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Article ; Online: c-Jun NH

Gunarta, I Ketut / Yuliana, Dewi / Erdenebaatar, Purev / Kishi, Yuhei / Boldbaatar, Jambaldorj / Suzuki, Ryusuke / Odongoo, Ravdandorj / Davaakhuu, Gantulga / Hohjoh, Hirohiko / Yoshioka, Katsuji

Drug discoveries & therapeutics

2021 Volume 15, Issue 2, Page(s) 66–72

Abstract: ... scaffold protein c-Jun NH ...

Abstract	Curcumin, a major component of turmeric, is known to exhibit multiple biological functions including antitumor activity. We previously reported that the mitogen-activated protein kinase (MAPK) scaffold protein c-Jun NH
MeSH term(s)	Adaptor Proteins, Signal Transducing/metabolism ; Adaptor Proteins, Signal Transducing/pharmacology ; Antineoplastic Agents/adverse effects ; Antineoplastic Agents/pharmacology ; Autophagy/drug effects ; Autophagy/genetics ; Cell Culture Techniques ; Cell Death/drug effects ; Cell Death/genetics ; Curcumin/adverse effects ; Curcumin/pharmacology ; Drug Development/methods ; Humans ; Leucine Zippers/genetics ; Lysosomes/drug effects ; Lysosomes/genetics ; MAP Kinase Signaling System/drug effects ; Mitogen-Activated Protein Kinase 9/metabolism ; Mitogen-Activated Protein Kinases/drug effects ; Mitogen-Activated Protein Kinases/metabolism ; Neoplasms/drug therapy ; Nerve Tissue Proteins/metabolism ; Nerve Tissue Proteins/pharmacology ; Protective Agents ; Reactive Oxygen Species/metabolism
Chemical Substances	Adaptor Proteins, Signal Transducing ; Antineoplastic Agents ; MAPK8IP3 protein, human ; Nerve Tissue Proteins ; Protective Agents ; Reactive Oxygen Species ; Mitogen-Activated Protein Kinase 9 (EC 2.7.1.24) ; Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Curcumin (IT942ZTH98)
Language	English
Publishing date	2021-03-14
Publishing country	Japan
Document type	Journal Article
ZDB-ID	2568828-5
ISSN	1881-784X ; 1881-784X
ISSN (online)	1881-784X
ISSN	1881-784X
DOI	10.5582/ddt.2021.01021
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Article ; Online: Functional role of c-Jun NH

Suzuki, Ryusuke / Gunarta, I Ketut / Boldbaatar, Jambaldorj / Erdenebaatar, Purev / Odongoo, Ravdandorj / Yoshioka, Katsuji

Drug discoveries & therapeutics

2020 Volume 14, Issue 1, Page(s) 35–41

Abstract: ... fully elucidated. In this study we analyzed c-Jun NH ...

Abstract	Lysosomes are involved in many cellular functions, and in turn lysosomal dysfunction underlies a variety of diseases, including cancer and neurodegenerative diseases. Lysosomes are distributed broadly in the cytoplasm and can move throughout the cell in kinesin- and dynein-dependent manners. Although many mechanisms of lysosomal transport have been reported, how lysosomal transport is regulated has yet to be fully elucidated. In this study we analyzed c-Jun NH
MeSH term(s)	Adaptor Proteins, Signal Transducing/metabolism ; Autophagy ; Dynactin Complex/metabolism ; Humans ; Kinesin/metabolism ; Lysosomes/metabolism ; Mitogen-Activated Protein Kinase 9/metabolism
Chemical Substances	Adaptor Proteins, Signal Transducing ; DCTN1 protein, human ; Dynactin Complex ; SPAG9 protein, human ; Mitogen-Activated Protein Kinase 9 (EC 2.7.1.24) ; Kinesin (EC 3.6.4.4)
Language	English
Publishing date	2020-02-05
Publishing country	Japan
Document type	Journal Article
ISSN	1881-784X
ISSN (online)	1881-784X
DOI	10.5582/ddt.2020.01001
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Article ; Online: Protective role of c-Jun NH

Boldbaatar, Jambaldorj / Gunarta, I Ketut / Suzuki, Ryusuke / Erdenebaatar, Purev / Davaakhuu, Gantulga / Hohjoh, Hirohiko / Yoshioka, Katsuji

Biochemical and biophysical research communications

2019 Volume 522, Issue 3, Page(s) 697–703

Abstract: ... The c-Jun NH ...

Abstract	Previous studies have established the antitumor activity of curcumin, a major component of turmeric. Increasing evidence indicates that curcumin induces autophagy, the activation of mitogen-activated protein kinase (MAPK) intracellular signaling pathways, and reactive oxygen species (ROS)-mediated cell death. The c-Jun NH
MeSH term(s)	Adaptor Proteins, Signal Transducing/metabolism ; Antineoplastic Agents/pharmacology ; Autophagy/drug effects ; Cell Death/drug effects ; Cell Line, Tumor ; Curcumin/pharmacology ; Humans ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Reactive Oxygen Species/metabolism
Chemical Substances	Adaptor Proteins, Signal Transducing ; Antineoplastic Agents ; Reactive Oxygen Species ; SPAG9 protein, human ; Curcumin (IT942ZTH98)
Language	English
Publishing date	2019-11-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2019.11.154
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Article ; Online: Enhanced phosphorylation of c-Jun by cisplatin treatment as a potential predictive biomarker for cisplatin response in combination with patient-derived tumor organoids.

Tsukamoto, Yoshiyuki / Kurogi, Shusaku / Shibata, Tomotaka / Suzuki, Kosuke / Hirashita, Yuka / Fumoto, Shoichi / Yano, Shinji / Yanagihara, Kazuyoshi / Nakada, Chisato / Mieno, Fumi / Kinoshita, Keisuke / Fuchino, Takafumi / Mizukami, Kazuhiro / Ueda, Yoshitake / Etoh, Tsuyoshi / Uchida, Tomohisa / Hanada, Toshikatsu / Takekawa, Mutsuhiro / Daa, Tsutomu /

Shirao, Kuniaki / Hironaka, Shuichi / Murakami, Kazunari / Inomata, Masafumi / Hijiya, Naoki / Moriyama, Masatsugu

Laboratory investigation; a journal of technical methods and pathology

2022 Volume 102, Issue 12, Page(s) 1355–1366

Abstract: ... Jun (p-c-Jun) within 24 h after cisplatin treatment. We also compared the responses of 6 PDOs ... matched patients. Mechanistically, the c-Jun induction was partly related to TNF signaling induced ... by cisplatin. Our data suggest that enhanced phosphorylation of c-Jun in response to cisplatin treatment ...

Abstract	Despite recent advances in sequencing technology and large-scale drug screenings employing hundreds of cell lines, the predictive accuracy of mutation-based biomarkers is still insufficient as a guide for cancer therapy. Therefore, novel types of diagnostic methods using alternative biomarkers would be highly desirable. We have hypothesized that sensitivity-specific changes in the phosphorylation of signaling molecules could be useful in this respect. Here, with the aim of developing a method for predicting the response of cancers to cisplatin using a combination of specific biomarker(s) and patient-derived tumor organoids (PDOs), we found that cisplatin-sensitive cell lines or PDOs showed enhanced phosphorylation of c-Jun (p-c-Jun) within 24 h after cisplatin treatment. We also compared the responses of 6 PDOs to cisplatin with the therapeutic effect of neoadjuvant chemotherapy (docetaxel/cisplatin/5-fluorouracil) in 6 matched patients. Mechanistically, the c-Jun induction was partly related to TNF signaling induced by cisplatin. Our data suggest that enhanced phosphorylation of c-Jun in response to cisplatin treatment could be a predictive biomarker for the efficacy of cisplatin in selected cancer patients.
MeSH term(s)	Humans ; Cisplatin/pharmacology ; Cisplatin/therapeutic use ; Organoids/pathology ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Phosphorylation ; Docetaxel/pharmacology ; Neoplasms/pathology ; Biomarkers
Chemical Substances	Cisplatin (Q20Q21Q62J) ; Antineoplastic Agents ; Docetaxel (15H5577CQD) ; Biomarkers
Language	English
Publishing date	2022-08-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80178-1
ISSN	1530-0307 ; 0023-6837
ISSN (online)	1530-0307
ISSN	0023-6837
DOI	10.1038/s41374-022-00827-2
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Article ; Online: Inhibition of the Phospholipase Cε-c-Jun N-Terminal Kinase Axis Suppresses Glioma Stem Cell Properties.

Okada, Masashi / Nakagawa-Saito, Yurika / Mitobe, Yuta / Sugai, Asuka / Togashi, Keita / Suzuki, Shuhei / Kitanaka, Chifumi

International journal of molecular sciences

2022 Volume 23, Issue 15

Abstract: Glioma stem cells (GSCs), the cancer stem cells of glioblastoma multiforme (GBM), contribute to the malignancy of GBM due to their resistance to therapy and tumorigenic potential; therefore, the development of GSC-targeted therapies is urgently needed to ...

Abstract	Glioma stem cells (GSCs), the cancer stem cells of glioblastoma multiforme (GBM), contribute to the malignancy of GBM due to their resistance to therapy and tumorigenic potential; therefore, the development of GSC-targeted therapies is urgently needed to improve the poor prognosis of GBM patients. The molecular mechanisms maintaining GSCs need to be elucidated in more detail for the development of GSC-targeted therapy. In comparison with patient-derived GSCs and their differentiated counterparts, we herein demonstrated for the first time that phospholipase C (PLC)ε was highly expressed in GSCs, in contrast to other PLC isoforms. A broad-spectrum PLC inhibitor suppressed the viability of GSCs, but not their stemness. Nevertheless, the knockdown of PLCε suppressed the survival of GSCs and induced cell death. The stem cell capacity of residual viable cells was also suppressed. Moreover, the survival of mice that were transplanted with PLCε knockdown-GSCs was longer than the control group. PLCε maintained the stemness of GSCs via the activation of JNK. The present study demonstrated for the first time that PLCε plays a critical role in maintaining the survival, stemness, and tumor initiation capacity of GSCs. Our study suggested that PLCε is a promising anti-GSC therapeutic target.
MeSH term(s)	Animals ; Brain Neoplasms/metabolism ; Cell Line, Tumor ; Glioblastoma/metabolism ; Glioma/drug therapy ; Glioma/genetics ; Glioma/metabolism ; JNK Mitogen-Activated Protein Kinases/metabolism ; Mice ; Neoplastic Stem Cells/metabolism ; Phosphoinositide Phospholipase C ; Type C Phospholipases/metabolism
Chemical Substances	JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Type C Phospholipases (EC 3.1.4.-) ; Phosphoinositide Phospholipase C (EC 3.1.4.11) ; phospholipase C epsilon (EC 3.1.4.11)
Language	English
Publishing date	2022-08-07
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/ijms23158785
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Article ; Online: m6A RNA methylation regulates the transcription factors JUN and JUNB in TGF-β-induced epithelial-mesenchymal transition of lung cancer cells.

Suphakhong, Kusuma / Terashima, Minoru / Wanna-Udom, Sasithorn / Takatsuka, Risa / Ishimura, Akihiko / Takino, Takahisa / Suzuki, Takeshi

The Journal of biological chemistry

2022 Volume 298, Issue 11, Page(s) 102554

Abstract: ... in many pathological processes including various cancers. In this study, we investigated the m6A-dependent regulation of JUN and ... within this process remains to be clarified. We found that JUN and JUNB played an important and nonredundant role ... regulation of JUN expression is associated with the translation process of JUN protein but not ...

Abstract	N6-methyladenosine (m6A) is the most common internal chemical modification of mRNAs involved in many pathological processes including various cancers. In this study, we investigated the m6A-dependent regulation of JUN and JUNB transcription factors (TFs) during transforming growth factor-beta-induced epithelial-mesenchymal transition (EMT) of A549 and LC2/ad lung cancer cell lines, as the function and regulation of these TFs within this process remains to be clarified. We found that JUN and JUNB played an important and nonredundant role in the EMT-inducing gene expression program by regulating different mesenchymal genes and that their expressions were controlled by methyltransferase-like 3 (METTL3) m6A methyltransferase. METTL3-mediated regulation of JUN expression is associated with the translation process of JUN protein but not with the stability of JUN protein or mRNA, which is in contrast with the result of m6A-mediated regulation of JUNB mRNA stability. We identified the specific m6A motifs responsible for the regulation of JUN and JUNB in EMT within 3'UTR of JUN and JUNB. Furthermore, we discovered that different m6A reader proteins interacted with JUN and JUNB mRNA and controlled m6A-dependent expression of JUN protein and JUNB mRNA. These results demonstrate that the different modes of m6A-mediated regulation of JUN and JUNB TFs provide critical input in the gene regulatory network during transforming growth factor-beta-induced EMT of lung cancer cells.
MeSH term(s)	Humans ; Epithelial-Mesenchymal Transition/genetics ; Transforming Growth Factor beta/metabolism ; Methylation ; Lung Neoplasms/genetics ; Lung Neoplasms/metabolism ; RNA, Messenger/genetics ; Transcription Factor AP-1/metabolism ; Methyltransferases/genetics ; Methyltransferases/metabolism ; Transforming Growth Factors/metabolism ; Transcription Factors/genetics ; Transcription Factors/metabolism
Chemical Substances	Transforming Growth Factor beta ; RNA, Messenger ; Transcription Factor AP-1 ; Methyltransferases (EC 2.1.1.-) ; Transforming Growth Factors (76057-06-2) ; METTL3 protein, human (EC 2.1.1.62) ; JunB protein, human ; Transcription Factors
Language	English
Publishing date	2022-09-29
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1016/j.jbc.2022.102554
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Article ; Online: Pirfenidone attenuates acetaminophen-induced liver injury via suppressing c-Jun N-terminal kinase phosphorylation.

Tashiro, Shigeki / Tanaka, Masatake / Goya, Takeshi / Aoyagi, Tomomi / Kurokawa, Miho / Imoto, Koji / Kuwano, Akifumi / Takahashi, Motoi / Suzuki, Hideo / Kohjima, Motoyuki / Kato, Masaki / Ogawa, Yoshihiro

Toxicology and applied pharmacology

2021 Volume 434, Page(s) 115817

Abstract: ... PFD suppressed APAP-induced c-Jun N-terminal kinase (JNK) phosphorylation despite no effect on JNK ...

Abstract	Acetaminophen (APAP)-induced liver injury is the most frequent cause of acute liver failure in Western countries. Pirfenidone (PFD), an orally bioavailable pyridone derivative, is clinically used for idiopathic pulmonary fibrosis treatment and has antifibrotic, anti-inflammatory, and antioxidant effects. Here we examined the PFD effect on APAP-induced liver injury. In a murine model, APAP caused serum alanine aminotransferase elevation attenuated by PFD treatment. We performed terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL) and vital propidium iodide (PI) stainings simultaneously. APAP induced TUNEL-positive/PI-negative necrosis around the central vein and subsequent TUNEL-negative/PI-positive oncotic necrosis with hemorrhage and caused the upregulation of hypercoagulation- and hypoxia-associated gene expressions. PFD treatment suppressed these findings. Western blotting revealed PFD suppressed APAP-induced c-Jun N-terminal kinase (JNK) phosphorylation despite no effect on JNK phosphatase expressions. In conclusion, simultaneous TUNEL and vital PI staining is useful for discriminating APAP-induced necrosis from typical oncotic necrosis. Our results indicated that PFD attenuated APAP-induced liver injury by suppressing TUNEL-positive necrosis by directly blocking JNK phosphorylation. PFD is promising as a new option to prevent APAP-induced liver injury.
MeSH term(s)	Acetaminophen/toxicity ; Analgesics, Non-Narcotic/toxicity ; Animals ; Anti-Inflammatory Agents, Non-Steroidal/pharmacology ; Chemical and Drug Induced Liver Injury/drug therapy ; Gene Expression Regulation, Enzymologic/drug effects ; JNK Mitogen-Activated Protein Kinases/antagonists & inhibitors ; JNK Mitogen-Activated Protein Kinases/genetics ; JNK Mitogen-Activated Protein Kinases/metabolism ; Male ; Mice ; Phosphorylation ; Pyridones/therapeutic use
Chemical Substances	Analgesics, Non-Narcotic ; Anti-Inflammatory Agents, Non-Steroidal ; Pyridones ; Acetaminophen (362O9ITL9D) ; pirfenidone (D7NLD2JX7U) ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2021-12-08
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.2021.115817
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Book: Jun Aoki

Aoki, Jun / Suzuki, Risaku

: complete works

2006

Language	English ; Japanese
Size	217, 28 S., überw. Ill.
Edition	1. publ.
Publisher	INAX Publ
Publishing place	Tokyo
Document type	Book
Note	Text engl. und japan.
ISBN	4872751361 ; 9784872751369
Database	Library catalogue of the German National Library of Science and Technology (TIB), Hannover

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Article ; Online: Inhibition of the Phospholipase Cε–c-Jun N-Terminal Kinase Axis Suppresses Glioma Stem Cell Properties

Masashi Okada / Yurika Nakagawa-Saito / Yuta Mitobe / Asuka Sugai / Keita Togashi / Shuhei Suzuki / Chifumi Kitanaka

International Journal of Molecular Sciences, Vol 23, Iss 15, p

2022 Volume 8785

Abstract	Glioma stem cells (GSCs), the cancer stem cells of glioblastoma multiforme (GBM), contribute to the malignancy of GBM due to their resistance to therapy and tumorigenic potential; therefore, the development of GSC-targeted therapies is urgently needed to improve the poor prognosis of GBM patients. The molecular mechanisms maintaining GSCs need to be elucidated in more detail for the development of GSC-targeted therapy. In comparison with patient-derived GSCs and their differentiated counterparts, we herein demonstrated for the first time that phospholipase C (PLC)ε was highly expressed in GSCs, in contrast to other PLC isoforms. A broad-spectrum PLC inhibitor suppressed the viability of GSCs, but not their stemness. Nevertheless, the knockdown of PLCε suppressed the survival of GSCs and induced cell death. The stem cell capacity of residual viable cells was also suppressed. Moreover, the survival of mice that were transplanted with PLCε knockdown-GSCs was longer than the control group. PLCε maintained the stemness of GSCs via the activation of JNK. The present study demonstrated for the first time that PLCε plays a critical role in maintaining the survival, stemness, and tumor initiation capacity of GSCs. Our study suggested that PLCε is a promising anti-GSC therapeutic target.
Keywords	glioma initiating cell ; brain tumor initiating cell ; phospholipase Cε ; c-Jun N-terminal kinase ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Language	English
Publishing date	2022-08-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Ablation of aryl hydrocarbon receptor promotes angiotensin II-induced cardiac fibrosis through enhanced c-Jun/HIF-1α signaling.

Ichihara, Sahoko / Li, Ping / Mise, Nathan / Suzuki, Yuka / Izuoka, Kiyora / Nakajima, Tamie / Gonzalez, Frank / Ichihara, Gaku

Archives of toxicology

2019 Volume 93, Issue 6, Page(s) 1543–1553

Abstract: Aryl hydrocarbon receptor (AHR) is a transcription factor that binds to DNA as a heterodimer with the AHR nuclear translocator (ARNT) after interaction with ligands, such as polycyclic and halogenated aromatic hydrocarbons and other xenobiotics. The ... ...

Abstract	Aryl hydrocarbon receptor (AHR) is a transcription factor that binds to DNA as a heterodimer with the AHR nuclear translocator (ARNT) after interaction with ligands, such as polycyclic and halogenated aromatic hydrocarbons and other xenobiotics. The endogenous ligands and functions of AHR have been the subject of many investigations. In the present study, the potential role of AHR signaling in the development of left ventricular hypertrophy and cardiac fibrosis by angiotensin II (Ang II) infusion was investigated in mice lacking the AHR gene (Ahr
MeSH term(s)	Angiotensin II/toxicity ; Animals ; Basic Helix-Loop-Helix Transcription Factors/genetics ; Basic Helix-Loop-Helix Transcription Factors/metabolism ; Blood Pressure/drug effects ; Fenofibrate/pharmacology ; Fibrosis ; Hypertrophy, Left Ventricular/pathology ; Hypoxia-Inducible Factor 1, alpha Subunit/genetics ; JNK Mitogen-Activated Protein Kinases/genetics ; Male ; Mice ; Mice, Knockout ; Myocardium/pathology ; PPAR alpha/agonists ; Receptors, Aryl Hydrocarbon/genetics ; Receptors, Aryl Hydrocarbon/metabolism ; Signal Transduction/drug effects ; Signal Transduction/genetics ; Vascular Endothelial Growth Factor A/biosynthesis ; Vascular Endothelial Growth Factor A/genetics
Chemical Substances	Ahr protein, mouse ; Basic Helix-Loop-Helix Transcription Factors ; Hif1a protein, mouse ; Hypoxia-Inducible Factor 1, alpha Subunit ; PPAR alpha ; Receptors, Aryl Hydrocarbon ; Vascular Endothelial Growth Factor A ; vascular endothelial growth factor A, mouse ; Angiotensin II (11128-99-7) ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Fenofibrate (U202363UOS)
Language	English
Publishing date	2019-04-23
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	124992-7
ISSN	1432-0738 ; 0340-5761
ISSN (online)	1432-0738
ISSN	0340-5761
DOI	10.1007/s00204-019-02446-1
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