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Article ; Online: S100P facilitates LUAD progression via PKA/c-Jun-mediated tumor-associated macrophage recruitment and polarization.

Gao, Lu / Bai, Ying / Zhou, Jiawei / Liang, Chao / Dong, Yunjia / Han, Tao / Liu, Yafeng / Guo, Jianqiang / Wu, Jing / Hu, Dong

Cellular signalling

2024 , Page(s) 111179

Abstract: ... of chemokines and polarizing factors by activating the PKA/c-Jun pathway, which is implicated in TAM recruitment ... and polarization towards the M2 phenotype. Moreover, inhibition of c-Jun expression impedes ... that S100P facilitates LUAD cells growth by recruiting M2 TAMs through PKA/c-Jun signaling, resulting ...

Abstract	S100P, a member of the S100 calcium-binding protein family, is closely associated with abnormal proliferation, invasion, and metastasis of various cancers. However, its role in the lung adenocarcinoma (LUAD) tumor microenvironment (TME) remains unclear. In this study, we observed specific expression of S100P on tumor cells in LUAD patients through tissue immunofluorescence analysis. Furthermore, this expression was strongly correlated with the recruitment and polarization of tumor-associated macrophages (TAMs). Bioinformatics analysis revealed that high S100P expression is associated with poorer overall survival in LUAD patients. Subsequently, a subcutaneous mouse model demonstrated that S100P promotes recruitment and polarization of TAMs towards the M2 type. Finally, in vitro studies on LUAD cells revealed that S100P enhances the secretion of chemokines and polarizing factors by activating the PKA/c-Jun pathway, which is implicated in TAM recruitment and polarization towards the M2 phenotype. Moreover, inhibition of c-Jun expression impedes the ability of TAMs to infiltrate and polarize towards the M2 phenotype. In conclusion, our study demonstrates that S100P facilitates LUAD cells growth by recruiting M2 TAMs through PKA/c-Jun signaling, resulting in the production of various cytokines. Considering these findings, S100P holds promise as an important diagnostic marker and potential therapeutic target for LUAD.
Language	English
Publishing date	2024-04-17
Publishing country	England
Document type	Journal Article
ZDB-ID	1002702-6
ISSN	1873-3913 ; 0898-6568
ISSN (online)	1873-3913
ISSN	0898-6568
DOI	10.1016/j.cellsig.2024.111179
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Zs.A 2579: Show issues

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Article ; Online: NNMT contributes to high metastasis of triple negative breast cancer by enhancing PP2A/MEK/ERK/c-Jun/ABCA1 pathway mediated membrane fluidity.

Wang, Yanzhong / Zhou, Xi / Lei, Yinjiao / Chu, Yadong / Yu, Xingtong / Tong, Qingchao / Zhu, Tao / Yu, Haitao / Fang, Sining / Li, Guoli / Wang, Linbo / Wang, Gavin Y / Xie, Xinyou / Zhang, Jun

Cancer letters

2022 Volume 547, Page(s) 215884

Abstract: ... levels in the cytoplasm and cell membrane. Mechanistically, NNMT activated MEK/ERK/c-Jun/ABCA1 pathway ...

Abstract	Elucidating the mechanism for high metastasis capacity of triple negative breast cancers (TNBC) is crucial to improve treatment outcomes of TNBC. We have recently reported that nicotinamide N-methyltransferase (NNMT) is overexpressed in breast cancer, especially in TNBC, and predicts poor survival of patients undergoing chemotherapy. Here, we aimed to determine the function and mechanism of NNMT on metastasis of TNBC. Additionally, analysis of public datasets indicated that NNMT is involved in cholesterol metabolism. In vitro, NNMT overexpression promoted migration and invasion of TNBCs by reducing cholesterol levels in the cytoplasm and cell membrane. Mechanistically, NNMT activated MEK/ERK/c-Jun/ABCA1 pathway by repressing protein phosphatase 2A (PP2A) activity leading to cholesterol efflux and membrane fluidity enhancement, thereby promoting the epithelial-mesenchymal transition (EMT) of TNBCs. In vivo, the metastasis capacity of TNBCs was weakened by targeting NNMT. Collectively, our findings suggest a new molecular mechanism involving NNMT in metastasis and poor survival of TNBC mediated by PP2A and affecting cholesterol metabolism.
MeSH term(s)	Humans ; ATP Binding Cassette Transporter 1/metabolism ; Cell Line, Tumor ; Cell Proliferation ; Cholesterol ; Epithelial-Mesenchymal Transition ; Membrane Fluidity ; Mitogen-Activated Protein Kinase Kinases/metabolism ; Neoplasm Metastasis ; Nicotinamide N-Methyltransferase/metabolism ; Protein C/metabolism ; Protein C/therapeutic use ; Triple Negative Breast Neoplasms/metabolism
Chemical Substances	ABCA1 protein, human ; ATP Binding Cassette Transporter 1 ; Cholesterol (97C5T2UQ7J) ; Mitogen-Activated Protein Kinase Kinases (EC 2.7.12.2) ; Nicotinamide N-Methyltransferase (EC 2.1.1.1) ; NNMT protein, human (EC 2.1.1.1) ; Protein C
Language	English
Publishing date	2022-08-19
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.2022.215884
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Zs.A 1177: Show issues

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Article: NR0B1 suppresses ferroptosis through upregulation of NRF2/c-JUN-CBS signaling pathway in lung cancer cells.

Zhang, Xin-Yue / Zhang, Hao / Hu, Si-Jing / Liao, Shun-Yao / Tao, Da-Chang / Tan, Xiao-Lan / Yi, Ming / Leng, Xiang-You / Wang, Zhao-Kun / Shi, Jia-Ying / Xie, Sheng-Yu / Yang, Yuan / Liu, Yun-Qiang

American journal of cancer research

2023 Volume 13, Issue 11, Page(s) 5174–5196

Abstract: ... and the expression level of NR0B1 positively correlated with that of c-JUN, NRF2, and CBS. We further ... revealed that NR0B1 suppression of ferroptosis depended on the activities of c-JUN, NRF2, and CBS. NR0B1 ... directly promoted the expression of NRF2 and c-JUN and indirectly upregulated CBS expression ...

Abstract	Ferroptosis has demonstrated significant potential in treating radiochemotherapy-resistant cancers, but its efficacy can be affected by recently discovered ferroptosis suppressors. In this study, we discovered that NR0B1 protects against erastin- or RSL3-induced ferroptosis in lung cancer cells. Transcriptomic analysis revealed that NR0B1 significantly interfered with the expression of 12 ferroptosis-related genes, and the expression level of NR0B1 positively correlated with that of c-JUN, NRF2, and CBS. We further revealed that NR0B1 suppression of ferroptosis depended on the activities of c-JUN, NRF2, and CBS. NR0B1 directly promoted the expression of NRF2 and c-JUN and indirectly upregulated CBS expression through enhancing NRF2 and/or c-JUN transcription. Moreover, we showed that NR0B1 depletion restrained xenograft tumor growth and facilitated RSL3-induced ferroptosis in the tumors. In conclusion, our findings uncover that NR0B1 suppresses ferroptosis by activating the c-JUN/NRF2-CBS signaling pathway in lung cancer cells, providing new evidence for the involvement of NR0B1 in drug resistance during cancer therapy.
Language	English
Publishing date	2023-11-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	2589522-9
ISSN	2156-6976
ISSN	2156-6976
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Article: CDK2 regulates aminoglycoside-induced hair cell death through modulating c-Jun activity: Inhibiting CDK2 to preserve hearing.

Tao, Litao / Segil, Neil

Frontiers in molecular neuroscience

2022 Volume 15, Page(s) 1013383

Abstract: Sensory hair cell death caused by the ototoxic side effects of many clinically used drugs leads to permanent sensorineural hearing loss in patients. Aminoglycoside antibiotics are widely used and well-known for their ototoxicity, but the molecular ... ...

Abstract	Sensory hair cell death caused by the ototoxic side effects of many clinically used drugs leads to permanent sensorineural hearing loss in patients. Aminoglycoside antibiotics are widely used and well-known for their ototoxicity, but the molecular mechanisms of aminoglycoside-induced hair cell death are not well understood. This creates challenges in our attempts to alleviate or prevent such adverse side effects. Here, we report a regulatory role of CDK2 in aminoglycoside-induced hair cell death. Utilizing organotypic cultures of cochleae from neonatal mice, we show that blocking CDK2 activity by either pharmaceutical inhibition or by
Language	English
Publishing date	2022-10-13
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2452967-9
ISSN	1662-5099
ISSN	1662-5099
DOI	10.3389/fnmol.2022.1013383
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Article ; Online: p38-dependent c-Jun degradation contributes to reduced PGE2 production in sodium orthovanadate-treated macrophages.

Aziz, Nur / Kim, Eunji / Yang, Yanyan / Kim, Han Gyung / Yu, Tao / Cho, Jae Youl

BMB reports

2022 Volume 55, Issue 8, Page(s) 389–394

Abstract: In particular, the phenomenon of c-Jun degradation within the inflammatory response has not ... which regulate c-Jun degradation within the inflammatory response. Through our study, we found that SO suppressed ... Additionally, SO decreased total c-Jun levels, without altering the amount of mRNA, although the phospho-levels ...

Abstract	In particular, the phenomenon of c-Jun degradation within the inflammatory response has not yet been fully analyzed. In order to verify this, we investigated LPS-stimulated murine macrophages pre-treated with sodium orthovanadate (SO) in order to uncover the regulatory mechanisms of the MAPKs which regulate c-Jun degradation within the inflammatory response. Through our study, we found that SO suppressed the production of prostaglandin E2 (PGE2) and the expression of COX-2 in LPS-stimulated RAW264.7 cells. Additionally, SO decreased total c-Jun levels, without altering the amount of mRNA, although the phospho-levels of p38, ERK, and JNK were strongly enhanced. Through the usage of selective MAPK inhibitors, and knockdown and overexpression strategies, p38 was revealed to be a major MAPK which regulates c-Jun degradation. Further analysis indicates that the phosphorylation of p38 is a determinant for c-Jun degradation, and is sufficient to induce ubiquitination-dependent c-Jun degradation, recovered through MG132 treatment. Therefore, our results suggest that the hyperphosphorylation of p38 by SO contributes to c-Jun degradation, which is linked to the suppression of PGE2 secretion in inflammatory responses; and thus, finding drugs to increase p38 activity could be a novel strategy for the development of anti-inflammatory drugs. [BMB Reports 2022; 55(8): 389-394].
MeSH term(s)	Animals ; Cyclooxygenase 2/genetics ; Cyclooxygenase 2/metabolism ; Dinoprostone/metabolism ; Lipopolysaccharides/metabolism ; Lipopolysaccharides/pharmacology ; Macrophages/metabolism ; Mice ; NF-kappa B/metabolism ; Sodium/metabolism ; Ubiquitination ; Vanadates/metabolism ; Vanadates/pharmacology ; p38 Mitogen-Activated Protein Kinases/metabolism
Chemical Substances	Lipopolysaccharides ; NF-kappa B ; Vanadates (3WHH0066W5) ; Sodium (9NEZ333N27) ; Cyclooxygenase 2 (EC 1.14.99.1) ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Dinoprostone (K7Q1JQR04M)
Language	English
Publishing date	2022-04-11
Publishing country	Korea (South)
Document type	News
ZDB-ID	2410389-5
ISSN	1976-670X ; 1976-6696
ISSN (online)	1976-670X
ISSN	1976-6696
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Zs.A 4202: Show issues

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Article ; Online: MUC1-C Dictates JUN and BAF-Mediated Chromatin Remodeling at Enhancer Signatures in Cancer Stem Cells.

Bhattacharya, Atrayee / Fushimi, Atsushi / Yamashita, Nami / Hagiwara, Masayuki / Morimoto, Yoshihiro / Rajabi, Hasan / Long, Mark D / Abdulla, Maha / Ahmad, Rehan / Street, Kelly / Liu, Song / Liu, Tao / Kufe, Donald

Molecular cancer research : MCR

2022 Volume 20, Issue 4, Page(s) 556–567

Abstract: ... induced DARs align with genes regulated by the JUN/AP-1 family of transcription factors. MUC1-C activates ... the BAF chromatin remodeling complex, which is recruited by JUN in enhancer selection. In studies ... necessary for (i) occupancy of JUN and ARID1A/BAF, (ii) increases in H3K27ac and H3K4me3 signals, and (iii ...

Abstract	The oncogenic MUC1-C protein promotes dedifferentiation of castrate-resistant prostate cancer (CRPC) and triple-negative breast cancer (TNBC) cells. Chromatin remodeling is critical for the cancer stem cell (CSC) state; however, there is no definitive evidence that MUC1-C regulates chromatin accessibility and thereby expression of stemness-associated genes. We demonstrate that MUC1-C drives global changes in chromatin architecture in the dedifferentiation of CRPC and TNBC cells. Our results show that MUC1-C induces differentially accessible regions (DAR) across their genomes, which are significantly associated with differentially expressed genes (DEG). Motif and cistrome analysis further demonstrated MUC1-C-induced DARs align with genes regulated by the JUN/AP-1 family of transcription factors. MUC1-C activates the BAF chromatin remodeling complex, which is recruited by JUN in enhancer selection. In studies of the NOTCH1 gene, which is required for CRPC and TNBC cell self-renewal, we demonstrate that MUC1-C is necessary for (i) occupancy of JUN and ARID1A/BAF, (ii) increases in H3K27ac and H3K4me3 signals, and (iii) opening of chromatin accessibility on a proximal enhancer-like signature. Studies of the EGR1 and LY6E stemness-associated genes further demonstrate that MUC1-C-induced JUN/ARID1A complexes regulate chromatin accessibility on proximal and distal enhancer-like signatures. These findings uncover a role for MUC1-C in chromatin remodeling that is mediated at least in part by JUN/AP-1 and ARID1A/BAF in association with driving the CSC state. Implications: These findings show that MUC1-C, which is necessary for the CRPC and TNBC CSC state, activates a novel pathway involving JUN/AP-1 and ARID1A/BAF that regulates chromatin accessibility of stemness-associated gene enhancers.
MeSH term(s)	Carcinogenesis/genetics ; Chromatin/genetics ; Chromatin/metabolism ; Chromatin Assembly and Disassembly ; Gene Expression Regulation, Neoplastic ; Humans ; Male ; Mucin-1/metabolism ; Neoplastic Stem Cells/metabolism ; Oncogenes
Chemical Substances	Chromatin ; MUC1 protein, human ; Mucin-1
Language	English
Publishing date	2022-01-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2098788-2
ISSN	1557-3125 ; 1541-7786
ISSN (online)	1557-3125
ISSN	1541-7786
DOI	10.1158/1541-7786.MCR-21-0672
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Zs.A 5744: Show issues

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Article ; Online: GRP75-mediated upregulation of HMGA1 stimulates stage I lung adenocarcinoma progression by activating JNK/c-JUN signaling.

Qiao, Guo-Bing / Wang, Ren-Tao / Wang, Shu-Nan / Tao, Shao-Lin / Tan, Qun-You / Jin, Hua

Thoracic cancer

2021 Volume 12, Issue 10, Page(s) 1558–1569

Abstract: ... In addition, the GRP75/HMGA1 axis played its role by activating JNK/c-JUN signaling in LUAD.: Conclusions ... The activation of GRP75/HMGA1/JNK/c-JUN signaling is an important mechanism that promotes the progression ...

Abstract	Background: Recurrence is a major challenge in early-stage lung adenocarcinoma (LUAD) treatment. Here, we investigated the role and mechanism of high-mobility group AT-hook 1 (HMGA1) and glucose-regulated protein 75-kDa (GRP75) in stage I LUAD and evaluated their potential as biomarkers for predicting the recurrence and prognosis of stage I LUAD. Methods: The TCGA dataset was used to investigate the clinical significance of HMGA1 and GRP75 in early-stage LUAD. The biological functions of HMGA1 and GRP75 in LUAD were investigated both in vitro and in vivo through overexpression and knockdown experiments. The interaction and regulation between HMGA1 and GRP75 were evaluated with coimmunoprecipitation and ubiquitination assays. The downstream signaling pathway of the GRP75/HMGA1 axis was investigated by mRNA-sequencing analysis. Results: Both HMGA1 expression levels and GRP75 expression levels were associated with recurrence in stage I LUAD patients. In particular, HMGA1 had potential as an independent prognostic factor in stage I LUAD patients. Overexpression of GRP75 or HMGA1 significantly stimulated LUAD cell growth and metastasis, while silencing GRP75 or HMGA1 inhibited LUAD cell growth and metastasis in vitro and in vivo. Importantly, GRP75 inhibited ubiquitination-mediated HMGA1 degradation by directly binding to HMGA1, thereby causes HMGA1 upregulation in LUAD. In addition, the GRP75/HMGA1 axis played its role by activating JNK/c-JUN signaling in LUAD. Conclusions: The activation of GRP75/HMGA1/JNK/c-JUN signaling is an important mechanism that promotes the progression of stage I LUAD, and a high level of HMGA1 is a novel biomarker for predicting recurrence and a poor prognosis in stage I LUAD patients.
MeSH term(s)	A549 Cells ; Adenocarcinoma of Lung/genetics ; Adenocarcinoma of Lung/metabolism ; Adenocarcinoma of Lung/pathology ; Animals ; Disease Progression ; Female ; HMGA1a Protein/metabolism ; HSP70 Heat-Shock Proteins/metabolism ; Humans ; Lung Neoplasms/genetics ; Lung Neoplasms/metabolism ; Lung Neoplasms/pathology ; MAP Kinase Signaling System ; Mice ; Mitochondrial Proteins/metabolism ; Mitogen-Activated Protein Kinase 8/metabolism ; Neoplasm Staging ; Prognosis ; Transfection ; Up-Regulation
Chemical Substances	HMGA1 protein, human ; HSP70 Heat-Shock Proteins ; HSPA9 protein, human ; Mitochondrial Proteins ; HMGA1a Protein (124544-67-8) ; Mitogen-Activated Protein Kinase 8 (EC 2.7.11.24)
Language	English
Publishing date	2021-03-23
Publishing country	Singapore
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2625856-0
ISSN	1759-7714 ; 1759-7706
ISSN (online)	1759-7714
ISSN	1759-7706
DOI	10.1111/1759-7714.13944
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Zs.A 6921: Show issues

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Article ; Online: Glutamine exerts a protective effect on osteoarthritis development by inhibiting the Jun N-terminal kinase and nuclear factor kappa-B signaling pathways.

Zhong, Lin / Cao, Le / Song, Rui / Yang, Xue-Fei / Li, Jia-Le / Yang, Hai-Tao / Zhou, Hong-Xiang / Fan, Hai-Tao

Scientific reports

2022 Volume 12, Issue 1, Page(s) 11957

Abstract: Strategies for treating osteoarthritis (OA) have become a research focus because an effective treatment for OA is unavailable. The objective of this study was to explore the effects and underlying mechanisms of glutamine (Gln) in OA. First, the ... ...

Abstract	Strategies for treating osteoarthritis (OA) have become a research focus because an effective treatment for OA is unavailable. The objective of this study was to explore the effects and underlying mechanisms of glutamine (Gln) in OA. First, the chondrocytes were identified and a standard IL-1β-induced OA model was established. After treatment with Gln or saline, the viability and apoptosis of chondrocytes were evaluated using a CCK-8 assay and flow cytometry analysis, which revealed that Gln can improve the IL-1β-induced OA cells. Meanwhile, Gln can enhance the expression of aggrecan and collagen II, which are protective proteins for articular cartilage. Instead, Gln inhibited the expression of matrix metalloproteinase-1 (MMP-1) and matrix metalloproteinase-13 (MMP-13), which can degrade cartilage. To better understand the underlying mechanisms of Gln in IL-1β-induced chondrocytes, the classical OA pathways of JNK and NF-κB were examined at the protein and mRNA levels using western blot and qRT-PCR analyses. We found that JNK and NF-κB were downregulated gradually depending on the Gln dose and protective and destructive factors changed based on changes of JNK and NF-κB. The effects of high-dose Gln were more effective than low-dose. Moreover, Gln was applied to the animal OA model to check the effects in vivo. The results showed that Gln attenuated cartilage degeneration and decreased OARSI scores, which demonstrated that Gln can improve OA. The experiments showed that Gln can benefit mice with OA by inhibiting the JNK and NF-κB signaling pathways.
MeSH term(s)	Animals ; Cartilage, Articular/metabolism ; Cells, Cultured ; Chondrocytes/metabolism ; Disease Models, Animal ; Glutamine/metabolism ; Interleukin-1beta/metabolism ; JNK Mitogen-Activated Protein Kinases/metabolism ; Mice ; NF-kappa B/metabolism ; Osteoarthritis/drug therapy ; Osteoarthritis/metabolism ; Signal Transduction
Chemical Substances	Interleukin-1beta ; NF-kappa B ; Glutamine (0RH81L854J) ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2022-07-13
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-022-16093-7
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Article: Erratum: lncRNA RP11-147L13.8 suppresses metastasis and chemo-resistance by modulating the phosphorylation of c-Jun protein in GBC.

Zheng, Bohao / Wang, Jiwen / Fan, Kun / Sun, Wentao / Wan, Wenze / Gao, Zhihui / Ni, Xiaojian / Zhang, Dexiang / Ni, Xiaoling / Suo, Tao / Liu, Han / Liu, Houbao / Shen, Sheng

Molecular therapy oncolytics

2021 Volume 23, Page(s) 531–533

Abstract: This corrects the article DOI: 10.1016/j.omto.2021.08.016.]. ...

Abstract	[This corrects the article DOI: 10.1016/j.omto.2021.08.016.].
Language	English
Publishing date	2021-11-29
Publishing country	United States
Document type	Published Erratum
ISSN	2372-7705
ISSN	2372-7705
DOI	10.1016/j.omto.2021.11.015
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Article ; Online: Long-term instillation to four natural representative chrysotile of China induce the inactivation of P53 and P16 and the activation of C-JUN and C-FOS in the lung tissues of Wistar rats.

Luo, Yingyu / Deng, Jianjun / Cui, Yan / Li, Tao / Bai, Jun / Huang, Liuwen / Sun, Yaochuan / Dong, Faqin / Zhang, Qingbi

Toxicology letters

2020 Volume 333, Page(s) 140–149

Abstract: ... of the tumor suppressor gene P53 and P16 and activation of the protooncogene C-JUN and C-FOS both in the messenger RNA and ...

Abstract	Chrysotile is the only type of asbestos still widely exploited, and all kinds of asbestos including chrysotile was classified as a group I carcinogen by the IARC. There is a wealth of evidence that chrysotile can cause a range of cancers, including cancer of the lung, larynx, ovary, and mesothelioma. As the second largest chrysotile producer, China is at great risk of occupational exposure. Moreover, our previous experiment and some other studies have shown that the toxicity of mineral fibre from various mining areas may be different. To explore the oncogenic potential of chrysotile from different mining areas of China, Wistar rats were administered 0.5 mL chrysotile asbestos suspension of 2.0 mg/mL (from Akesai, Gansu; Mangnai, Qinghai; XinKang, Sichuan; and Shannan, Shaanxi) dissolved in saline by intratracheal instillation once-monthly and were sacrificed at 1 mo, 6 mo, and 12 mo. Our results found that chrysotile caused lung inflammation and lung tissue damage. Moreover, prolonged exposure of chrysotile can induce inactivation of the tumor suppressor gene P53 and P16 and activation of the protooncogene C-JUN and C-FOS both in the messenger RNA and protein level. In addition, chrysotile from Shannan and XinKang has a stronger effect which may link to cancer than that from Akesai and Mangnai.
MeSH term(s)	Animals ; Asbestos, Serpentine/chemistry ; Asbestos, Serpentine/toxicity ; Bronchoalveolar Lavage Fluid/cytology ; China ; Cyclin-Dependent Kinase Inhibitor p16/genetics ; Cyclin-Dependent Kinase Inhibitor p16/metabolism ; Cytokines/metabolism ; Environmental Pollutants/chemistry ; Environmental Pollutants/toxicity ; Gene Expression/drug effects ; Inhalation Exposure/adverse effects ; JNK Mitogen-Activated Protein Kinases/genetics ; JNK Mitogen-Activated Protein Kinases/metabolism ; Leukocyte Count ; Leukocytes/cytology ; Leukocytes/drug effects ; Lung/drug effects ; Lung/immunology ; Lung/metabolism ; Lung/pathology ; Male ; Mineral Fibers/toxicity ; Proto-Oncogene Proteins c-fos/genetics ; Proto-Oncogene Proteins c-fos/metabolism ; Rats, Wistar ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	Asbestos, Serpentine ; Cyclin-Dependent Kinase Inhibitor p16 ; Cytokines ; Environmental Pollutants ; Mineral Fibers ; Proto-Oncogene Proteins c-fos ; Tumor Suppressor Protein p53 ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2020-08-02
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	433788-8
ISSN	1879-3169 ; 0378-4274
ISSN (online)	1879-3169
ISSN	0378-4274
DOI	10.1016/j.toxlet.2020.07.033
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