LIVIVO - The Search Portal for Life Sciences

zur deutschen Oberfläche wechseln
Advanced search

Search results

Result 1 - 10 of total 41

Search options

  1. Article ; Online: Alleviating CB2-Dependent ER Stress and Mitochondrial Dysfunction Improves Chronic Cerebral Hypoperfusion-Induced Cognitive Impairment.

    Wang, Da Peng / Kang, Kai / Hai, Jian / Lv, Qiao Li / Wu, Zhe Bao

    Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology

    2024  Volume 19, Issue 1, Page(s) 1

    Abstract: Augmentation of endoplasmic reticulum (ER) stress may trigger excessive oxidative stress, which induces mitochondrial dysfunction. The fatty acid amide hydrolase inhibitor, URB597, shows anti-oxidation characteristics in multiple neurological disorders. ... ...

    Abstract Augmentation of endoplasmic reticulum (ER) stress may trigger excessive oxidative stress, which induces mitochondrial dysfunction. The fatty acid amide hydrolase inhibitor, URB597, shows anti-oxidation characteristics in multiple neurological disorders. The present study aimed to determine whether inhibition of ER stress was involved in the protective effects of URB597 against chronic cerebral hypoperfusion (CCH)-induced cognitive impairment. Hippocampal HT-22 cells were exposed to oxygen-glucose deprivation. The cell viability, apoptosis, ER stress, mitochondrial ATP, and oxidative stress levels were assessed following treatment with URB597, benzenebutyric acid (4-PBA), and thapsigargin (TG). Furthermore, the effects of URB597 on ER stress and related pathways were investigated in the CCH animal model, including Morris water maze testing of cognition, western blotting analysis of ER stress signaling, and transmission electron microscopy of mitochondrial and ER ultrastructure changes. The results suggested that cerebral ischemia caused ER stress with upregulation of ER stress signaling-related proteins, mitochondrial dysfunction, neuronal apoptosis, ultrastructural injuries of mitochondria-associated ER membranes, and cognitive decline. Co-immunoprecipitation experiments confirmed the interaction between CB2 and β-Arrestin1. Inhibiting ER stress by URB597 improved these changes by activating CB2/β-Arrestin1 signaling, which was reversed by the CB2 antagonist, AM630. Together, the results identified a novel mechanism of URB597, involving CCH-induced cognitive impairment alleviation of CB2-dependent ER stress and mitochondrial dysfunction. Furthermore, this study identified CB2 as a potential target for therapy of ischemic cerebrovascular diseases.
    MeSH term(s) Rats ; Animals ; Rats, Sprague-Dawley ; Brain Ischemia/drug therapy ; Cognitive Dysfunction/drug therapy ; Cognitive Dysfunction/etiology ; Mitochondrial Diseases ; Endoplasmic Reticulum Stress ; Apoptosis ; Benzamides ; Carbamates
    Chemical Substances cyclohexyl carbamic acid 3'-carbamoylbiphenyl-3-yl ester ; Benzamides ; Carbamates
    Language English
    Publishing date 2024-01-12
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2227405-4
    ISSN 1557-1904 ; 1557-1890
    ISSN (online) 1557-1904
    ISSN 1557-1890
    DOI 10.1007/s11481-024-10098-x
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

    More links

    Kategorien

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  2. Article ; Online: Roles of lncRNA-MALAT1 in the Progression and Prognosis of Gliomas.

    Ji, Yu-Long / Kang, Kai / Lv, Qiao-Li / Wang, Da-Peng

    Mini reviews in medicinal chemistry

    2023  

    Abstract: Long noncoding RNAs (lncRNAs) represent a large subgroup of RNA transcripts that lack the function of coding proteins and may be essential universal genes involved in carcinogenesis and metastasis. LncRNA metastasis-associated lung adenocarcinoma ... ...

    Abstract Long noncoding RNAs (lncRNAs) represent a large subgroup of RNA transcripts that lack the function of coding proteins and may be essential universal genes involved in carcinogenesis and metastasis. LncRNA metastasis-associated lung adenocarcinoma transcript 1 (lncRNAMALAT1) is overexpressed in various human tumors, including gliomas. However, the biological function and molecular mechanism of action of lncRNA-MALAT1 in gliomas have not yet been systematically elucidated. Accumulating evidence suggests that the abnormal expression of lncRNA-MALAT1 in gliomas is associated with various physical properties of the glioma, such as tumor growth, metastasis, apoptosis, drug resistance, and prognosis. Furthermore, lncRNAs, as tumor progression and prognostic markers in gliomas, may affect tumorigenesis, proliferation of glioma stem cells, and drug resistance. In this review, we summarize the knowledge on the biological functions and prognostic value of lncRNA-MALAT1 in gliomas. This mini-review aims to deepen the understanding of lncRNA-MALAT1 as a novel potential therapeutic target for the individualized precision treatment of gliomas.
    Language English
    Publishing date 2023-10-06
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 2104081-3
    ISSN 1875-5607 ; 1389-5575
    ISSN (online) 1875-5607
    ISSN 1389-5575
    DOI 10.2174/0113895575253875230922055711
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 5891: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  3. Article ; Online: VEGF-A ameliorates ischemia hippocampal neural injury via regulating autophagy and Akt/CREB signaling in a rat model of chronic cerebral hypoperfusion.

    Kang, Kai / Wang, Da-Peng / Lv, Qiao-Li / Chen, Feng

    Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association

    2023  Volume 32, Issue 11, Page(s) 107367

    Abstract: Objective: Chronic cerebral hypoperfusion (CCH) can cause a series of pathophysiological processes, including neuronal autophagy and apoptosis. VEGF-A has been reported to affect angiogenesis and neurogenesis in many CNS diseases. However, its effects ... ...

    Abstract Objective: Chronic cerebral hypoperfusion (CCH) can cause a series of pathophysiological processes, including neuronal autophagy and apoptosis. VEGF-A has been reported to affect angiogenesis and neurogenesis in many CNS diseases. However, its effects on neuronal autophagy and apoptosis, as well as the underlying mechanisms in CCH remain unclear.
    Methods: To address these issues, the CCH model was established by permanent bilateral common carotid artery occlusion (2VO). Rats were sacrificed at different stages of CCH. Hippocampal morphological and ultrastructural changes were detected using HE staining and electron microscopy. The immunoreactivities of microtubule-associated protein 1 light chain 3 (LC3) and phospho-cAMP response element binding protein (p-CREB) were examined by immunofluorescence staining. The neuronal apoptosis was detected via TUNEL staining. The levels of LC3-II, Beclin-1, Akt, p-Akt, CREB, p-CREB, Caspase-3, and Bad were accessed by Western blotting. Furthermore, mouse hippocampal HT22 neurons received the oxygen and glucose deprivation (OGD) treatment, VEGF-A treatment, and GSK690693 (an Akt inhibitor) treatment, respectively.
    Results: LC3-II protein started to increase at 3 days of CCH, peaked at 4 weeks of CCH, then decreased. CCH increased the levels of LC3-II, Caspase-3, and Bad, and decreased the levels of p-Akt, CREB, and p-CREB, which were reversed by VEGF-A treatment. VEGF-A also improved CCH-induced neuronal ultrastructural injuries and apoptosis in the hippocampus in vitro. In HT22, the anti-apoptosis and pro-phosphorylation of VEGF-A were reversed by GSK690693.
    Conclusion: Present results provide a novel neuroprotective effect of VEGF-A in CCH that is related to the inhibition of neuronal autophagy and activation of the Akt/CREB signaling, suggesting a potential therapeutic strategy for ischemic brain damage.
    Language English
    Publishing date 2023-09-19
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1131675-5
    ISSN 1532-8511 ; 1052-3057
    ISSN (online) 1532-8511
    ISSN 1052-3057
    DOI 10.1016/j.jstrokecerebrovasdis.2023.107367
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 3519: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  4. Article ; Online: CircRNAs in tumor immunity and immunotherapy: Perspectives from innate and adaptive immunity.

    Yu, Lu-Lu / Xiao, Qi / Yu, Bing / Lv, Qiao-Li / Liu, Zhao-Qian / Yin, Ji-Ye

    Cancer letters

    2023  Volume 564, Page(s) 216219

    Abstract: Tumor immunotherapy is a new therapeutic approach that has been evolving in the last decade and has dramatically changed the treatment options for cancer. Circular RNAs (circRNAs) are non-coding RNAs (ncRNAs) with high stability, tissue-specific and cell- ...

    Abstract Tumor immunotherapy is a new therapeutic approach that has been evolving in the last decade and has dramatically changed the treatment options for cancer. Circular RNAs (circRNAs) are non-coding RNAs (ncRNAs) with high stability, tissue-specific and cell-specific expression. There is growing evidence that circRNAs are involved in the regulation of both adaptive and innate immunity. They play important roles in tumor immunotherapy by affecting macrophage, NK and T cell function. The high stability and tissue specificity make them ideal candidate biomarkers for therapeutic effects. CircRNAs also represent one of promising targets or adjuvant for immunotherapy. Investigations in this field progress rapidly and provide essential support for the diagnosis, prognosis and treatment guidance of cancers in the future. In this review, we summarize the role of circRNAs on tumor immunity from the viewpoint of innate and adaptive immunity, and explore the role of circRNAs in tumor immunotherapy.
    MeSH term(s) Humans ; RNA, Circular/genetics ; Biomarkers ; Neoplasms/genetics ; Neoplasms/therapy ; Adaptive Immunity/genetics ; Immunotherapy
    Chemical Substances RNA, Circular ; Biomarkers
    Language English
    Publishing date 2023-05-03
    Publishing country Ireland
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 195674-7
    ISSN 1872-7980 ; 0304-3835
    ISSN (online) 1872-7980
    ISSN 0304-3835
    DOI 10.1016/j.canlet.2023.216219
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 1177: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  5. Article ; Online: URB597 and Andrographolide Improve Brain Microvascular Endothelial Cell Permeability and Apoptosis by Reducing Oxidative Stress and Inflammation Associated with Activation of Nrf2 Signaling in Oxygen-Glucose Deprivation.

    Wang, Da-Peng / Kang, Kai / Sun, Jun / Lin, Qi / Lv, Qiao-Li / Hai, Jian

    Oxidative medicine and cellular longevity

    2022  Volume 2022, Page(s) 4139330

    Abstract: Ischemic stroke, a cerebrovascular disease worldwide, triggers a cascade of pathophysiological events, including blood-brain barrier (BBB) breakdown. Brain microvascular endothelial cells (BMECs) play a vital role in maintaining BBB function. The injury ... ...

    Abstract Ischemic stroke, a cerebrovascular disease worldwide, triggers a cascade of pathophysiological events, including blood-brain barrier (BBB) breakdown. Brain microvascular endothelial cells (BMECs) play a vital role in maintaining BBB function. The injury of BMECs may worsen neurovascular dysfunction and patients' prognosis. Therefore, uncover the principal molecular mechanisms involved in BBB disruption in stroke becomes pressing. The endocannabinoid system (ECS) has been implicated in increasingly physiological functions, both in neurometabolism and cerebrovascular regulation. Modulating its activities by the fatty acid amide hydrolase (FAAH) shows anti-inflammatory characteristics. Andrographolide (AG), one Chinese herbal ingredient, has also attracted attention for its role in immunomodulatory and as a therapeutic target in BBB disorders. Recently, the FAAH inhibitor URB597 and AG have important regulatory effects on neuronal and vascular cells in ischemia. However, the effects of URB597 and AG on BMEC permeability and apoptosis in oxygen-glucose deprivation (OGD) and the underlying mechanisms remain unclear. To address these issues, cultured BMECs (bEnd.3 cells) were exposed to OGD. The cell viability, permeability, tube formation, and apoptosis were assessed following treatment with URB597, AG, and cotreatment. Mitochondrial membrane potential (MMP), reactive oxygen species (ROS), superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA), proinflammatory factors, tight junction (TJ) proteins, and oxidative stress-mediated Nrf2 signaling were also investigated. Results revealed that OGD broke the endothelial barrier, cell viability, MMP, and tube formation, which was reversed by URB597 and AG. OGD-induced enhancement of ROS, MDA, and apoptosis was reduced after drug interventions. URB597 and AG exhibited antioxidant/anti-inflammatory and mitochondrial protective effects by activating Nrf2 signaling. These findings indicated that URB597 and AG protect BMECs against OGD-induced endothelial permeability impairment and apoptosis by reducing mitochondrial oxidative stress and inflammation associated with activation of Nrf2 signaling. URB597 and AG showing the vascular protection may have therapeutic potential for the BBB damage in ischemic cerebrovascular diseases.
    MeSH term(s) Anti-Inflammatory Agents/metabolism ; Anti-Inflammatory Agents/pharmacology ; Apoptosis ; Benzamides ; Brain/metabolism ; Carbamates ; Diterpenes ; Endothelial Cells/metabolism ; Glucose/metabolism ; Humans ; Inflammation/drug therapy ; Inflammation/metabolism ; Matrix Metalloproteinases/metabolism ; NF-E2-Related Factor 2/metabolism ; Oxidative Stress ; Oxygen/metabolism ; Permeability ; Reactive Oxygen Species/metabolism
    Chemical Substances Anti-Inflammatory Agents ; Benzamides ; Carbamates ; Diterpenes ; NF-E2-Related Factor 2 ; Reactive Oxygen Species ; cyclohexyl carbamic acid 3'-carbamoylbiphenyl-3-yl ester ; andrographolide (410105JHGR) ; Matrix Metalloproteinases (EC 3.4.24.-) ; Glucose (IY9XDZ35W2) ; Oxygen (S88TT14065)
    Language English
    Publishing date 2022-05-12
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2455981-7
    ISSN 1942-0994 ; 1942-0994
    ISSN (online) 1942-0994
    ISSN 1942-0994
    DOI 10.1155/2022/4139330
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  6. Article ; Online: Bacoside a inhibits the growth of glioma by promoting apoptosis and autophagy in U251 and U87 cells.

    Liu, Hai-Yun / Ji, Yu-Long / Du, Hong / Chen, Shu-Hui / Wang, Da-Peng / Lv, Qiao-Li

    Naunyn-Schmiedeberg's archives of pharmacology

    2023  Volume 397, Issue 4, Page(s) 2105–2120

    Abstract: Bacoside A (gypenoside, Gyp) is a potent bioactive compound derived from Gynostemma pentaphyllum, known to exert inhibitory effects on various malignant tumors. However, the effects of Gyp on glioma as well as the underlying mechanisms remain unclear. In ...

    Abstract Bacoside A (gypenoside, Gyp) is a potent bioactive compound derived from Gynostemma pentaphyllum, known to exert inhibitory effects on various malignant tumors. However, the effects of Gyp on glioma as well as the underlying mechanisms remain unclear. In the present study, we first conducted a comprehensive investigation into the anti-glioma potential of gypenosides using network pharmacology to identify potential glioma-related targets. Protein-protein interaction networks were assembled, and GO and KEGG enrichment analyses were performed for shared targets. Experimental validation involved assessing the viability of U251 and U87 cell lines using the MTS method. Furthermore, trans-well and scratch migration assays evaluated the cell migration, while flow cytometry and Hoechst 33342 staining were utilized for apoptosis assessment. The study also monitored changes in autophagy flow through fluorescence microscopy. The expression levels of proteins pertinent to migration, apoptosis, and autophagy were tested using Western blotting. Findings revealed that Gyp upregulated apoptosis-related proteins (Bax and cleaved caspase-9), downregulated anti-apoptotic protein Bcl-2, and migration-associated matrix metalloproteinases (MMP-2 and MMP-9). Furthermore, autophagy-related proteins (Beclin1 and LC3 II) were upregulated, and p62 protein expression was downregulated. Gyp displayed considerable potential in suppressing glioma progression by inhibiting cell proliferation, invasion, and migration and promoting apoptosis and autophagy. Gyp may offer potential clinical therapeutic choices in glioma management.
    MeSH term(s) Humans ; Apoptosis ; Glioma/drug therapy ; Glioma/pathology ; Apoptosis Regulatory Proteins/metabolism ; Cell Proliferation ; Autophagy ; Cell Line, Tumor ; Saponins ; Triterpenes
    Chemical Substances bacoside A ; Apoptosis Regulatory Proteins ; Saponins ; Triterpenes
    Language English
    Publishing date 2023-10-02
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 121471-8
    ISSN 1432-1912 ; 0028-1298
    ISSN (online) 1432-1912
    ISSN 0028-1298
    DOI 10.1007/s00210-023-02724-x
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Ud II Zs.5: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  7. Article ; Online: Progress of engineered bacteria for tumour therapy.

    Xia, Xue / Zhang, Jing-Wen / Zhao, Bing / Zhang, Min / Chen, Zhang-Ren / Zhang, Bing-Feng / Ji, Yu-Long / Wang, Xia / Xiong, Wen-Min / Li, Jia-Wei / Lv, Qiao-Li

    International immunopharmacology

    2024  Volume 132, Page(s) 111935

    Abstract: Finding novel therapeutic modalities, improving drug delivery efficiency and targeting, and reducing the immune escape of tumor cells are currently hot topics in the field of tumor therapy. Bacterial therapeutics have proven highly effective in ... ...

    Abstract Finding novel therapeutic modalities, improving drug delivery efficiency and targeting, and reducing the immune escape of tumor cells are currently hot topics in the field of tumor therapy. Bacterial therapeutics have proven highly effective in preventing tumor spread and recurrence, used alone or in combination with traditional therapies. In recent years, a growing number of researchers have significantly improved the targeting and penetration of bacteria by using genetic engineering technology, which has received widespread attention in the field of tumor therapy. In this paper, we provide an overview and assessment of the advancements made in the field of tumor therapy using genetically engineered bacteria. We cover three major aspects: the development of engineered bacteria, their integration with other therapeutic techniques, and the current state of clinical trials. Lastly, we discuss the limitations and challenges that are currently being faced in the utilization of engineered bacteria for tumor therapy.
    MeSH term(s) Humans ; Neoplasms/therapy ; Neoplasms/immunology ; Animals ; Genetic Engineering ; Bacteria/genetics ; Immunotherapy/methods ; Drug Delivery Systems
    Language English
    Publishing date 2024-04-09
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 2043785-7
    ISSN 1878-1705 ; 1567-5769
    ISSN (online) 1878-1705
    ISSN 1567-5769
    DOI 10.1016/j.intimp.2024.111935
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 5408: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  8. Article ; Online: Correction to: Akt/FoxM1 signaling pathway-mediated upregulation of MYBL2 promotes progression of human glioma.

    Zhang, Xue / Lv, Qiao-Li / Huang, Yuan-Tao / Zhang, Li-Hua / Zhou, Hong-Hao

    Journal of experimental & clinical cancer research : CR

    2021  Volume 40, Issue 1, Page(s) 181

    Language English
    Publishing date 2021-06-02
    Publishing country England
    Document type Published Erratum
    ZDB-ID 803138-1
    ISSN 1756-9966 ; 0392-9078
    ISSN (online) 1756-9966
    ISSN 0392-9078
    DOI 10.1186/s13046-021-01992-w
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 2065: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  9. Article ; Online: lncRNA ZNF674-AS1 inhibits the migration, invasion and epithelial-mesenchymal transition of thyroid cancer cells by modulating the miR-181a/SOCS4 axis.

    Le, Fei / Li, Hong-Mi / Lv, Qiao-Li / Chen, Jun-Jun / Lin, Qian-Xia / Ji, Yu-Long / Yi, Bo

    Molecular and cellular endocrinology

    2022  Volume 544, Page(s) 111551

    Abstract: Thyroid cancer (TC) is a very common endocrine cancer worldwide. Further understanding and revealing the molecular mechanism underlying thyroid cancer are indispensable for the development of effective diagnosis and treatments. Long non-coding RNAs ( ... ...

    Abstract Thyroid cancer (TC) is a very common endocrine cancer worldwide. Further understanding and revealing the molecular mechanism underlying thyroid cancer are indispensable for the development of effective diagnosis and treatments. Long non-coding RNAs (lncRNAs), a series of non-coding RNAs with a length of >200 nts, have been regarded as crucial regulators of many cancers playing a tumor suppressive or oncogenic role, depending on circumstances. lncRNA ZNF674-AS1 was reported to be abnormally expressed in TC, but the exact mechanism remains unclear. This study aims to probe the mechanism and roles of ZNF674-AS1 in TC. The expression patterns of RNAs and proteins were determined via qRT-PCR and western blotting, respectively. Cell proliferation, migration and invasion were detected using MTT and Transwell assays. ZNF674-AS1 and SOCS4 expression were remarkably reduced while miR-181a was upregulated in TC tissues and cells. Enforced expression of ZNF674-AS1 inhibited proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) in vitro and reduced tumour growth in vivo. Mechanistic assays verified that ZNF674-AS1 directly interacted with miR-181a to increase SOCS4 expression. In addition, miR-181a overexpression aggravated proliferation, metastasis and EMT by inhibiting SOCS4. Interestingly, inhibition of miR-181a diminished the promoting effects of ZNF674-AS1 silencing on the malignant behaviours of TC cells. These data illustrated that ZNF674-AS1 alleviated TC progression by modulating the miR-181a/SOCS4 axis (graphical abstract), further suggesting that ZNF674-AS1 might be used as a therapheutic target in TC treatment.
    MeSH term(s) Cell Line, Tumor ; Cell Movement/genetics ; Cell Proliferation/genetics ; Epithelial-Mesenchymal Transition/genetics ; Gene Expression Regulation, Neoplastic ; Humans ; MicroRNAs/genetics ; MicroRNAs/metabolism ; RNA, Long Noncoding/genetics ; Suppressor of Cytokine Signaling Proteins/genetics ; Suppressor of Cytokine Signaling Proteins/metabolism ; Thyroid Neoplasms/genetics
    Chemical Substances MicroRNAs ; RNA, Long Noncoding ; SOCS4 protein, human ; Suppressor of Cytokine Signaling Proteins
    Language English
    Publishing date 2022-01-04
    Publishing country Ireland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 187438-x
    ISSN 1872-8057 ; 0303-7207
    ISSN (online) 1872-8057
    ISSN 0303-7207
    DOI 10.1016/j.mce.2021.111551
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 1127: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  10. Article ; Online: Drug screening against F13 protein, the target of tecovirimat, as potential therapies for monkeypox virus.

    Chen, Zhang-Ren / Lv, Qiao-Li / Peng, Hong-Wei / Liu, Xiao-Yi / Hu, Wen-Lei / Hu, Jin-Fang

    The Journal of infection

    2022  Volume 86, Issue 2, Page(s) 154–225

    MeSH term(s) Humans ; Monkeypox virus ; Drug Evaluation, Preclinical ; Benzamides
    Chemical Substances Benzamides
    Language English
    Publishing date 2022-11-25
    Publishing country England
    Document type Letter ; Research Support, Non-U.S. Gov't
    ZDB-ID 424417-5
    ISSN 1532-2742 ; 0163-4453
    ISSN (online) 1532-2742
    ISSN 0163-4453
    DOI 10.1016/j.jinf.2022.11.018
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 1501: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MG 48: Show issues

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

To top