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Article ; Online: Repositioning VU-0365114 as a novel microtubule-destabilizing agent for treating cancer and overcoming drug resistance.

Hsieh, Yao-Yu / Du, Jia-Ling / Yang, Pei-Ming

2023 Volume 18, Issue 2, Page(s) 386–414

Abstract: Microtubule-targeting agents represent one of the most successful classes of anticancer agents. However, the development of drug resistance and the appearance of adverse effects hamper their clinical implementation. Novel microtubule-targeting agents ... ...

Abstract	Microtubule-targeting agents represent one of the most successful classes of anticancer agents. However, the development of drug resistance and the appearance of adverse effects hamper their clinical implementation. Novel microtubule-targeting agents without such limitations are urgently needed. By employing a gene expression-based drug repositioning strategy, this study identifies VU-0365114, originally synthesized as a positive allosteric modulator of human muscarinic acetylcholine receptor M5 (M5 mAChR), as a novel type of tubulin inhibitor by destabilizing microtubules. VU-0365114 exhibits a broad-spectrum in vitro anticancer activity, especially in colorectal cancer cells. A tumor xenograft study in nude mice shows that VU-0365114 slowed the in vivo colorectal tumor growth. The anticancer activity of VU-0365114 is not related to its original target, M5 mAChR. In addition, VU-0365114 does not serve as a substrate of multidrug resistance (MDR) proteins, and thus, it can overcome MDR. Furthermore, a kinome analysis shows that VU-0365114 did not exhibit other significant off-target effects. Taken together, our study suggests that VU-0365114 primarily targets microtubules, offering potential for repurposing in cancer treatment, although more studies are needed before further drug development.
MeSH term(s)	Mice ; Animals ; Humans ; Drug Repositioning ; Cell Line, Tumor ; Mice, Nude ; Drug Resistance, Neoplasm ; Microtubules/metabolism ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Colorectal Neoplasms/drug therapy ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/metabolism
Chemical Substances	Antineoplastic Agents
Language	English
Publishing date	2023-10-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	2415106-3
ISSN	1878-0261 ; 1574-7891
ISSN (online)	1878-0261
ISSN	1574-7891
DOI	10.1002/1878-0261.13536
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Article: A Bioinformatics Analysis Identifies the Telomerase Inhibitor MST-312 for Treating High-STMN1-Expressing Hepatocellular Carcinoma.

Wang, Szu-Jen / Yang, Pei-Ming

Journal of personalized medicine

2021 Volume 11, Issue 5

Abstract: Hepatocellular carcinoma (HCC) is a relatively chemo-resistant tumor. Several multi-kinase inhibitors have been approved for treating advanced HCC. However, most HCC patients are highly refractory to these drugs. Therefore, the development of more ... ...

Abstract	Hepatocellular carcinoma (HCC) is a relatively chemo-resistant tumor. Several multi-kinase inhibitors have been approved for treating advanced HCC. However, most HCC patients are highly refractory to these drugs. Therefore, the development of more effective therapies for advanced HCC patients is urgently needed. Stathmin 1 (STMN1) is an oncoprotein that destabilizes microtubules and promotes cancer cell migration and invasion. In this study, cancer genomics data mining identified STMN1 as a prognosis biomarker and a therapeutic target for HCC. Co-expressed gene analysis indicated that STMN1 expression was positively associated with cell-cycle-related gene expression. Chemical sensitivity profiling of HCC cell lines suggested that High-STMN1-expressing HCC cells were the most sensitive to MST-312 (a telomerase inhibitor). Drug-gene connectivity mapping supported that MST-312 reversed the STMN1-co-expressed gene signature (especially BUB1B, MCM2/5/6, and TTK genes). In vitro experiments validated that MST-312 inhibited HCC cell viability and related protein expression (STMN1, BUB1B, and MCM5). In addition, overexpression of STMN1 enhanced the anticancer activity of MST-312 in HCC cells. Therefore, MST-312 can be used for treating STMN1-high expression HCC.
Language	English
Publishing date	2021-04-22
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2662248-8
ISSN	2075-4426
ISSN	2075-4426
DOI	10.3390/jpm11050332
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Article: PF-429242 exhibits anticancer activity in hepatocellular carcinoma cells via FOXO1-dependent autophagic cell death and IGFBP1-dependent anti-survival signaling.

Lin, Jiunn-Chang / Liu, Tsang-Pai / Chen, Yan-Bin / Yang, Pei-Ming

American journal of cancer research

2023 Volume 13, Issue 9, Page(s) 4125–4144

Abstract: Effective therapies for hepatocellular carcinoma (HCC) are urgently needed, as it is a type of cancer resistant to chemotherapy. Recent evidence showed that PF-429242, a membrane-bound transcription factor site-1 protease (MBTPS1) inhibitor, exhibited ... ...

Abstract	Effective therapies for hepatocellular carcinoma (HCC) are urgently needed, as it is a type of cancer resistant to chemotherapy. Recent evidence showed that PF-429242, a membrane-bound transcription factor site-1 protease (MBTPS1) inhibitor, exhibited anticancer activities against glioblastomas, renal cell carcinoma, and pancreatic cancer. However, its anticancer activity against HCC has yet to be investigated. In this study, we found that PF-429242 induced autophagy-dependent cell death in HCC cells. RNA-sequencing analysis indicated that the primary effect of PF-429242 was inhibition of the sterol regulatory element-binding protein (SREBP) signaling pathway. However, overexpression of SREBP proteins did not efficiently rescue PF-429242-induced autophagy and cell death. Mechanistically, PF-429242 induced forkhead box protein O1 (FOXO1)-dependent autophagic cell death. Additionally, PF-429242 caused FOXO1-independent upregulation of insulin-like growth factor-binding protein 1 (IGFBP1), ultimately leading to autophagy-independent cell death. The
Language	English
Publishing date	2023-09-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	2589522-9
ISSN	2156-6976
ISSN	2156-6976
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Article ; Online: Long Non-Coding RNA

Ko, Ching-Chung / Hsieh, Yao-Yu / Yang, Pei-Ming

International journal of molecular sciences

2022 Volume 23, Issue 12

Abstract: The epithelial-to-mesenchymal transition (EMT) describes a biological process in which polarized epithelial cells are converted into highly motile mesenchymal cells. It promotes cancer cell dissemination, allowing them to form distal metastases, and also ...

Abstract	The epithelial-to-mesenchymal transition (EMT) describes a biological process in which polarized epithelial cells are converted into highly motile mesenchymal cells. It promotes cancer cell dissemination, allowing them to form distal metastases, and also involves drug resistance in metastatic cancers. Transforming growth factor β (TGFβ) is a multifunctional cytokine that plays essential roles in development and carcinogenesis. It is a major inducer of the EMT. The MIR31 host gene (
MeSH term(s)	Carcinoma, Pancreatic Ductal/pathology ; Cell Line, Tumor ; Cell Movement ; Epithelial-Mesenchymal Transition ; Gene Expression Regulation, Neoplastic ; Humans ; Pancreatic Neoplasms/pathology ; RNA, Long Noncoding/genetics ; Transforming Growth Factor beta/metabolism ; Pancreatic Neoplasms
Chemical Substances	RNA, Long Noncoding ; Transforming Growth Factor beta
Language	English
Publishing date	2022-06-12
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/ijms23126559
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Article ; Online: Scutellaria baicalensis

Wu, Tung-Ho / Lin, Tung-Yi / Yang, Pei-Ming / Li, Wen-Tai / Yeh, Chau-Ting / Pan, Tai-Long

International journal of molecular sciences

2024 Volume 25, Issue 5

Abstract: Hepatocellular carcinoma is one of the most common malignant tumors in the world and shows strong metastatic potential. Current medicine for hepatocellular carcinoma therapy is invalid, ... ...

Abstract	Hepatocellular carcinoma is one of the most common malignant tumors in the world and shows strong metastatic potential. Current medicine for hepatocellular carcinoma therapy is invalid, while
MeSH term(s)	Humans ; Apoptosis ; Carcinoma, Hepatocellular/drug therapy ; Liver Neoplasms/drug therapy ; Plant Extracts/pharmacology ; Scutellaria baicalensis ; Tumor Suppressor Protein p53
Chemical Substances	Plant Extracts ; Scutellaria baicalensis extract ; Tumor Suppressor Protein p53
Language	English
Publishing date	2024-03-06
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/ijms25053073
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Article ; Online: Overexpression of miR-21-5p in colorectal cancer cells promotes self-assembly of E-cadherin-dependent multicellular tumor spheroids.

Li, Albert / Yang, Pei-Ming

Tissue & cell

2020 Volume 65, Page(s) 101365

Abstract: Three-dimensional (3D) multicellular tumor spheroid (MCTS) cultures are increasingly popular as an in vitro tumor model for drug screening because they can mimic the complexity and heterogeneity of tumors compared to 2D monolayer cell cultures. The ... ...

Abstract	Three-dimensional (3D) multicellular tumor spheroid (MCTS) cultures are increasingly popular as an in vitro tumor model for drug screening because they can mimic the complexity and heterogeneity of tumors compared to 2D monolayer cell cultures. The oncogenic microRNA, miR-21-5p (hereafter denoted as miR-21), is one of the most upregulated miRNAs in colorectal cancer (CRC). Herein, we established a stable miR-21-overexpressing clone in the DLD-1 human CRC cell line to investigate its impact on MCTS formation. We found that miR-21 overexpression enhanced cell-cell interactions/aggregations in both 2D monolayer and 3D suspension cultures. Cell aggregates in 3D suspension culture further formed MCTSs in miR-21-overexpressing cells. miR-21 overexpression was associated with the upregulation of proteins involved in E-cadherin-associated cell-cell adhesion. Furthermore, miR-21 induction of MCTSs could be reversed by the antibody-induced blockade of E-cadherin. Our results showed that miR-21 overexpression promoted MCTS formation through enhancing E-cadherin-dependent cell-cell interactions, which represents an advance in vitro model for investigating CRC biology.
MeSH term(s)	Cadherins/metabolism ; Cell Adhesion/drug effects ; Cell Line, Tumor ; Colorectal Neoplasms/genetics ; Culture Media/pharmacology ; Gene Expression Regulation, Neoplastic ; Humans ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Neoplastic Stem Cells/metabolism ; Neoplastic Stem Cells/pathology ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Spheroids, Cellular/metabolism ; Spheroids, Cellular/pathology
Chemical Substances	Cadherins ; Culture Media ; MIRN21 microRNA, human ; MicroRNAs ; RNA, Messenger
Language	English
Publishing date	2020-04-10
Publishing country	Scotland
Document type	Journal Article
ZDB-ID	204424-9
ISSN	1532-3072 ; 0040-8166
ISSN (online)	1532-3072
ISSN	0040-8166
DOI	10.1016/j.tice.2020.101365
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Article ; Online: Long Non-Coding RNA MIR31HG Promotes the Transforming Growth Factor β-Induced Epithelial-Mesenchymal Transition in Pancreatic Ductal Adenocarcinoma Cells

Ching-Chung Ko / Yao-Yu Hsieh / Pei-Ming Yang

International Journal of Molecular Sciences, Vol 23, Iss 6559, p

2022 Volume 6559

Abstract	The epithelial-to-mesenchymal transition (EMT) describes a biological process in which polarized epithelial cells are converted into highly motile mesenchymal cells. It promotes cancer cell dissemination, allowing them to form distal metastases, and also involves drug resistance in metastatic cancers. Transforming growth factor β (TGFβ) is a multifunctional cytokine that plays essential roles in development and carcinogenesis. It is a major inducer of the EMT. The MIR31 host gene ( MIR31HG ) is a newly identified long non-coding (lnc)RNA that exhibits ambiguous roles in cancer. In this study, a cancer genomics analysis predicted that MIR31HG overexpression was positively correlated with poorer disease-free survival of pancreatic ductal adenocarcinoma (PDAC) patients, which was associated with upregulation of genes related to TGFβ signaling and the EMT. In vitro evidence demonstrated that TGFβ induced MIR31HG expression in PDAC cells, and knockdown of MIR31HG expression reversed TGFβ-induced EMT phenotypes and cancer cell migration. Therefore, MIR31HG has an oncogenic role in PDAC by promoting the EMT.
Keywords	epithelial-to-mesenchymal transition ; long non-coding RNA ; metastasis ; pancreatic ductal adenocarcinoma ; transforming growth factor β ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	610
Language	English
Publishing date	2022-06-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: A Bioinformatics Analysis Identifies the Telomerase Inhibitor MST-312 for Treating High-STMN1-Expressing Hepatocellular Carcinoma

Szu-Jen Wang / Pei-Ming Yang

Journal of Personalized Medicine, Vol 11, Iss 332, p

2021 Volume 332

Abstract	Hepatocellular carcinoma (HCC) is a relatively chemo-resistant tumor. Several multi-kinase inhibitors have been approved for treating advanced HCC. However, most HCC patients are highly refractory to these drugs. Therefore, the development of more effective therapies for advanced HCC patients is urgently needed. Stathmin 1 (STMN1) is an oncoprotein that destabilizes microtubules and promotes cancer cell migration and invasion. In this study, cancer genomics data mining identified STMN1 as a prognosis biomarker and a therapeutic target for HCC. Co-expressed gene analysis indicated that STMN1 expression was positively associated with cell-cycle-related gene expression. Chemical sensitivity profiling of HCC cell lines suggested that High-STMN1-expressing HCC cells were the most sensitive to MST-312 (a telomerase inhibitor). Drug–gene connectivity mapping supported that MST-312 reversed the STMN1-co-expressed gene signature (especially BUB1B, MCM2/5/6, and TTK genes). In vitro experiments validated that MST-312 inhibited HCC cell viability and related protein expression (STMN1, BUB1B, and MCM5). In addition, overexpression of STMN1 enhanced the anticancer activity of MST-312 in HCC cells. Therefore, MST-312 can be used for treating STMN1-high expression HCC.
Keywords	bioinformatics ; cancer genomics ; cell cycle ; hepatocellular carcinoma ; stathmin 1 ; Medicine ; R
Language	English
Publishing date	2021-04-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Repurposing of ingenol mebutate for treating human colorectal cancer by targeting S100 calcium-binding protein A4 (S100A4).

Hsieh, Yao-Yu / Cheng, Ya-Wen / Wei, Po-Li / Yang, Pei-Ming

Toxicology and applied pharmacology

2022 Volume 449, Page(s) 116134

Abstract: Colorectal cancer (CRC) is the world's second most common cause of cancer-related death. Novel treatments are still urgently needed. S100 calcium-binding protein A4 (S100A4) was demonstrated to be an anticancer therapeutic target. Herein, we found that ... ...

Abstract	Colorectal cancer (CRC) is the world's second most common cause of cancer-related death. Novel treatments are still urgently needed. S100 calcium-binding protein A4 (S100A4) was demonstrated to be an anticancer therapeutic target. Herein, we found that higher S100A4 expression was associated with a poorer prognosis in publicly available cohorts and a Taiwanese CRC patient cohort. To identify repurposed S100A4 inhibitors, we mined the Connectivity Map (CMap) database for clinical drugs mimicking the S100A4-knockdown gene signature. Ingenol mebutate, derived from the sap of the plant Euphorbia peplus, is approved as a topical treatment for actinic keratosis. The CMap analysis predicted ingenol mebutate as a potent S100A4 inhibitor. Indeed, both messenger RNA and protein levels of S100A4 were attenuated by ingenol mebutate in human CRC cells. In addition, CRC cells with higher S100A4 expressions and/or the wild-type p53 gene were more sensitive to ingenol mebutate, and their migration and invasion were inhibited by ingenol mebutate. Therefore, our results suggest the repurposing of ingenol mebutate for treating CRC by targeting S100A4.
MeSH term(s)	Colorectal Neoplasms/drug therapy ; Colorectal Neoplasms/genetics ; Diterpenes/pharmacology ; Diterpenes/therapeutic use ; Drug Repositioning ; Humans ; S100 Calcium-Binding Protein A4/antagonists & inhibitors ; S100 Calcium-Binding Protein A4/genetics
Chemical Substances	3-ingenyl angelate ; Diterpenes ; S100 Calcium-Binding Protein A4 ; S100A4 protein, human (142662-27-9)
Language	English
Publishing date	2022-06-18
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	204477-8
ISSN	1096-0333 ; 0041-008X
ISSN (online)	1096-0333
ISSN	0041-008X
DOI	10.1016/j.taap.2022.116134
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Article ; Online: PERK/ATF4-Dependent ZFAS1 Upregulation Is Associated with Sorafenib Resistance in Hepatocellular Carcinoma Cells.

Lin, Jiunn-Chang / Yang, Pei-Ming / Liu, Tsang-Pai

International journal of molecular sciences

2021 Volume 22, Issue 11

Abstract: Sorafenib, a multi-kinase inhibitor, is the first-line treatment for advanced hepatocellular carcinoma (HCC) patients. However, this drug only provides a short improvement of patients' overall survival, and drug resistance is commonly developed. Thus, ... ...

Abstract	Sorafenib, a multi-kinase inhibitor, is the first-line treatment for advanced hepatocellular carcinoma (HCC) patients. However, this drug only provides a short improvement of patients' overall survival, and drug resistance is commonly developed. Thus, the identification of resistant factor(s) or biomarker(s) is needed to develop more efficient therapeutic strategies. Long, non-coding RNAs (lncRNAs) have recently been viewed as attractive cancer biomarkers and drive many important cancer phenotypes. A lncRNA,
MeSH term(s)	Activating Transcription Factor 4/metabolism ; Carcinoma, Hepatocellular/genetics ; Carcinoma, Hepatocellular/metabolism ; Carcinoma, Hepatocellular/mortality ; Carcinoma, Hepatocellular/pathology ; Cell Line, Tumor ; Drug Resistance, Neoplasm/genetics ; Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; Humans ; Kaplan-Meier Estimate ; Liver Neoplasms/genetics ; Liver Neoplasms/metabolism ; Liver Neoplasms/mortality ; Liver Neoplasms/pathology ; Prognosis ; Protein Kinase Inhibitors/pharmacology ; RNA, Long Noncoding/genetics ; Sequence Analysis, RNA ; Sorafenib/pharmacology ; eIF-2 Kinase/metabolism
Chemical Substances	ATF4 protein, human ; Protein Kinase Inhibitors ; RNA, Long Noncoding ; ZFAS1 long non-coding RNA, human ; Activating Transcription Factor 4 (145891-90-3) ; Sorafenib (9ZOQ3TZI87) ; EIF2AK3 protein, human (EC 2.7.11.1) ; eIF-2 Kinase (EC 2.7.11.1)
Language	English
Publishing date	2021-05-29
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/ijms22115848
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