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Article ; Online: NF2 alteration in mesothelioma.

Sekido, Yoshitaka / Sato, Tatsuhiro

Frontiers in toxicology

2023 Volume 5, Page(s) 1161995

Abstract: ... ...

Abstract	The
Language	English
Publishing date	2023-04-25
Publishing country	Switzerland
Document type	Journal Article ; Review
ISSN	2673-3080
ISSN (online)	2673-3080
DOI	10.3389/ftox.2023.1161995
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Article: Targeting the Hippo Pathway Is a New Potential Therapeutic Modality for Malignant Mesothelioma.

Sekido, Yoshitaka

Cancers

2018 Volume 10, Issue 4

Abstract: Malignant mesothelioma (MM) constitutes a very aggressive tumor that arises from the pleural or peritoneal cavities and is highly refractory to conventional therapies. Several key genetic alterations are associated with the development and progression of ...

Abstract	Malignant mesothelioma (MM) constitutes a very aggressive tumor that arises from the pleural or peritoneal cavities and is highly refractory to conventional therapies. Several key genetic alterations are associated with the development and progression of MM including mutations of the
Language	English
Publishing date	2018-03-22
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers10040090
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Article ; Online: Aberrant expression of NPPB through YAP1 and TAZ activation in mesothelioma with Hippo pathway gene alterations.

Sato, Tatsuhiro / Akao, Ken / Sato, Ayuko / Tsujimura, Tohru / Mukai, Satomi / Sekido, Yoshitaka

Cancer medicine

2023 Volume 12, Issue 12, Page(s) 13586–13598

Abstract: Background: Mesothelioma is a neoplastic disease associated with asbestos exposure. It is highly malignant and has a poor prognosis; thus, early detection is desirable. Recent whole-genome analysis has revealed that mesothelioma is characterized by a ... ...

Abstract	Background: Mesothelioma is a neoplastic disease associated with asbestos exposure. It is highly malignant and has a poor prognosis; thus, early detection is desirable. Recent whole-genome analysis has revealed that mesothelioma is characterized by a high frequency of mutations in a set of genes involved in the Hippo pathway, such as NF2 and LATS2. However, a rapid, simple, and precise method for finding mesothelioma with these mutations has not yet been established. Methods: Clustering of Hippo pathway gene alteration groups and the differential expression of each gene in mesothelioma patients were analyzed using The Cancer Genome Atlas database. Gene expression levels in various tumors and normal tissues were analyzed using public databases. Knockdown or transient expression of YAP1 or TAZ was performed to evaluate the regulation of gene expression by these genes. NT-proBNP was measured in the pleural effusions of 18 patients and was compared with NF2 expression in five cases where cell lines had been successfully established. Results: NPPB mRNA expression was markedly higher in the group of mesothelioma patients with Hippo pathway gene mutations than in the group without them. NPPB expression was low in all normal tissues except heart, and was highest in mesothelioma. Mesothelioma patients in the high NPPB expression group had a significantly worse prognosis than those in the low NPPB expression group. NPPB expression was suppressed by knockdown of YAP1 or TAZ. NT-proBNP was abundant in the effusions of mesothelioma patients and was particularly high in those with impaired NF2 expression. Conclusions: NPPB, whose levels can be measured in pleural effusions of mesothelioma patients, has the potential to act as a biomarker to detect NF2-Hippo pathway gene alterations and/or predict patient prognosis. Additionally, it may provide useful molecular insights for a better understanding of mesothelioma pathogenesis and for the development of novel therapies.
MeSH term(s)	Humans ; Hippo Signaling Pathway ; Mesothelioma, Malignant ; Mesothelioma/genetics ; Pleural Effusion ; Protein Serine-Threonine Kinases/genetics ; Protein Serine-Threonine Kinases/metabolism ; Tumor Suppressor Proteins/metabolism
Chemical Substances	5-nitro-2-(3-phenylpropylamino)benzoic acid (3A35O9G3YZ) ; LATS2 protein, human (EC 2.7.1.11) ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Tumor Suppressor Proteins
Language	English
Publishing date	2023-05-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2659751-2
ISSN	2045-7634 ; 2045-7634
ISSN (online)	2045-7634
ISSN	2045-7634
DOI	10.1002/cam4.6056
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Article ; Online: PCBP2 knockdown promotes ferroptosis in malignant mesothelioma.

Yue, Lin / Luo, Yaguang / Jiang, Li / Sekido, Yoshitaka / Toyokuni, Shinya

Pathology international

2022 Volume 72, Issue 4, Page(s) 242–251

Abstract: Malignant mesothelioma (MM) is still increasing worldwide. The pathogenesis depends on asbestos-induced iron accumulation, which eventually leads to ferroptosis-resistance of mesothelial cells via somatic mutations. Poly (rC)-binding proteins 1 and 2 ( ... ...

Abstract	Malignant mesothelioma (MM) is still increasing worldwide. The pathogenesis depends on asbestos-induced iron accumulation, which eventually leads to ferroptosis-resistance of mesothelial cells via somatic mutations. Poly (rC)-binding proteins 1 and 2 (PCBP1/2) are recently recognized cytosolic Fe(II) chaperones. Here we studied the role of PCBP1/2 in rat/human mesothelial and MM cells as well as rat/human MM specimens. Normal peritoneal mesothelial cells in rats exhibited PCBP1 but not PCBP2 immunopositivity whereas primary/immortalized mesothelial cells showed PCBP1/2 immunopositivity. Rat MM specimens induced by intraperitoneal injection of chrysotile, including in situ lesion, revealed PCBP1/2 immunopositivity (90% for both) in the nucleus and cytoplasm with a tendency of higher expression in epithelioid subtype. Knockdown of PCBP2 but not PCBP1 significantly decreased both TfR1 and FTH expression in MM cells with inhibition of proliferation, indicating stagnation of intracellular iron transport. Erastin, a cysteine-deprivation type ferroptosis inducer, decreased the expression of both PCBP1/2 in MM cells. Furthermore, PCBP2 knockdown significantly increased the sensitivity of MM cells to erastin-induced ferroptosis with increased catalytic Fe(II). In conclusion, PCBP2 works for ferroptosis-resistance not only during mesothelial carcinogenesis but also in MM, which warrants further investigation as a novel therapeutic target.
MeSH term(s)	Animals ; Ferroptosis ; Ferrous Compounds/metabolism ; Gene Knockdown Techniques ; Humans ; Iron/metabolism ; Mesothelioma, Malignant/genetics ; Mesothelioma, Malignant/metabolism ; RNA-Binding Proteins/genetics ; RNA-Binding Proteins/metabolism ; Rats
Chemical Substances	Ferrous Compounds ; PCBP2 protein, human ; RNA-Binding Proteins ; poly(rC) binding protein 2, rat ; Iron (E1UOL152H7)
Language	English
Publishing date	2022-01-28
Publishing country	Australia
Document type	Journal Article
ZDB-ID	1194850-4
ISSN	1440-1827 ; 1320-5463
ISSN (online)	1440-1827
ISSN	1320-5463
DOI	10.1111/pin.13209
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Article ; Online: Molecular pathogenesis of malignant mesothelioma.

Sekido, Yoshitaka

Carcinogenesis

2013 Volume 34, Issue 7, Page(s) 1413–1419

Abstract: Malignant mesothelioma (MM) is an aggressive tumor arising primarily from the pleural or peritoneal cavities. It develops by asbestos exposure after a long latency, which is characterized by insidious growth and clinical presentation at an advanced stage ...

Abstract	Malignant mesothelioma (MM) is an aggressive tumor arising primarily from the pleural or peritoneal cavities. It develops by asbestos exposure after a long latency, which is characterized by insidious growth and clinical presentation at an advanced stage of disease. MM is highly refractory to conventional therapies even with a combination of aggressive surgical intervention and multimodality strategies, with cure remaining elusive. Molecular genetic analysis has revealed several key genetic alterations, which are responsible for the development and progression of MM. The cyclin-dependent kinase inhibitor 2A/alternative reading frame (CDKN2A/ARF), neurofibromatosis type 2 (NF2) and BRCA1-associated protein-1 (BAP1) genes are the most frequently mutated tumor suppressor genes detected in MM cells; the alterations of the latter two are relatively characteristic of MM. Merlin, which is encoded by NF2, regulates multiple cell signaling cascades including the Hippo and mammalian target of rapamycin pathways, which regulate cell proliferation and growth. BAP1 is involved in histone modification and its inactivation induces the disturbance of global gene expression profiling. The discovery of a new familial cancer syndrome with germline mutation of BAP1 also indicates the importance of genetic factors in MM susceptibility. Meanwhile, although frequent expression and functional activations of oncogene products such as receptor tyrosine kinases are observed in MM cells, activating mutations of these genes are rare. With further comprehensive genome analyses, new genetic and epigenetic alterations in MM cells are expected to be revealed more precisely, and the new knowledge based on them will be applied for developing new diagnostic tools and new target therapies against MMs.
MeSH term(s)	Asbestos/adverse effects ; Cell Transformation, Neoplastic/chemically induced ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/pathology ; Disease Progression ; Disease Susceptibility/pathology ; Epigenesis, Genetic ; Gene Expression Regulation, Neoplastic ; Gene Frequency ; Genes, p16 ; Humans ; Mesothelioma/chemically induced ; Mesothelioma/genetics ; Mesothelioma/pathology ; Neurofibromin 2/genetics ; Neurofibromin 2/metabolism ; TOR Serine-Threonine Kinases/genetics ; TOR Serine-Threonine Kinases/metabolism ; Tumor Suppressor Proteins/genetics ; Tumor Suppressor Proteins/metabolism ; Ubiquitin Thiolesterase/genetics ; Ubiquitin Thiolesterase/metabolism
Chemical Substances	BAP1 protein, human ; Neurofibromin 2 ; Tumor Suppressor Proteins ; Asbestos (1332-21-4) ; MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Ubiquitin Thiolesterase (EC 3.4.19.12)
Language	English
Publishing date	2013-05-14
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	603134-1
ISSN	1460-2180 ; 0143-3334
ISSN (online)	1460-2180
ISSN	0143-3334
DOI	10.1093/carcin/bgt166
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Article ; Online: NF2/Merlin Inactivation and Potential Therapeutic Targets in Mesothelioma.

Sato, Tatsuhiro / Sekido, Yoshitaka

International journal of molecular sciences

2018 Volume 19, Issue 4

Abstract: The neurofibromatosis type 2 ( ...

Abstract	The neurofibromatosis type 2 (
MeSH term(s)	Actins/metabolism ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Gene Expression Regulation, Neoplastic/drug effects ; Genetic Variation ; Humans ; Lung Neoplasms/drug therapy ; Lung Neoplasms/genetics ; Lung Neoplasms/metabolism ; Mesothelioma/drug therapy ; Mesothelioma/genetics ; Mesothelioma/metabolism ; Mesothelioma, Malignant ; Neurofibromin 2/genetics ; Neurofibromin 2/metabolism ; Protein-Serine-Threonine Kinases/metabolism ; Signal Transduction ; TOR Serine-Threonine Kinases/metabolism
Chemical Substances	Actins ; Antineoplastic Agents ; Neurofibromin 2 ; MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Hippo protein, human (EC 2.7.11.1) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2018-03-26
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms19040988
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Article ; Online: Inactivation of Merlin in malignant mesothelioma cells and the Hippo signaling cascade dysregulation.

Sekido, Yoshitaka

Pathology international

2011 Volume 61, Issue 6, Page(s) 331–344

Abstract: Malignant mesothelioma (MM) is an aggressive tumor arising primarily from pleural or peritoneal cavities, which is caused by asbestos exposure after long latency. One of the most frequently mutated genes detected in MM cells is the neurofibromatosis type ...

Abstract	Malignant mesothelioma (MM) is an aggressive tumor arising primarily from pleural or peritoneal cavities, which is caused by asbestos exposure after long latency. One of the most frequently mutated genes detected in MM cells is the neurofibromatosis type 2 (NF2) tumor suppressor gene which is located at chromosome 22q12. The NF2 gene encodes Merlin, an ERM (Ezrin/Radixin/Moesin) protein. The underphosphorylated form of Merlin is active and acts as a tumor suppressor by regulating several distinct cellular signaling pathways. One of the downstream pathways regulated by Merlin is the Hippo signaling pathway, which is conserved from Drosophila to mammalian cells and plays important roles in organ size control and cancer development. Recent studies have identified alterations of the components in the Hippo signaling cascade in MM cells, including overexpression of Yes-associated protein (YAP) and inactivation of large tumor suppressor homolog 2 (LATS2). Dysregulation of the Merlin-Hippo signaling cascade is one of the frequent and key events of MM cell development and/or progression. Thus, a strategy to normalize this signaling cascade may be the rationale for developing a new target therapy against MM.
MeSH term(s)	Animals ; Cell Line, Tumor ; Chromosomes, Human, Pair 22 ; Disease Models, Animal ; Drosophila ; Drosophila Proteins/genetics ; Drosophila Proteins/physiology ; Genes, Tumor Suppressor ; Humans ; Intracellular Signaling Peptides and Proteins/genetics ; Intracellular Signaling Peptides and Proteins/metabolism ; Intracellular Signaling Peptides and Proteins/physiology ; Mesothelioma/genetics ; Mesothelioma/pathology ; Mutation ; Neurofibromin 2/chemistry ; Neurofibromin 2/genetics ; Neurofibromin 2/physiology ; Phosphorylation ; Pleural Neoplasms/genetics ; Pleural Neoplasms/pathology ; Protein-Serine-Threonine Kinases/genetics ; Protein-Serine-Threonine Kinases/physiology ; Signal Transduction/physiology ; Tumor Suppressor Proteins/genetics
Chemical Substances	Drosophila Proteins ; Intracellular Signaling Peptides and Proteins ; Neurofibromin 2 ; Tumor Suppressor Proteins ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; hpo protein, Drosophila (EC 2.7.11.1)
Language	English
Publishing date	2011-06
Publishing country	Australia
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1194850-4
ISSN	1440-1827 ; 1320-5463
ISSN (online)	1440-1827
ISSN	1320-5463
DOI	10.1111/j.1440-1827.2011.02666.x
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Article ; Online: Elaborate cooperation of poly(rC)-binding proteins 1/2 and glutathione in ferroptosis induced by plasma-activated Ringer's lactate.

Jiang, Li / Zheng, Hao / Ishida, Moe / Lyu, Qinying / Akatsuka, Shinya / Motooka, Yashiro / Sato, Kotaro / Sekido, Yoshitaka / Nakamura, Kae / Tanaka, Hiromasa / Ishikawa, Kenji / Kajiyama, Hiroaki / Mizuno, Masaaki / Hori, Masaru / Toyokuni, Shinya

Free radical biology & medicine

2024 Volume 214, Page(s) 28–41

Abstract: Reactive species are involved in various aspects of neoplastic diseases, including carcinogenesis, cancer-specific metabolism and therapeutics. Non-thermal plasma (NTP) can directly provide reactive species, by integrating atmospheric and interjacent ... ...

Abstract	Reactive species are involved in various aspects of neoplastic diseases, including carcinogenesis, cancer-specific metabolism and therapeutics. Non-thermal plasma (NTP) can directly provide reactive species, by integrating atmospheric and interjacent molecules as substrates, to represent a handy strategy to load oxidative stress in situ. NTP causes apoptosis and/or ferroptosis specifically in cancer cells of various types. Plasma-activated Ringer's lactate (PAL) is another modality at the preclinical stage as cancer therapeutics, based on more stable reactive species. PAL specifically kills malignant mesothelioma (MM) cells, employing lysosomal ·NO as a switch from autophagy to ferroptosis. However, the entire molecular mechanisms have not been elucidated yet. Here we studied cytosolic iron regulations in MM and other cancer cells in response to PAL exposure. We discovered that cells with higher catalytic Fe(II) are more susceptible to PAL-induced ferroptosis. PAL caused a cytosolic catalytic Fe(II)-associated pathology through iron chaperones, poly (rC)-binding proteins (PCBP)1/2, inducing a disturbance in glutathione-regulated iron homeostasis. PCBP1/NCOA4-mediated ferritinophagy started at a later phase, further increasing cytosolic catalytic Fe(II), ending in ferroptosis. In contrast, PCBP2 after PAL exposure contributed to iron loading to mitochondria, leading to mitochondrial dysfunction. Therapeutic effect of PAL was successfully applied to an orthotopic MM xenograft model in mice. In conclusion, PAL can selectively sensitize MM cells to ferroptosis by remodeling cytoplasmic iron homeostasis, where glutathione and PCBPs play distinct roles, resulting in lethal ferritinophagy and mitochondrial dysfunction. Our findings indicate the clinical application of PAL as a ferroptosis-inducer and the potential of PCBPs as novel targets in cancer therapeutics.
MeSH term(s)	Humans ; Animals ; Mice ; Carrier Proteins ; Ringer's Lactate ; Ferroptosis ; Mesothelioma, Malignant ; Mesothelioma ; Glutathione ; Iron ; Mitochondrial Diseases ; Ferrous Compounds ; RNA-Binding Proteins/genetics
Chemical Substances	Carrier Proteins ; Ringer's Lactate ; Glutathione (GAN16C9B8O) ; Iron (E1UOL152H7) ; Ferrous Compounds ; PCBP2 protein, human ; RNA-Binding Proteins
Language	English
Publishing date	2024-02-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	807032-5
ISSN	1873-4596 ; 0891-5849
ISSN (online)	1873-4596
ISSN	0891-5849
DOI	10.1016/j.freeradbiomed.2024.02.001
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Article ; Online: NF2/Merlin Inactivation and Potential Therapeutic Targets in Mesothelioma

Tatsuhiro Sato / Yoshitaka Sekido

International Journal of Molecular Sciences, Vol 19, Iss 4, p

2018 Volume 988

Abstract: The neurofibromatosis type 2 (NF2) gene encodes merlin, a tumor suppressor protein frequently inactivated in schwannoma, meningioma, and malignant mesothelioma (MM). The sequence of merlin is similar to that of ezrin/radixin/moesin (ERM) proteins which ... ...

Abstract	The neurofibromatosis type 2 (NF2) gene encodes merlin, a tumor suppressor protein frequently inactivated in schwannoma, meningioma, and malignant mesothelioma (MM). The sequence of merlin is similar to that of ezrin/radixin/moesin (ERM) proteins which crosslink actin with the plasma membrane, suggesting that merlin plays a role in transducing extracellular signals to the actin cytoskeleton. Merlin adopts a distinct closed conformation defined by specific intramolecular interactions and regulates diverse cellular events such as transcription, translation, ubiquitination, and miRNA biosynthesis, many of which are mediated through Hippo and mTOR signaling, which are known to be closely involved in cancer development. MM is a very aggressive tumor associated with asbestos exposure, and genetic alterations in NF2 that abrogate merlin’s functional activity are found in about 40% of MMs, indicating the importance of NF2 inactivation in MM development and progression. In this review, we summarize the current knowledge of molecular events triggered by NF2/merlin inactivation, which lead to the development of mesothelioma and other cancers, and discuss potential therapeutic targets in merlin-deficient mesotheliomas.
Keywords	malignant mesothelioma ; neurofibromatosis type 2 (NF2) ; merlin ; Hippo signaling pathway ; PI3K/AKT/mTOR signaling pathway ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	572
Language	English
Publishing date	2018-03-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article ; Online: Genomic abnormalities and signal transduction dysregulation in malignant mesothelioma cells.

Sekido, Yoshitaka

Cancer science

2010 Volume 101, Issue 1, Page(s) 1–6

Abstract: Malignant mesothelioma (MM) is a tumor with poor prognosis associated with asbestos exposure. While it remains to be clarified how asbestos fibers confer genetic/epigenetic alterations and induce cellular transformation in normal mesothelial cells, the ... ...

Abstract	Malignant mesothelioma (MM) is a tumor with poor prognosis associated with asbestos exposure. While it remains to be clarified how asbestos fibers confer genetic/epigenetic alterations and induce cellular transformation in normal mesothelial cells, the understanding of key molecular mechanisms of MM cell development, proliferation, and invasion has progressed. MM shows frequent genetic inactivation of tumor suppressor genes of p16(INK4a)/p14(ARF) and neurofibromatosis type 2 (NF2) which encodes Merlin, and epigenetic inactivation of RASSF1A. However, no frequent mutations of well-known oncogenes such as K-RAS and PIK3CA have been identified. Activation of multiple receptor tyrosine kinases including the epidermal growth factor receptor (EGFR) family and MET, and subsequent deregulations of mitogen-activated protein kinase (MAPK) and phosphatidylinositol-3-kinase (PI3K)-AKT signaling cascades are frequently observed in most MM cells. The tumor suppressive function of Merlin in MM cells is also being investigated by dissecting its possible downstream signaling cascade called the Hippo pathway. Further comprehensive delineation of dysregulated signaling cascades in MM cells will lead to identification of key addiction pathways for cell survival and proliferation of MM cells, which strongly promote establishment of a new molecular target therapy for MM.
MeSH term(s)	Asbestos/toxicity ; Cyclin-Dependent Kinase Inhibitor p16/genetics ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Humans ; MAP Kinase Signaling System ; Mesothelioma/genetics ; Mesothelioma/metabolism ; Mesothelioma/therapy ; Mutation ; Neurofibromatosis 2/genetics ; Phosphatidylinositol 3-Kinases/physiology ; Proto-Oncogene Proteins c-akt/physiology ; Signal Transduction/physiology ; Tumor Suppressor Protein p14ARF/genetics
Chemical Substances	Cyclin-Dependent Kinase Inhibitor p16 ; Tumor Suppressor Protein p14ARF ; Asbestos (1332-21-4) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2010-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ISSN	1349-7006
ISSN (online)	1349-7006
DOI	10.1111/j.1349-7006.2009.01336.x
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