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Article: Editorial: High-Throughput Sequencing-Based Investigation of Chronic Disease Markers and Mechanisms.

Orlov, Yuriy L / Chen, Wen-Lian / Sekacheva, Marina I / Cai, Guoshuai / Li, Hua

2022 Volume 13, Page(s) 922206

Language	English
Publishing date	2022-06-21
Publishing country	Switzerland
Document type	Editorial
ZDB-ID	2606823-0
ISSN	1664-8021
ISSN	1664-8021
DOI	10.3389/fgene.2022.922206
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Article: Cisplatin-Resistant Gastric Cancer Cells Promote the Chemoresistance of Cisplatin-Sensitive Cells via the Exosomal RPS3-Mediated PI3K-Akt-Cofilin-1 Signaling Axis.

Sun, Meng-Yao / Xu, Bo / Wu, Qiu-Xue / Chen, Wen-Lian / Cai, Si / Zhang, Hui / Tang, Qing-Feng

Frontiers in cell and developmental biology

2021 Volume 9, Page(s) 618899

Abstract: Cisplatin is an important agent in first-line chemotherapy against gastric cancer (GC). However, consequential drug resistance limits its effectiveness for the treatment of GC. In this study, a cisplatin resistant gastric cancer cell line SGC7901R was ... ...

Abstract	Cisplatin is an important agent in first-line chemotherapy against gastric cancer (GC). However, consequential drug resistance limits its effectiveness for the treatment of GC. In this study, a cisplatin resistant gastric cancer cell line SGC7901R was determined by LC-MS/MS with increased exosomal levels of RPS3 protein. SGC7901R cell-derived exosomes were readily taken up by cisplatin-sensitive SGC7901S cells, thus triggering off a phenotype of chemoresistance in the receptor cells. Subsequently, it was demonstrated that exosomal RPS3 was essential for inducing chemoresistance of receptor cells as shown by the acquisition of this phenotype in SGC7901S cells with enforced expression of RPS3. Further mechanism study demonstrated that cisplatin-resistant gastric cancer cell-derived exosomal RPS3 enhanced the chemoresistance of cisplatin-sensitive gastric cancer cells through the PI3K-Akt-cofilin-1 signaling pathway. All these findings demonstrated that cisplatin-resistant gastric cancer cells communicate with sensitive cells through the intercellular delivery of exosomal RPS3 and activation of the PI3K-Akt-cofilin-1 signaling pathway. Targeting exosomal RPS3 protein in cisplatin-resistant gastric cancer cells may thus be a promising strategy to overcome cisplatin resistance in gastric cancer.
Language	English
Publishing date	2021-02-11
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2021.618899
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Article ; Online: Unveiling the methionine cycle: a key metabolic signature and NR4A2 as a methionine-responsive oncogene in esophageal squamous cell carcinoma.

Jin, Xing / Liu, Lei / Liu, Dan / Wu, Jia / Wang, Congcong / Wang, Siliang / Wang, Fengying / Yu, Guanzhen / Jin, Xiaoxia / Xue, Yu-Wen / Jiang, Dan / Ni, Yan / Yang, Xi / Wang, Ming-Song / Wang, Zhi-Wei / Orlov, Yuriy L / Jia, Wei / Melino, Gerry / Liu, Ji-Bin /

Chen, Wen-Lian

Cell death and differentiation

2024

Abstract: Esophageal squamous cell carcinoma (ESCC) is a deadly malignancy with notable metabolic reprogramming, yet the pivotal metabolic feature driving ESCC progression remains elusive. Here, we show that methionine cycle exhibits robust activation in ESCC and ... ...

Abstract	Esophageal squamous cell carcinoma (ESCC) is a deadly malignancy with notable metabolic reprogramming, yet the pivotal metabolic feature driving ESCC progression remains elusive. Here, we show that methionine cycle exhibits robust activation in ESCC and is reversely associated with patient survival. ESCC cells readily harness exogenous methionine to generate S-adenosyl-methionine (SAM), thus promoting cell proliferation. Mechanistically, methionine augments METTL3-mediated RNA m
Language	English
Publishing date	2024-04-03
Publishing country	England
Document type	Journal Article
ZDB-ID	1225672-9
ISSN	1476-5403 ; 1350-9047
ISSN (online)	1476-5403
ISSN	1350-9047
DOI	10.1038/s41418-024-01285-7
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Article ; Online: New Metabolic Alterations and A Predictive Marker Pipecolic Acid in Sera for Esophageal Squamous Cell Carcinoma.

Liu, Lei / Wu, Jia / Shi, Minxin / Wang, Fengying / Lu, Haimin / Liu, Jibing / Chen, Weiqin / Yu, Guanzhen / Liu, Dan / Yang, Jing / Luo, Qin / Ni, Yan / Jin, Xing / Jin, Xiaoxia / Chen, Wen-Lian

Genomics, proteomics & bioinformatics

2022 Volume 20, Issue 4, Page(s) 670–687

Abstract: Esophageal squamous cell carcinoma (ESCC) is a major histological subtype of esophageal cancer with a poor prognosis. Although several serum metabolomic investigations have been reported, ESCC tumor-associated metabolic alterations and predictive ... ...

Abstract	Esophageal squamous cell carcinoma (ESCC) is a major histological subtype of esophageal cancer with a poor prognosis. Although several serum metabolomic investigations have been reported, ESCC tumor-associated metabolic alterations and predictive biomarkers in sera have not been defined. Here, we enrolled 34 treatment-naive patients with ESCC and collected their pre- and post-esophagectomy sera together with the sera from 34 healthy volunteers for a metabolomic survey. Our comprehensive analysis identified ESCC tumor-associated metabolic alterations as represented by a panel of 12 serum metabolites. Notably, postoperative abrosia and parenteral nutrition substantially perturbed the serum metabolome. Furthermore, we performed an examination using sera from carcinogen-induced mice at the dysplasia and ESCC stages and identified three ESCC tumor-associated metabolites conserved between mice and humans. Notably, among these metabolites, the level of pipecolic acid was observed to be progressively increased in mouse sera from dysplasia to cancerization, and it could be used to accurately discriminate between mice at the dysplasia stage and healthy control mice. Furthermore, this metabolite is essential for ESCC cells to restrain oxidative stress-induced DNA damage and cell proliferation arrest. Together, this study revealed a panel of 12 ESCC tumor-associated serum metabolites with potential for monitoring therapeutic efficacy and disease relapse, presented evidence for refining parenteral nutrition composition, and highlighted serum pipecolic acid as an attractive biomarker for predicting ESCC tumorigenesis.
MeSH term(s)	Humans ; Animals ; Mice ; Esophageal Squamous Cell Carcinoma ; Esophageal Neoplasms/genetics ; Esophageal Neoplasms/pathology ; Esophageal Neoplasms/surgery ; Carcinoma, Squamous Cell/diagnosis ; Carcinoma, Squamous Cell/genetics ; Carcinoma, Squamous Cell/pathology ; Biomarkers, Tumor/genetics
Chemical Substances	pipecolic acid (H254GW7PVV) ; Biomarkers, Tumor
Language	English
Publishing date	2022-03-26
Publishing country	China
Document type	Journal Article
ZDB-ID	2240213-5
ISSN	2210-3244 ; 1672-0229
ISSN (online)	2210-3244
ISSN	1672-0229
DOI	10.1016/j.gpb.2021.08.016
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Article ; Online: An essential role for GLUT5-mediated fructose utilization in exacerbating the malignancy of clear cell renal cell carcinoma.

Jin, Xing / Liang, Yupei / Liu, Dan / Luo, Qin / Cai, Lili / Wu, Jia / Jia, Lijun / Chen, Wen-Lian

Cell biology and toxicology

2019 Volume 35, Issue 5, Page(s) 471–483

Abstract: Fructose is an important alternative carbon source for several tumors, and GLUT5 is the major fructose transporter which mediates most of fructose uptake in cells. So far, it is unclear whether GLUT5-mediated fructose utilization is important for clear ... ...

Abstract	Fructose is an important alternative carbon source for several tumors, and GLUT5 is the major fructose transporter which mediates most of fructose uptake in cells. So far, it is unclear whether GLUT5-mediated fructose utilization is important for clear cell renal cell carcinoma (ccRCC). Here, we demonstrated that GLUT5 was highly expressed in a panel of ccRCC cell lines. High GLUT5 expression exacerbated the neoplastic phenotypes of ccRCC cells, including cell proliferation and colony formation. On the other hand, deletion of the GLUT5-encoding gene SLC2A5 dramatically attenuated cellular malignancy via activating the apoptotic pathway. Moreover, administration of 2,5-anhydro-D-mannitol (2,5-AM), a competitive inhibitor of fructose uptake, could markedly suppress ccRCC cell growth. Together, we provide a new mechanistic insight for GLUT5-mediated fructose utilization in ccRCC cells and highlight the therapeutic potential for targeting this metabolic pathway against ccRCC.
MeSH term(s)	Animals ; Apoptosis/drug effects ; Apoptosis/physiology ; Biological Transport ; Carcinoma, Renal Cell/metabolism ; Carcinoma, Renal Cell/pathology ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cell Proliferation/physiology ; Female ; Fructose/antagonists & inhibitors ; Fructose/metabolism ; Glucose Transporter Type 5/metabolism ; HEK293 Cells ; Heterografts ; Humans ; Kidney Neoplasms/metabolism ; Kidney Neoplasms/pathology ; Mannitol/analogs & derivatives ; Mannitol/pharmacology ; Mice ; Mice, Inbred BALB C ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Xenograft Model Antitumor Assays
Chemical Substances	Glucose Transporter Type 5 ; RNA, Messenger ; SLC2A5 protein, human ; Fructose (30237-26-4) ; Mannitol (3OWL53L36A) ; 2,5-anhydromannitol (41107-82-8)
Language	English
Publishing date	2019-05-17
Publishing country	Netherlands
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/s10565-019-09478-4
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Article ; Online: Metabolic Profiling Revealed Prediction Biomarkers for Infantile Hemangioma in Umbilical Cord Blood Sera: A Prospective Study.

Jiang, Cheng-Hong / Lin, Peng-Fei / Chen, Fa-Chun / Chen, Jia-Yao / Xie, Wen-Jun / Li, Ming / Hu, Xiao-Jie / Chen, Wen-Lian / Cheng, Yu / Lin, Xiao-Xi

Journal of proteome research

2021 Volume 21, Issue 3, Page(s) 822–832

Abstract: Infantile hemangioma (IH), the most common benign tumor in infancy, mostly arises and has rapid growth before 3 months of age. Because irreversible skin changes occur in the early proliferative stage, early medical treatment is essential to reduce the ... ...

Abstract	Infantile hemangioma (IH), the most common benign tumor in infancy, mostly arises and has rapid growth before 3 months of age. Because irreversible skin changes occur in the early proliferative stage, early medical treatment is essential to reduce the permanent sequelae caused by IH. Yet there are still no early screening biomarkers for IH before its visible emergence. This study aimed to explore prediction biomarkers using noninvasive umbilical cord blood (UCB). A prospective study of the metabolic profiling approach was performed on UCB sera from 28 infants with IH and 132 matched healthy controls from a UCB population comprising over 1500 infants (PeptideAtlas: PASS01675) using liquid chromatography-mass spectrometry. The metabolic profiling results exhibited the characteristic metabolic aberrance of IH. Machine learning suggested a panel of biomarkers to predict the occurrence of IH, with the area under curve (AUC) values in the receiver operating characteristic analysis all >0.943. Phenylacetic acid had potential to predict infants with large IH (diameter >2 cm) from those with small IH (diameter <2 cm), with an AUC of 0.756. The novel biomarkers in noninvasive UCB sera for predicting IH before its emergence might lead to a revolutionary clinical utility.
MeSH term(s)	Biomarkers ; Chromatography, Liquid ; Fetal Blood ; Hemangioma/complications ; Hemangioma/diagnosis ; Hemangioma/drug therapy ; Humans ; Infant ; Prospective Studies
Chemical Substances	Biomarkers
Language	English
Publishing date	2021-07-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2078618-9
ISSN	1535-3907 ; 1535-3893
ISSN (online)	1535-3907
ISSN	1535-3893
DOI	10.1021/acs.jproteome.1c00430
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Article ; Online: Active post-transcriptional regulation and ACLY-mediated acetyl-CoA synthesis as a pivotal target of Shuang-Huang-Sheng-Bai formula for lung adenocarcinoma treatment.

Liu, Dan / Dong, Changsheng / Wang, Fengying / Liu, Wei / Jin, Xing / Qi, Sheng-Lan / Liu, Lei / Jin, Qiang / Wang, Siliang / Wu, Jia / Wang, Congcong / Yang, Jing / Deng, Haibin / Cai, Yuejiao / Yang, Lu / Qin, Jingru / Zhang, Chengcheng / Yang, Xi / Wang, Ming-Song /

Yu, Guanzhen / Xue, Yu-Wen / Wang, Zhongqi / Ge, Guang-Bo / Xu, Zhenye / Chen, Wen-Lian

Phytomedicine : international journal of phytotherapy and phytopharmacology

2023 Volume 113, Page(s) 154732

Abstract: Background: New therapeutic approaches are required to improve the outcomes of lung cancer (LC), a leading cause of cancer-related deaths worldwide. Chinese herbal medicine formulae widely used in China provide a unique opportunity for improving LC ... ...

Abstract	Background: New therapeutic approaches are required to improve the outcomes of lung cancer (LC), a leading cause of cancer-related deaths worldwide. Chinese herbal medicine formulae widely used in China provide a unique opportunity for improving LC treatment, and the Shuang-Huang-Sheng-Bai (SHSB) formula is a typical example. However, the underlying mechanisms of action remains unclear. Purpose: This study aimed to confirm the efficacy of SHSB against lung adenocarcinoma (LUAD), which is a major histological type of LC, unveil the downstream targets of this formula, and assess the clinical relevance and biological roles of the newly identified target. Methods: An experimental metastasis mouse model and a subcutaneous xenograft mouse model were used to evaluate the anti-cancer activity of SHSB. Multi-omics profiling of subcutaneous tumors and metabolomic profiling of sera were performed to identify downstream targets, especially the metabolic targets of SHSB. A clinical trial was conducted to verify the newly identified metabolic targets in patients. Next, the metabolites and enzymes engaged in the metabolic pathway targeted by SHSB were measured in clinical samples. Finally, routine molecular experiments were performed to decipher the biological functions of the metabolic pathways targeted by SHSB. Results: Oral SHSB administration showed overt anti-LUAD efficacy as revealed by the extended overall survival of the metastasis model and impaired growth of implanted tumors in the subcutaneous xenograft model. Mechanistically, SHSB administration altered protein expression in the post-transcriptional layer and modified the metabolome of LUAD xenografts. Integrative analysis demonstrated that SHSB markedly inhibited acetyl-CoA synthesis in tumors by post-transcriptionally downregulating ATP-citrate lyase (ACLY). Consistently, our clinical trial showed that oral SHSB administration declined serum acetyl-CoA levels of patients with LC. Moreover, acetyl-CoA synthesis and ACLY expression were both augmented in clinical LUAD tissues of patients, and high intratumoral ACLY expression predicted a detrimental prognosis. Finally, we showed that ACLY-mediated acetyl-CoA synthesis is essential for LUAD cell growth by promoting G1/S transition and DNA replication. Conclusion: Limited downstream targets of SHSB for LC treatment have been reported in previous hypothesis-driven studies. In this study, we conducted a comprehensive multi-omics investigation and demonstrated that SHSB exerted its anti-LUAD efficacy by actively and post-transcriptionally modulating protein expression and particularly restraining ACLY-mediated acetyl-CoA synthesis.
MeSH term(s)	Humans ; Mice ; Animals ; ATP Citrate (pro-S)-Lyase/genetics ; ATP Citrate (pro-S)-Lyase/metabolism ; Acetyl Coenzyme A/metabolism ; Drugs, Chinese Herbal/pharmacology ; Adenocarcinoma of Lung/drug therapy ; Lung Neoplasms/drug therapy
Chemical Substances	ATP Citrate (pro-S)-Lyase (EC 2.3.3.8) ; Acetyl Coenzyme A (72-89-9) ; Drugs, Chinese Herbal
Language	English
Publishing date	2023-02-26
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1205240-1
ISSN	1618-095X ; 0944-7113
ISSN (online)	1618-095X
ISSN	0944-7113
DOI	10.1016/j.phymed.2023.154732
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Article: New metabolic alterations and predictive marker pipecolic acid in sera for esophageal squamous cell carcinoma

Liu, Lei / Wu, Jia / Shi, Minxin / Wang, Fengying / Lu, Haimin / Liu, Jibing / Chen, Weiqin / Yu, Guanzhen / Liu, Dan / Yang, Jing / Luo, Qin / Ni, Yan / Jin, Xing / Jin, Xiaoxia / Chen, Wen-Lian

Genomics, proteomics & bioinformatics. 2021 Sept. 27,

2021

Abstract	Esophageal squamous cell carcinoma (ESCC) is a major histological subtype of esophageal cancer with a poor prognosis. Although several serum metabolomic investigations have been reported, ESCC tumor-associated metabolic alterations and predictive biomarkers in sera have not been defined. Here, we enrolled 34 treatment-naive patients with ESCC and collected their pre- and post-esophagectomy sera together with the sera from 34 healthy volunteers for a metabolomic survey. Our comprehensive analysis identified ESCC tumor-associated metabolic alterations as represented by a panel of 12 serum metabolites. Notably, postoperative abrosia and parenteral nutrition substantially perturbed the serum metabolome. Furthermore, we performed an examination using sera from carcinogen-induced mice at the dysplasia and ESCC stages and identified three ESCC tumor-associated metabolites conserved between mice and humans. Notably, among these metabolites, the level of pipecolic acid was observed to be progressively increasing in mouse sera from dysplasia to cancerization, and it could be used to accurately discriminate between mice at the dysplasia stage and healthy control mice. Furthermore, this metabolite is essential for ESCC cells to restrain oxidative stress-induced DNA damage and cell proliferation arrest. Together, this study revealed a panel of 12 ESCC tumor-associated serum metabolites with potential for monitoring therapeutic efficacy and disease relapse, presented evidence for refining parenteral nutrition composition, and highlighted serum pipecolic acid as an attractive biomarker for predicting ESCC tumorigenesis.
Keywords	DNA damage ; bioinformatics ; biomarkers ; blood serum ; carcinogenesis ; cell cycle checkpoints ; esophageal neoplasms ; genomics ; histology ; metabolites ; metabolome ; metabolomics ; mice ; parenteral feeding ; pipecolic acid ; prognosis ; proteomics ; relapse ; squamous cell carcinoma ; surveys
Language	English
Dates of publication	2021-0927
Publishing place	Elsevier B.V.
Document type	Article
Note	Pre-press version
ZDB-ID	2240213-5
ISSN	2210-3244 ; 1672-0229
ISSN (online)	2210-3244
ISSN	1672-0229
DOI	10.1016/j.gpb.2021.08.016
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Article: Metabolic Profiling Revealed Prediction Biomarkers for Infantile Hemangioma in Umbilical Cord Blood Sera: A Prospective Study

Jiang, Cheng-Hong / Lin, Peng-Fei / Chen, Fa-Chun / Chen, Jia-Yao / Xie, Wen-Jun / Li, Ming / Hu, Xiao-Jie / Chen, Wen-Lian / Cheng, Yu / Lin, Xiao-xi

Journal of proteome research. 2021 July 28, v. 21, no. 3

2021

Abstract	Infantile hemangioma (IH), the most common benign tumor in infancy, mostly arises and has rapid growth before 3 months of age. Because irreversible skin changes occur in the early proliferative stage, early medical treatment is essential to reduce the permanent sequelae caused by IH. Yet there are still no early screening biomarkers for IH before its visible emergence. This study aimed to explore prediction biomarkers using noninvasive umbilical cord blood (UCB). A prospective study of the metabolic profiling approach was performed on UCB sera from 28 infants with IH and 132 matched healthy controls from a UCB population comprising over 1500 infants (PeptideAtlas: PASS01675) using liquid chromatography–mass spectrometry. The metabolic profiling results exhibited the characteristic metabolic aberrance of IH. Machine learning suggested a panel of biomarkers to predict the occurrence of IH, with the area under curve (AUC) values in the receiver operating characteristic analysis all >0.943. Phenylacetic acid had potential to predict infants with large IH (diameter >2 cm) from those with small IH (diameter <2 cm), with an AUC of 0.756. The novel biomarkers in noninvasive UCB sera for predicting IH before its emergence might lead to a revolutionary clinical utility.
Keywords	biomarkers ; complications (disease) ; hemangioma ; infancy ; liquid chromatography ; mass spectrometry ; medical treatment ; phenylacetic acid ; prediction ; prospective studies ; proteome ; research ; umbilical cord
Language	English
Dates of publication	2021-0728
Size	p. 822-832.
Publishing place	American Chemical Society
Document type	Article
ZDB-ID	2078618-9
ISSN	1535-3907 ; 1535-3893
ISSN (online)	1535-3907
ISSN	1535-3893
DOI	10.1021/acs.jproteome.1c00430
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Article: Oleanolic acid blocks the purine salvage pathway for cancer therapy by inactivating SOD1 and stimulating lysosomal proteolysis.

Liu, Dan / Jin, Xing / Yu, Guanzhen / Wang, Mingsong / Liu, Lei / Zhang, Wenjuan / Wu, Jia / Wang, Fengying / Yang, Jing / Luo, Qin / Cai, Lili / Yang, Xi / Ke, Xisong / Qu, Yi / Xu, Zhenye / Jia, Lijun / Chen, Wen-Lian

Molecular therapy oncolytics

2021 Volume 23, Page(s) 107–123

Abstract: Metabolic reprogramming is a core hallmark of cancer and is key for tumorigenesis and tumor progression. Investigation of metabolic perturbation by anti-cancer compounds would allow a thorough understanding of the underlying mechanisms of these agents ... ...

Abstract	Metabolic reprogramming is a core hallmark of cancer and is key for tumorigenesis and tumor progression. Investigation of metabolic perturbation by anti-cancer compounds would allow a thorough understanding of the underlying mechanisms of these agents and identification of new anti-cancer targets. Here, we demonstrated that the administration of oleanolic acid (OA) rapidly altered cancer metabolism, particularly suppressing the purine salvage pathway (PSP). PSP restoration significantly opposed OA-induced DNA replication and cell proliferation arrest, underscoring the importance of this pathway for the anti-cancer activity of OA. Hypoxanthine-guanine phosphoribosyltransferase (HGPRT) and 5'-nucleotidase (5'-NT), two metabolic enzymes essential for PSP activity, were promptly degraded by OA via the lysosome pathway. Mechanistically, OA selectively targeted superoxide dismutase 1 (SOD1) and yielded reactive oxygen species (ROS) to activate the AMP-activated protein kinase (AMPK)/mammalian target of rapamycin complex 1 (mTORC1)/macroautophagy pathway, thus eliciting lysosomal degradation of HGPRT and 5'-NT. Furthermore, we found that the PSP was overactivated in human lung and breast cancers, with a negative correlation with patient survival. The results of this study elucidated a new anti-cancer mechanism of OA by restraining the PSP via the SOD1/ROS/AMPK/mTORC1/macroautophagy/lysosomal pathway. We also identified the PSP as a new target for cancer treatment and highlighted OA as a potential therapeutic agent for cancers with high PSP activity.
Language	English
Publishing date	2021-08-28
Publishing country	United States
Document type	Journal Article
ISSN	2372-7705
ISSN	2372-7705
DOI	10.1016/j.omto.2021.08.013
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