analysis.

Wang, Wensheng / Zhu, Guangxi / Lai, Shujie / Guo, Yan / Yin, Xinru / Chen, Dongfeng / Wen, Liangzhi

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

2020 Volume 26, Page(s) e919896

Abstract: BACKGROUND Angiogenic factor with G patch and FHA domains 1 (AGGF1) is a novel identified initiator of angiogenesis through promoting the proliferation of endothelial cells. The continuous angiogenesis plays a key role in the growth, invasion, and ... ...

Abstract	BACKGROUND Angiogenic factor with G patch and FHA domains 1 (AGGF1) is a novel identified initiator of angiogenesis through promoting the proliferation of endothelial cells. The continuous angiogenesis plays a key role in the growth, invasion, and metastasis of hepatocellular carcinoma (HCC), while the diagnostic and prognostic roles of AGGF1 for HCC need to be further studied. MATERIAL AND METHODS The mRNA sequencing datasets and clinical features of HCC patients were extracted from The Cancer Genome Atlas database. The relationship between clinical features and AGGF1 expression was analyzed by Wilcoxon test. Further validation explorations were carried out using online database Oncomine. The diagnostic receiver operating characteristic curves of AGGF1 and alpha-fetoprotein were compared to examine the diagnostic efficacy of AGGF1. Survival analysis and Gene Set Enrichment Analysis were performed to explore the prediction value and potential mechanism of AGGF1 dysregulation in HCC. RESULTS Comprehensive overexpression of AGGF1 was observed in HCC, correlating with poor overall survival. Upregulated level of AGGF1 was statistically associated with poor differentiated histological grade, advanced cancer stage and T classification. AGGF1 was a more effective diagnostic marker than alpha-fetoprotein in HCC. Several important pathways related to HCC including pathway in cancer and P53 signaling pathway were differentially enriched in the high AGGF1 expression phenotype. CONCLUSIONS AGGF1 was a potential diagnostic and prognostic marker for poor clinical outcomes in HCC patients. Moreover, vital pathways regulated by AGGF1 in HCC may include regulation of autophagy, Wnt signaling pathway, pathway in cancer, cell cycle, and P53 signaling pathway.
MeSH term(s)	Angiogenic Proteins/metabolism ; Biomarkers, Tumor/metabolism ; Carcinoma, Hepatocellular/genetics ; Carcinoma, Hepatocellular/pathology ; Computational Biology ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Liver Neoplasms/genetics ; Liver Neoplasms/pathology ; Male ; Middle Aged ; Multivariate Analysis ; Neoplasm Grading ; Phenotype ; Prognosis ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Signal Transduction
Chemical Substances	AGGF1 protein, human ; Angiogenic Proteins ; Biomarkers, Tumor ; RNA, Messenger
Language	English
Publishing date	2020-02-24
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.919896
Database	MEDical Literature Analysis and Retrieval System OnLINE

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