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Article ; Online: Cancer-Related Unconventional Protein Secretion: A New Role of the Endoplasmic Reticulum.

Yamada, Kohji / Yoshida, Kiyotsugu

2023 Volume 42, Issue 5, Page(s) 225–228

Abstract: Unconventional protein secretion (UPS) is a crucial mechanism controlling the localization of cytosolic proteins lacking signal peptides and is implicated in inflammation, neurodegenerative diseases, and cancer. Several previous studies on immune cells ... ...

Abstract	Unconventional protein secretion (UPS) is a crucial mechanism controlling the localization of cytosolic proteins lacking signal peptides and is implicated in inflammation, neurodegenerative diseases, and cancer. Several previous studies on immune cells have demonstrated the mechanisms of UPS. In cancer, the active secretion of several cytosolic proteins, including PKCδ and nucleolin, has been described. Moreover, we have recently demonstrated that extended synaptotagmin 1, one of the membrane proteins of the endoplasmic reticulum, plays a critical role in UPS in liver cancer cells. Importantly, UPS in cancer cells shows characteristics that are markedly different from those of the previously known UPS, and therefore, we categorize them as cancer-related UPS (CUPS). In this article, we provide an overview of UPS mechanisms and discuss the process that leads to the naming of cancer-specific UPS as CUPS.
MeSH term(s)	Secretory Pathway ; Endoplasmic Reticulum/metabolism ; Protein Transport ; Cell Membrane/metabolism ; Membrane Proteins/metabolism ; Neoplasms/metabolism
Chemical Substances	Membrane Proteins
Language	English
Publishing date	2023-03-17
Publishing country	United States
Document type	Journal Article
ZDB-ID	1024454-2
ISSN	1557-7430 ; 0198-0238 ; 1044-5498
ISSN (online)	1557-7430
ISSN	0198-0238 ; 1044-5498
DOI	10.1089/dna.2023.0044
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Zs.A 2061: Show issues

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Article ; Online: Leakage? or Secretion? unconventional protein secretion in cancer.

Yamada, Kohji / Yoshida, Kiyotsugu

Oncotarget

2023 Volume 14, Page(s) 146–147

MeSH term(s)	Humans ; Neoplasms ; Proteins
Chemical Substances	Proteins
Language	English
Publishing date	2023-02-20
Publishing country	United States
Document type	Editorial ; Research Support, Non-U.S. Gov't
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.28368
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Article ; Online: Functional Roles of DYRK2 as a Tumor Regulator.

Mochimaru, Yuta / Yoshida, Kiyotsugu

Current issues in molecular biology

2023 Volume 45, Issue 10, Page(s) 8539–8551

Abstract: The dual-specificity tyrosine phosphorylation-regulated kinase 2 (DYRK2) regulates the induction of apoptosis and DNA repair, metastasis inhibition, cell cycle G1/S transition, protein scaffold stability for E3 ligase complexes, and embryogenesis. Owing ... ...

Abstract	The dual-specificity tyrosine phosphorylation-regulated kinase 2 (DYRK2) regulates the induction of apoptosis and DNA repair, metastasis inhibition, cell cycle G1/S transition, protein scaffold stability for E3 ligase complexes, and embryogenesis. Owing to these functions, DYRK2 is thought to regulate tumorigenesis, and its function in cancer has been investigated. Notably, DYRK2 has been reported to function as a tumor suppressor; however, it has also been reported to act as an oncogene in some cancers. This discrepancy makes it difficult to elucidate the conserved functions of DYRK2 in cancer. Here, we reviewed the functions of DYRK2 in various cancers. Patient tissue samples were evaluated for each cancer type. Although some studies have used cell lines and/or xenografts to elucidate the mechanism of DYRK2 function, these studies are not sufficient to understand the role of DYRK2 in cancers. In particular, studies using genetically modified mice would help us to understand the reported functional duality of DYRK2 in cancer.
Language	English
Publishing date	2023-10-23
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2000024-8
ISSN	1467-3045 ; 1467-3037
ISSN (online)	1467-3045
ISSN	1467-3037
DOI	10.3390/cimb45100538
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Zs.A 5122: Show issues

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Article ; Online: The diverse functions of DYRK2 in response to cellular stress.

Kawamura, Akira / Yoshida, Saishu / Yoshida, Kiyotsugu

Histology and histopathology

2024 , Page(s) 18744

Abstract: To maintain microenvironmental and cellular homeostasis, cells respond to multiple stresses by activating characteristic cellular mechanisms consisting of receptors, signal transducers, and effectors. Dysfunction of these mechanisms can trigger multiple ... ...

Abstract	To maintain microenvironmental and cellular homeostasis, cells respond to multiple stresses by activating characteristic cellular mechanisms consisting of receptors, signal transducers, and effectors. Dysfunction of these mechanisms can trigger multiple human diseases as well as cancers. Dual-specificity tyrosine-regulated kinases (DYRKs) are members of the CMGC group and are evolutionarily conserved from yeast to mammals. Previous studies revealed that DYRK2 has important roles in the regulation of the cell cycle and survival in cancer cells. On the other hand, recent studies show that DYRK2 also exhibits significant functions in multiple cellular stress responses and in maintaining cellular homeostasis. Hence, the further elucidation of mechanisms underlying DYRK2's diverse responses to various stresses helps to promote the advancement of innovative clinical therapies and pharmacological drugs. This review summarizes the molecular mechanisms of DYRK2, particularly focusing on cellular stress responses.
Language	English
Publishing date	2024-04-08
Publishing country	Spain
Document type	Journal Article ; Review
ZDB-ID	83911-5
ISSN	1699-5848 ; 0213-3911
ISSN (online)	1699-5848
ISSN	0213-3911
DOI	10.14670/HH-18-744
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Article ; Online: New insights into the roles for DYRK family in mammalian development and congenital diseases.

Yoshida, Saishu / Yoshida, Kiyotsugu

Genes & diseases

2022 Volume 10, Issue 3, Page(s) 758–770

Abstract: The dual-specificity tyrosine-regulated kinase (DYRK) family is evolutionarily conserved from invertebrate to mammals. DYRKs regulate cell proliferation, apoptosis, survival, and differentiation by modifying the protein activation state, cellular ... ...

Abstract	The dual-specificity tyrosine-regulated kinase (DYRK) family is evolutionarily conserved from invertebrate to mammals. DYRKs regulate cell proliferation, apoptosis, survival, and differentiation by modifying the protein activation state, cellular localization, and turnover. In contrast to several studies in cellular models, the available evidence regarding the
Language	English
Publishing date	2022-01-06
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	2821806-1
ISSN	2352-3042 ; 2352-3042
ISSN (online)	2352-3042
ISSN	2352-3042
DOI	10.1016/j.gendis.2021.12.004
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Article ; Online: Multiple subcellular localizations and functions of protein kinase Cδ in liver cancer.

Yamada, Kohji / Yoshida, Kiyotsugu

World journal of gastroenterology

2021 Volume 28, Issue 2, Page(s) 188–198

Abstract: Protein kinase Cδ (PKCδ) is a member of the PKC family, and its implications have been reported in various biological and cancerous processes, including cell proliferation, cell death, tumor suppression, and tumor progression. In liver cancer cells, ... ...

Abstract	Protein kinase Cδ (PKCδ) is a member of the PKC family, and its implications have been reported in various biological and cancerous processes, including cell proliferation, cell death, tumor suppression, and tumor progression. In liver cancer cells, accumulating reports show the bi-functional regulation of PKCδ in cell death and survival. PKCδ function is defined by various factors, such as phosphorylation, catalytic domain cleavage, and subcellular localization. PKCδ has multiple intracellular distribution patterns, ranging from the cytosol to the nucleus. We recently found a unique extracellular localization of PKCδ in liver cancer and its growth factor-like function in liver cancer cells. In this review, we first discuss the structural features of PKCδ and then focus on the functional diversity of PKCδ based on its subcellular localization, such as the nucleus, cell surface, and extracellular space. These findings improve our knowledge of PKCδ involvement in the progression of liver cancer.
MeSH term(s)	Cell Line ; Cell Nucleus/metabolism ; Humans ; Liver Neoplasms/metabolism ; Phosphorylation ; Protein Kinase C-delta/metabolism
Chemical Substances	Protein Kinase C-delta (EC 2.7.11.13)
Language	English
Publishing date	2021-01-12
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2185929-2
ISSN	2219-2840 ; 1007-9327
ISSN (online)	2219-2840
ISSN	1007-9327
DOI	10.3748/wjg.v28.i2.188
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Zs.A 6039: Show issues

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Article ; Online: Dual-specificity tyrosine-regulated kinase 2 exerts anti-tumor effects by induction of G1 arrest in lung adenocarcinoma.

Harada, Eriko / Yoshida, Saishu / Imaizumi, Yuta / Kawamura, Akira / Ohtsuka, Takashi / Yoshida, Kiyotsugu

Biochimica et biophysica acta. General subjects

2024 Volume 1868, Issue 6, Page(s) 130600

Abstract: Objectives: Lung cancer is a leading cause of cancer-related mortality and remains one of the most poorly prognosed disease worldwide. Therefore, it is necessary to identify novel molecular markers with potential therapeutic effects. Recent findings ... ...

Abstract	Objectives: Lung cancer is a leading cause of cancer-related mortality and remains one of the most poorly prognosed disease worldwide. Therefore, it is necessary to identify novel molecular markers with potential therapeutic effects. Recent findings have suggested that dual-specificity tyrosine-regulated kinase 2 (DYRK2) plays a tumor suppressive role in colorectal, breast, and hepatic cancers; however, its effect and mechanism in lung cancer remain poorly understood. Therefore, this study aimed to investigate the tumor-suppressive role and molecular mechanism of DYRK2 in lung adenocarcinoma (LUAD) by in vitro experiments and xenograft models. Materials and methods: The evaluation of DYRK2 expression was carried out using lung cancer cell lines and normal bronchial epithelial cells. Overexpression of DYRK2 was induced by an adenovirus vector, and cell proliferation was assessed through MTS assay and Colony Formation Assay. Cell cycle analysis was performed using flow cytometry. Additionally, proliferative capacity was evaluated in a xenograft model by subcutaneously implanting A549 cells into SCID mice (C·B17/Icr-scidjcl-scid/scid). Results: Immunoblotting assays showed that DYRK2 was downregulated in most LUAD cell lines. DYRK2 overexpression using adenovirus vectors significantly suppressed cell proliferation compared with that in the control group. Additionally, DYRK2 overexpression suppressed tumor growth in a murine subcutaneous xenograft model. Mechanistically, DYRK2 overexpression inhibited the proliferation of LUAD cells via p21-mediated G1 arrest, which was contingent on p53. Conclusion: Taken together, these findings suggest that DYRK2 may serve as potential prognostic biomarker and therapeutic target for LUAD.
MeSH term(s)	Animals ; Humans ; Mice ; A549 Cells ; Adenocarcinoma of Lung/pathology ; Adenocarcinoma of Lung/metabolism ; Adenocarcinoma of Lung/genetics ; Cell Line, Tumor ; Cell Proliferation ; Dyrk Kinases ; G1 Phase Cell Cycle Checkpoints/genetics ; Gene Expression Regulation, Neoplastic ; Lung Neoplasms/pathology ; Lung Neoplasms/metabolism ; Lung Neoplasms/genetics ; Mice, SCID ; Protein Serine-Threonine Kinases/metabolism ; Protein Serine-Threonine Kinases/genetics ; Protein-Tyrosine Kinases/metabolism ; Protein-Tyrosine Kinases/genetics ; Xenograft Model Antitumor Assays
Chemical Substances	Dyrk Kinases (EC 2.7.1.-) ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Protein-Tyrosine Kinases (EC 2.7.10.1) ; DYRK2 protein, human
Language	English
Publishing date	2024-03-18
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	60-7
ISSN	1872-8006 ; 1879-2596 ; 1879-260X ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1872-8006 ; 1879-2596 ; 1879-260X ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbagen.2024.130600
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Article ; Online: Enforced dual-specificity tyrosine-regulated kinase 2 expression by adenovirus-mediated gene transfer inhibits tumor growth and metastasis of colorectal cancer.

Imaizumi, Yuta / Yoshida, Saishu / Kanegae, Yumi / Eto, Ken / Yoshida, Kiyotsugu

Cancer science

2022 Volume 113, Issue 3, Page(s) 960–970

Abstract: Colorectal cancer is one of the most common gastrointestinal tumors with good outcomes; however, with distant metastasis, the outcomes are poor. Novel treatment methods are urgently needed. Our in vitro studies indicate that dual-specificity tyrosine- ... ...

Abstract	Colorectal cancer is one of the most common gastrointestinal tumors with good outcomes; however, with distant metastasis, the outcomes are poor. Novel treatment methods are urgently needed. Our in vitro studies indicate that dual-specificity tyrosine-regulated kinase 2 (DYRK2) functions as a tumor suppressor in colorectal cancer by regulating cell survival, proliferation, and apoptosis induction. In addition, DYRK2 expression is decreased in tumor tissues compared to nontumor tissues in colorectal cancer, indicating a correlation with clinical prognosis. In this context, we devised a novel therapeutic strategy to overexpress DYRK2 in tumors by adenovirus-mediated gene transfer. The present study shows that overexpression of DYRK2 in colon cancer cell lines by adenovirus inhibits cell proliferation and induces apoptosis in vitro. Furthermore, in mouse subcutaneous xenograft and liver metastasis models, enforced expression of DYRK2 by direct or intravenous injection of adenovirus to the tumor significantly inhibits tumor growth. Taken together, these findings show that adenovirus-based overexpression of DYRK2 could be a novel gene therapy for liver metastasis of colorectal cancer.
MeSH term(s)	Adenoviridae/genetics ; Animals ; Apoptosis/genetics ; Cell Line, Tumor ; Cell Proliferation/genetics ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/pathology ; Colorectal Neoplasms/therapy ; Genetic Therapy/methods ; Genetic Vectors ; Humans ; Liver Neoplasms/genetics ; Liver Neoplasms/secondary ; Liver Neoplasms/therapy ; Mice ; Protein Serine-Threonine Kinases/genetics ; Protein-Tyrosine Kinases/genetics ; Tumor Suppressor Proteins/genetics ; Xenograft Model Antitumor Assays ; Dyrk Kinases
Chemical Substances	Tumor Suppressor Proteins ; Protein-Tyrosine Kinases (EC 2.7.10.1) ; Protein Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2022-01-10
Publishing country	England
Document type	Journal Article
ZDB-ID	2115647-5
ISSN	1349-7006 ; 1349-7006
ISSN (online)	1349-7006
ISSN	1349-7006
DOI	10.1111/cas.15247
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Article ; Online: Mechanical insights into the regulation of programmed cell death by p53 via mitochondria.

Yamada, Kohji / Yoshida, Kiyotsugu

Biochimica et biophysica acta. Molecular cell research

2019 Volume 1866, Issue 5, Page(s) 839–848

Abstract: All organisms end with their death, and many parts of cells die through intrinsic suicide machineries in response to diverse stimuli. These intrinsic cell death pathways are often termed as programmed cell deaths (PCDs), and are critical for organism ... ...

Abstract	All organisms end with their death, and many parts of cells die through intrinsic suicide machineries in response to diverse stimuli. These intrinsic cell death pathways are often termed as programmed cell deaths (PCDs), and are critical for organism development, tissue homeostasis and various diseases. Recent evidence has revealed that most of PCDs involve a tumor suppressor p53 and components of the intra-mitochondria. Furthermore, the movement and positioning of p53 in cells affect the induction of each PCD pathway. Here we provide a comprehensive review on p53-related PCD mechanisms via the mitochondria, namely classical apoptosis, non-classical apoptosis, autophagic cell death, ferroptosis, necroptosis. In addition, we discuss the roles of p53 in each PCD pathway by focusing its altered intracellular localization in response to diverse cellular stresses.
MeSH term(s)	Animals ; Apoptosis ; Autophagy ; Humans ; Mitochondria/genetics ; Mitochondria/metabolism ; Signal Transduction ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	Tumor Suppressor Protein p53
Language	English
Publishing date	2019-02-18
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	60-7
ISSN	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbamcr.2019.02.009
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Article ; Online: Multiple functions of DYRK2 in cancer and tissue development.

Yoshida, Saishu / Yoshida, Kiyotsugu

FEBS letters

2019 Volume 593, Issue 21, Page(s) 2953–2965

Abstract: Dual-specificity tyrosine-regulated kinases (DYRKs) are evolutionarily conserved from yeast to mammals. Accumulating studies have revealed that DYRKs have important roles in regulation of the cell cycle and survival. DYRK2, a member of the class II DYRK ... ...

Abstract	Dual-specificity tyrosine-regulated kinases (DYRKs) are evolutionarily conserved from yeast to mammals. Accumulating studies have revealed that DYRKs have important roles in regulation of the cell cycle and survival. DYRK2, a member of the class II DYRK family protein, is a key regulator of p53, and phosphorylates it at Ser46 to induce apoptosis in response to DNA damage. Moreover, recent studies have uncovered that DYRK2 regulates G1/S transition, epithelial-mesenchymal-transition, and stemness in human cancer cells. DYRK2 also appears to have roles in tissue development in lower eukaryotes. Thus, the elucidation of mechanisms for DYRK2 during mammalian tissue development will promote the understanding of cell differentiation, tissue homeostasis, and congenital diseases as well as cancer. In this review, we discuss the roles of DYRK2 in tumor cells. Moreover, we focus on DYRK2-dependent developmental mechanisms in several species including fly (Drosophila), worm (Caenorhabditis elegans), zebrafish (Danio rerio), and mammals.
MeSH term(s)	Animals ; Apoptosis ; Cell Proliferation ; DNA Damage ; Epithelial-Mesenchymal Transition ; Gene Expression Regulation, Neoplastic ; Humans ; Neoplasms/genetics ; Neoplasms/metabolism ; Neoplastic Stem Cells/metabolism ; Protein Serine-Threonine Kinases/metabolism ; Protein-Tyrosine Kinases/metabolism ; Dyrk Kinases
Chemical Substances	Protein-Tyrosine Kinases (EC 2.7.10.1) ; Protein Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2019-09-18
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	212746-5
ISSN	1873-3468 ; 0014-5793
ISSN (online)	1873-3468
ISSN	0014-5793
DOI	10.1002/1873-3468.13601
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