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Article ; Online: Systematic analyses to explore immune gene sets-based signature in hepatocellular carcinoma, in which IGF2BP3 contributes to tumor progression.

Zhang, Baohui / Tang, Bufu / Lv, Jiarui / Gao, Jianyao / Qin, Ling

2022 Volume 241, Page(s) 109073

Abstract: Tumor immune microenvironment (TIME) is of critical importance for the development and therapeutic response of hepatocellular carcinoma (HCC). However, limited studies have investigated immune-related indicators for clinical supervision and decision. The ...

Abstract	Tumor immune microenvironment (TIME) is of critical importance for the development and therapeutic response of hepatocellular carcinoma (HCC). However, limited studies have investigated immune-related indicators for clinical supervision and decision. The current study aimed to develop an improved prognostic signature based on TIME. HCC patients from TCGA and ICGC database were classified into three subtypes (Immunity High, Immunity Medium and Immunity Low) according to ssGSEA scores of 29 immune gene sets. Differentially expressed immune-related genes (DE IRGs) between Immune High and Low groups were screened with an adjusted P < 0.05. Weighted gene co-expression network analysis (WGCNA) was used to establish gene co-expression modules of differentially expressed genes (DEGs) between tumor and normal tissues. 45 survival-related immune genes (SRIGs) were identified at points of intersection between hub genes and DE IRGs. By performing Cox regression and LASSO analysis, 3 of the 45 SRIGs were screened to establish a prognostic model. Patients with high risk scores exhibited worse survival outcome and poorer response to chemotherapy. Potential mechanisms of chemotherapy resistance also have been discussed. More significantly, high -risk patients showed increased immune cell infiltration and checkpoints, which suggested a benefit of immunotherapy. In addition, knockdown of IGF2BP3 was determined to significantly inhibit cell proliferation and migration in HCC. Our immune-related model may be an effective tool for precise diagnosis and treatment of HCC. It may help to select patients suitable for chemotherapy, and immunotherapy.
MeSH term(s)	Biomarkers, Tumor/genetics ; Carcinoma, Hepatocellular/genetics ; Computational Biology ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Humans ; Liver Neoplasms ; Prognosis ; Tumor Microenvironment/genetics
Chemical Substances	Biomarkers, Tumor
Language	English
Publishing date	2022-07-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	1459903-x
ISSN	1521-7035 ; 1521-6616
ISSN (online)	1521-7035
ISSN	1521-6616
DOI	10.1016/j.clim.2022.109073
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Article ; Online: Emerging Mechanisms and Targeted Therapy of Ferroptosis in Neurological Diseases and Neuro-oncology.

Wang, Yajie / Tang, Bufu / Zhu, Jinyu / Yu, Junchao / Hui, Junguo / Xia, Shuiwei / Ji, Jiansong

International journal of biological sciences

2022 Volume 18, Issue 10, Page(s) 4260–4274

Abstract: Ferroptosis is a novel type of cell death characterized by iron-dependent lipid peroxidation that involves a variety of biological processes, such as iron metabolism, lipid metabolism, and oxidative stress. A growing body of research suggests that ... ...

Abstract	Ferroptosis is a novel type of cell death characterized by iron-dependent lipid peroxidation that involves a variety of biological processes, such as iron metabolism, lipid metabolism, and oxidative stress. A growing body of research suggests that ferroptosis is associated with cancer and neurodegenerative diseases, such as glioblastoma, Alzheimer's disease, Parkinson's disease, and stroke. Building on these findings, we can selectively induce ferroptosis for the treatment of certain cancers, or we can treat neurodegenerative diseases by inhibiting ferroptosis. This review summarizes the relevant advances in ferroptosis, the regulatory mechanisms of ferroptosis, the participation of ferroptosis in brain tumors and neurodegenerative diseases, and the corresponding drug therapies to provide new potential targets for its treatment.
MeSH term(s)	Cell Death/physiology ; Ferroptosis ; Humans ; Iron/metabolism ; Lipid Peroxidation ; Neoplasms/metabolism ; Neurodegenerative Diseases/drug therapy
Chemical Substances	Iron (E1UOL152H7)
Language	English
Publishing date	2022-06-27
Publishing country	Australia
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2179208-2
ISSN	1449-2288 ; 1449-2288
ISSN (online)	1449-2288
ISSN	1449-2288
DOI	10.7150/ijbs.72251
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Article ; Online: Risk assessment of pneumothorax in colorectal lung metastases treated by percutaneous thermal ablation: a multicenter retrospective cohort study.

Fan, Hongjie / Xie, Xuancheng / Pang, Zhenzhu / Zhang, Licai / Ding, Rong / Wan, Cheng / Li, Xinghai / Yang, Zebin / Sun, Jihong / Kan, Xuefeng / Tang, Bufu / Zheng, Chuansheng

International journal of surgery (London, England)

2024 Volume 110, Issue 1, Page(s) 261–269

Abstract: Purpose: To evaluate the risk of pneumothorax in the percutaneous image-guided thermal ablation (IGTA) treatment of colorectal lung metastases (CRLM).: Methods: Data regarding patients with CRLM treated with IGTA from five medical institutions in ... ...

Abstract	Purpose: To evaluate the risk of pneumothorax in the percutaneous image-guided thermal ablation (IGTA) treatment of colorectal lung metastases (CRLM). Methods: Data regarding patients with CRLM treated with IGTA from five medical institutions in China from 2016 to 2023 were reviewed retrospectively. Pneumothorax and non-pneumothorax were compared using the Student's t -test, χ 2 test and Fisher's exact test. Univariate logistic regression analysis was conducted to identify potential risk factors, followed by multivariate logistic regression analysis to evaluate the predictors of pneumothorax. Interactions between variables were examined and used for model construction. Receiver operating characteristic curves and nomograms were generated to assess the performance of the model. Results: A total of 254 patients with 376 CRLM underwent 299 ablation sessions. The incidence of pneumothorax was 45.5%. The adjusted multivariate logistic regression model, incorporating interaction terms, revealed that tumour number [odds ratio (OR)=8.34 (95% CI: 1.37-50.64)], puncture depth [OR=0.53 (95% CI: 0.31-0.91)], pre-procedure radiotherapy [OR=3.66 (95% CI: 1.17-11.40)], peribronchial tumour [OR=2.32 (95% CI: 1.04-5.15)], and emphysema [OR=56.83 (95% CI: 8.42-383.57)] were significant predictive factors of pneumothorax (all P <0.05). The generated nomogram model demonstrated a significant prediction performance, with an area under the receiver operating characteristic curve of 0.800 (95% CI: 0.751-0.850). Conclusions: Pre-procedure radiotherapy, tumour number, peribronchial tumour, and emphysema were identified as risk factors for pneumothorax in the treatment of CRLM using percutaneous IGTA. Puncture depth was found to be a protective factor against pneumothorax.
MeSH term(s)	Humans ; Pneumothorax/etiology ; Retrospective Studies ; Lung Neoplasms/surgery ; Risk Assessment ; Risk Factors ; Nomograms ; Colorectal Neoplasms/surgery ; Colorectal Neoplasms/complications ; Emphysema/complications
Language	English
Publishing date	2024-01-01
Publishing country	United States
Document type	Multicenter Study ; Journal Article
ZDB-ID	2212038-5
ISSN	1743-9159 ; 1743-9191
ISSN (online)	1743-9159
ISSN	1743-9191
DOI	10.1097/JS9.0000000000000782
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Article ; Online: TKI resistant-based prognostic immune related gene signature in LUAD, in which FSCN1 contributes to tumor progression.

Shi, Yueli / Xu, Yun / Xu, Zhiyong / Wang, Huan / Zhang, Jingnan / Wu, Yuan / Tang, Bufu / Zheng, Shenfei / Wang, Kai

Cancer letters

2022 Volume 532, Page(s) 215583

Abstract: Drug resistance reflects the evolution of tumors, which is the main cause of recurrence and death. Currently, EGFR-TKI treatment is the first-line therapy for lung adenocarcinoma (LUAD) patients. Although EGFR-TKI achieved good effects at the beginning, ... ...

Abstract	Drug resistance reflects the evolution of tumors, which is the main cause of recurrence and death. Currently, EGFR-TKI treatment is the first-line therapy for lung adenocarcinoma (LUAD) patients. Although EGFR-TKI achieved good effects at the beginning, most of the LUAD patients eventually acquired resistance. Therefore, it's urgently need to develop a strong criterion for identifying these patients who may benefit from additional therapy. In this study, we established a three TKI resistant-related gene signature (DDIT4, OAS3, FSCN1), and determined that's an accuracy, independent and specific prognostic model for LUAD patients. Patients categorized as high-risk by this signature showed more sensitive to chemotherapy, and exhibited higher expression of common immune checkpoints such as PD-L1/B7H3/PD-L2/IDO1. Moreover, these patients were characterized by increased infiltration of M0 macrophage and activated memory CD4
MeSH term(s)	Adenocarcinoma of Lung/drug therapy ; Adenocarcinoma of Lung/genetics ; Carrier Proteins ; ErbB Receptors ; Humans ; Lung Neoplasms/drug therapy ; Lung Neoplasms/genetics ; Microfilament Proteins ; Phosphatidylinositol 3-Kinases ; Prognosis
Chemical Substances	Carrier Proteins ; FSCN1 protein, human ; Microfilament Proteins ; ErbB Receptors (EC 2.7.10.1)
Language	English
Publishing date	2022-02-09
Publishing country	Ireland
Document type	Journal Article ; 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.2022.215583
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Article ; Online: Correlation between second and first primary cancer: systematic review and meta-analysis of 9 million cancer patients.

Wang, Xinyu / Zeng, Meiyuan / Ju, Xueming / Lin, Anqi / Zhou, Chaozheng / Shen, Junyi / Liu, Zaoqu / Tang, Bufu / Cheng, Quan / Wang, Youyu / Zhang, Jian / Luo, Peng

The British journal of surgery

2023 Volume 111, Issue 1

Abstract: Background: Many survivors of a first primary cancer (FPCs) are at risk of developing a second primary cancer (SPC), with effects on patient prognosis. Primary cancers have different frequencies of specific SPC development and the development of SPCs ... ...

Abstract	Background: Many survivors of a first primary cancer (FPCs) are at risk of developing a second primary cancer (SPC), with effects on patient prognosis. Primary cancers have different frequencies of specific SPC development and the development of SPCs may be closely related to the FPC. The aim of this study was to explore possible correlations between SPCs and FPCs. Methods: Relevant literature on SPCs was retrospectively searched and screened from four databases, namely, PubMed, EMBASE, Web of Science, and PMC. Data on the number of patients with SPC in 28 different organ sites were also collected from The Surveillance, Epidemiology, and End Results (SEER) 8 Registry and NHANES database. Results: A total of 9 617 643 patients with an FPC and 677 430 patients with an SPC were included in the meta-analysis. Patients with a first primary gynaecological cancer and thyroid cancer frequently developed a second primary breast cancer and colorectal cancer. Moreover, those with a first primary head and neck cancer, anal cancer and oesophageal cancer developed a second primary lung cancer more frequently. A second primary lung cancer and prostate cancer was also common among patients with first primary bladder cancer and penile cancer. Patients with second primary bladder cancer accounted for 56% of first primary ureteral cancer patients with SPCs. Conclusions: This study recommends close clinical follow-up, monitoring and appropriate interventions in patients with relevant FPCs for better screening and early diagnosis of SPCs.
MeSH term(s)	Humans ; Incidence ; Lung Neoplasms ; Neoplasms, Second Primary/epidemiology ; Nutrition Surveys ; Prostatic Neoplasms/epidemiology ; Retrospective Studies ; Risk Factors ; Urinary Bladder Neoplasms
Language	English
Publishing date	2023-12-06
Publishing country	England
Document type	Meta-Analysis ; Systematic Review ; Journal Article
ZDB-ID	2985-3
ISSN	1365-2168 ; 0263-1202 ; 0007-1323 ; 1355-7688
ISSN (online)	1365-2168
ISSN	0263-1202 ; 0007-1323 ; 1355-7688
DOI	10.1093/bjs/znad377
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Article: TACE responser NDRG1 acts as a guardian against ferroptosis to drive tumorgenesis and metastasis in HCC.

Tang, Bufu / Wang, Yajie / Zhu, Jinyu / Song, Jingjing / Fang, Shiji / Weng, Qiaoyou / Yang, Yang / Tu, Jianfei / Zhao, Zhongwei / Chen, Minjiang / Xu, Min / Chen, Weiqian / Ji, Jiansong

Biological procedures online

2023 Volume 25, Issue 1, Page(s) 13

Abstract: Background: The treatment efficacy of transarterial chemoembolization (TACE) for hepatocellular carcinoma (HCC) varies widely between individuals. The aim of this study was to identify subtype landscapes and responser related to TACE, and further ... ...

Abstract	Background: The treatment efficacy of transarterial chemoembolization (TACE) for hepatocellular carcinoma (HCC) varies widely between individuals. The aim of this study was to identify subtype landscapes and responser related to TACE, and further clarify the regulatory effect and corresponding mechanism of NDRG1 on HCC tumorgenesis and metastasis. Methods: The principal component analysis (PCA) algorithm was used to construct a TACE response scoring (TRscore) system. The random forest algorithm was applied to identify the TACE response-related core gene NDRG1 of HCC, and its role in the prognosis of HCC was explored. The role of NDRG1 in the progression and metastasis of HCC and functional mechanism were confirmed using several experimental methods. Results: Based on the GSE14520 and GSE104580 cohorts, we identified 2 TACE response-related molecular subtypes for HCC with significant differences in clinical features, and the TACE prognosis of Cluster A was significantly better than that of Cluster B (p < 0.0001). We then established the TRscore system and found that the low TRscore group showed a higher probability of survival and a lower rate of recurrence than the high TRscore group (p < 0.05) in both the HCC and TACE-treated HCC cohorts within the GSE14520 cohort. NDRG1 was determined to be the the hub gene associated with the TACE response of HCC and its high expression suggested a poor prognosis. Furthermore, The suppression of NDRG1 konckdown in tumorgenesis and metastasis of HCC was clarified in both vivo and vitro, which was importantly achieved through inducing ferroptosis in HCC cells, especially contributing to RLS3-induced ferroptosis. Conclusion: The constructed TACE response-related molecular subtypes and TRscores can specifically and accurately predict TACE prognosis for HCC. In addition, the TACE response-related hub gene NDRG1 may act as a guardian against ferroptosis to drive tumorgenesis and metastasis in HCC, which laid a new foundation for the development of new potential targeted therapy strategies to improve disease prognosis in HCC patients.
Language	English
Publishing date	2023-05-19
Publishing country	England
Document type	Journal Article
ZDB-ID	2027823-8
ISSN	1480-9222
ISSN	1480-9222
DOI	10.1186/s12575-023-00199-x
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Article ; Online: A hypoxia-related signature for clinically predicting diagnosis, prognosis and immune microenvironment of hepatocellular carcinoma patients

Baohui Zhang / Bufu Tang / Jianyao Gao / Jiatong Li / Lingming Kong / Ling Qin

Journal of Translational Medicine, Vol 18, Iss 1, Pp 1-

2020 Volume 17

Abstract: Abstract Background Hypoxia plays an indispensable role in the development of hepatocellular carcinoma (HCC). However, there are few studies on the application of hypoxia molecules in the prognosis predicting of HCC. We aim to identify the hypoxia- ... ...

Abstract	Abstract Background Hypoxia plays an indispensable role in the development of hepatocellular carcinoma (HCC). However, there are few studies on the application of hypoxia molecules in the prognosis predicting of HCC. We aim to identify the hypoxia-related genes in HCC and construct reliable models for diagnosis, prognosis and recurrence of HCC patients as well as exploring the potential mechanism. Methods Differentially expressed genes (DEGs) analysis was performed using The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) database and four clusters were determined by a consistent clustering analysis. Three DEGs closely related to overall survival (OS) were identified using Cox regression and LASSO analysis. Then the hypoxia-related signature was developed and validated in TCGA and International Cancer Genome Consortium (ICGC) database. The Gene Set Enrichment Analysis (GSEA) was performed to explore signaling pathways regulated by the signature. CIBERSORT was used for estimating the fractions of immune cell types. Results A total of 397 hypoxia-related DEGs in HCC were detected and three genes (PDSS1, CDCA8 and SLC7A11) among them were selected to construct a prognosis, recurrence and diagnosis model. Then patients were divided into high- and low-risk groups. Our hypoxia-related signature was significantly associated with worse prognosis and higher recurrence rate. The diagnostic model also accurately distinguished HCC from normal samples and nodules. Furthermore, the hypoxia-related signature could positively regulate immune response. Meanwhile, the high-risk group had higher fractions of macrophages, B memory cells and follicle-helper T cells, and exhibited higher expression of immunocheckpoints such as PD1and PDL1. Conclusions Altogether, our study showed that hypoxia-related signature is a potential biomarker for diagnosis, prognosis and recurrence of HCC, and it provided an immunological perspective for developing personalized therapies.
Keywords	Hypoxia ; Hepatocellular carcinoma ; Prognostic ; Diagnostic ; Immune microenvironment ; Medicine ; R
Subject code	610
Language	English
Publishing date	2020-09-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
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Article ; Online: Overexpressed PKM2 promotes macrophage phagocytosis and atherosclerosis

Gai, Xiaochen / Liu, Fangming / Wu, Yuting / Zhang, Baohui / Tang, Bufu / Shang, Kezhuo / Wang, Lianmei / Zhang, Haihong / Chen, Yixin / Yang, Shuhui / Deng, Weiwei / Li, Peng / Wang, Jing / Zhang, Hongbing

Animal Models and Experimental Medicine. 2023 Apr., v. 6, no. 2 p.92-102

2023

Abstract: BACKGROUND: The expression of pyruvate kinase muscle 2 (PKM2) is augmented in macrophages of patients with atherosclerotic coronary artery disease. The role of PKM2 in atherosclerosis is to be determined. METHODS: Global and myeloid cell‐specific PKM2 ... ...

Abstract	BACKGROUND: The expression of pyruvate kinase muscle 2 (PKM2) is augmented in macrophages of patients with atherosclerotic coronary artery disease. The role of PKM2 in atherosclerosis is to be determined. METHODS: Global and myeloid cell‐specific PKM2 knock‐in mice with ApoE⁻/⁻ background (ApoE⁻/⁻, PKM2ᴷᴵ/ᴷᴵ and Lyz2‐cre, ApoE⁻/⁻, and PKM2ᶠˡᵒˣ/ᶠˡᵒˣ) were produced to evaluate the clinical significance of PKM2 in atherosclerosis development. Wild‐type and PKM2 knock‐in macrophages were isolated to assess the function of PKM2 in macrophage phagocytosis. Atherosclerotic mice were treated with PKM2 inhibitor shikonin (SKN) to evaluate the therapeutic potential of PKM2 suppression in atherosclerosis. RESULTS: Oxidized low‐density lipoprotein (oxLDL) upregulated PKM2 in macrophages. PKM2 in return promoted the uptake of oxLDL by macrophages. Overexpressed PKM2 accelerated atherosclerosis in mice. SKN blocked the progress of mouse atherosclerosis. CONCLUSIONS: PKM2 accelerates macrophage phagocytosis and atherosclerosis. Targeting PKM2 is a potential therapy for atherosclerosis.
Keywords	atherosclerosis ; coronary artery disease ; low density lipoprotein ; macrophages ; medicine ; mice ; muscles ; oxidation ; phagocytosis ; pyruvate kinase ; shikonin ; therapeutics
Language	English
Dates of publication	2023-04
Size	p. 92-102.
Publishing place	John Wiley & Sons, Ltd
Document type	Article ; Online
Note	JOURNAL ARTICLE
ISSN	2576-2095
DOI	10.1002/ame2.12266
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: SHP2 deneddylation mediates tumor immunosuppression in colon cancer via the CD47/SIRPα axis

Yiqing Li / Hui Zhou / Pan Liu / Dandan Lv / Yichun Shi / Bufu Tang / Jiaqi Xu / Tingting Zhong / Wangting Xu / Jie Zhang / Jianying Zhou / Kejing Ying / Yongchao Zhao / Yi Sun / Zhinong Jiang / Hongqiang Cheng / Xue Zhang / Yuehai Ke

The Journal of Clinical Investigation, Vol 133, Iss

2023 Volume 4

Abstract: SIPRα on macrophages binds with CD47 to resist proengulfment signals, but how the downstream signal of SIPRα controls tumor-infiltrating macrophages (TIMs) is still poorly clarified. Here, we report that the CD47/signal regulatory protein α (SIRPα) axis ... ...

Abstract	SIPRα on macrophages binds with CD47 to resist proengulfment signals, but how the downstream signal of SIPRα controls tumor-infiltrating macrophages (TIMs) is still poorly clarified. Here, we report that the CD47/signal regulatory protein α (SIRPα) axis requires the deneddylation of tyrosine phosphatase SHP2. Mechanistically, Src homology region 2–containing protein tyrosine phosphatase 2 (SHP2) was constitutively neddylated on K358 and K364 sites; thus, its autoinhibited conformation was maintained. In response to CD47-liganded SIRPα, SHP2 was deneddylated by sentrin-specific protease 8 (SENP8), which led to the dephosphorylation of relevant substrates at the phagocytic cup and subsequent inhibition of macrophage phagocytosis. Furthermore, neddylation inactivated myeloid-SHP2 and greatly boosted the efficacy of colorectal cancer (CRC) immunotherapy. Importantly, we observed that supplementation with SHP2 allosteric inhibitors sensitized immune treatment–resistant CRC to immunotherapy. Our results emphasize that the CRC subtype that is unresponsive to immunotherapy relies on SIRPαhiSHP2hiNEDD8lo TIMs and highlight the need to further explore the strategy of SHP2 targeting in CRC therapy.
Keywords	Cell biology ; Medicine ; R
Subject code	616
Language	English
Publishing date	2023-02-01T00:00:00Z
Publisher	American Society for Clinical Investigation
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Celastrol inhibits colorectal cancer cell proliferation and migration through suppression of MMP3 and MMP7 by the PI3K/AKT signaling pathway.

Bufu, Tang / Di, Xu / Yilin, Zhao / Gege, Liang / Xi, Chen / Ling, Wang

Anti-cancer drugs

2018 Volume 29, Issue 6, Page(s) 530–538

Abstract: Colorectal cancer (CRC) is one of the most frequent malignant tumors. Signaling by the PI3K/AKT pathway is crucial for CRC development and progression, including proliferation and migration. Celastrol has an anticancer effect, but its mechanism needs to ... ...

Abstract	Colorectal cancer (CRC) is one of the most frequent malignant tumors. Signaling by the PI3K/AKT pathway is crucial for CRC development and progression, including proliferation and migration. Celastrol has an anticancer effect, but its mechanism needs to be determined. Here, we showed that celastrol suppressed CRC cell proliferation and migration. Celastrol treatment also decreased the PI3K/AKT pathway components, and MMP3 and MMP7 expression levels. In addition, knockdown of AKT, not mTOR, inhibited MMP3 and MMP7 expression levels and AKT silencing promoted the celastrol-induced effects on CRC cell proliferation and migration. Taken together, these findings indicated that the celastrol-induced antitumor effects were mediated through MMP3 and MMP7 by the PI3K/AKT signaling pathway.
MeSH term(s)	Cell Line, Tumor ; Cell Movement/drug effects ; Cell Proliferation/drug effects ; Colorectal Neoplasms/drug therapy ; Colorectal Neoplasms/enzymology ; Colorectal Neoplasms/pathology ; HCT116 Cells ; Humans ; Matrix Metalloproteinase 3/biosynthesis ; Matrix Metalloproteinase 3/genetics ; Matrix Metalloproteinase 3/metabolism ; Matrix Metalloproteinase 7/biosynthesis ; Matrix Metalloproteinase 7/genetics ; Matrix Metalloproteinase 7/metabolism ; Matrix Metalloproteinase Inhibitors/pharmacology ; Phosphatidylinositol 3-Kinases/biosynthesis ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphoinositide-3 Kinase Inhibitors ; Protein Kinase Inhibitors/pharmacology ; Proto-Oncogene Proteins c-akt/antagonists & inhibitors ; Proto-Oncogene Proteins c-akt/biosynthesis ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction/drug effects ; TOR Serine-Threonine Kinases/antagonists & inhibitors ; TOR Serine-Threonine Kinases/biosynthesis ; Triterpenes/pharmacology ; Up-Regulation/drug effects
Chemical Substances	Matrix Metalloproteinase Inhibitors ; Phosphoinositide-3 Kinase Inhibitors ; Protein Kinase Inhibitors ; Triterpenes ; MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; MMP3 protein, human (EC 3.4.24.17) ; Matrix Metalloproteinase 3 (EC 3.4.24.17) ; MMP7 protein, human (EC 3.4.24.23) ; Matrix Metalloproteinase 7 (EC 3.4.24.23) ; celastrol (L8GG98663L)
Language	English
Publishing date	2018-03-13
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1065301-6
ISSN	1473-5741 ; 0959-4973
ISSN (online)	1473-5741
ISSN	0959-4973
DOI	10.1097/CAD.0000000000000621
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