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Article ; Online: Emerging roles of transmembrane-type tight junction proteins in cancers.

Takasawa, Akira / Takasawa, Kumi / Murata, Masaki / Osanai, Makoto / Sawada, Norimasa

2023 Volume 73, Issue 8, Page(s) 331–340

Abstract: Tight junctions (TJs) are the most apical components of the cell-cell adhesion machinery in epithelial and endothelial cells and they play essential roles in homeostasis. Recent studies have revealed that aberrant expression of tight junction proteins ( ... ...

Abstract	Tight junctions (TJs) are the most apical components of the cell-cell adhesion machinery in epithelial and endothelial cells and they play essential roles in homeostasis. Recent studies have revealed that aberrant expression of tight junction proteins (TJPs) is frequently observed in various type of cancers. Here we review cancer-associated aberrant expression of TJPs with focus on transmembrane-type TJPs including claudins, junctional adhesion molecule-A (JAM-A), and occludin. Some transmembrane-type TJPs are upregulated at the early neoplastic stage and their expression persists during dedifferentiation. Aberrant expression of TJPs contributes to proliferation, invasion, and dysregulated signaling of cancer cells. In addition to an increase in their expression level, their localization is altered from a TJ-restricted pattern to distribution throughout the whole cell membrane, making them suitable as therapeutic targets. Extracellular domains of transmembrane-type TJPs can be approached by target drugs not only from the lumen side (apical side) but also from the extracellular matrix side (basal side), including blood vessels. Aberrantly expressed TJPs are potential useful diagnostic markers as well as therapeutic targets for cancers.
MeSH term(s)	Humans ; Tight Junction Proteins/metabolism ; Endothelial Cells ; Claudins ; Tight Junctions/metabolism ; Neoplasms/metabolism ; Occludin/metabolism
Chemical Substances	Tight Junction Proteins ; Claudins ; Occludin
Language	English
Publishing date	2023-07-14
Publishing country	Australia
Document type	Journal Article ; Review
ZDB-ID	1194850-4
ISSN	1440-1827 ; 1320-5463
ISSN (online)	1440-1827
ISSN	1320-5463
DOI	10.1111/pin.13349
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Article ; Online: Tight junction-related human diseases.

Sawada, Norimasa

Pathology international

2013 Volume 63, Issue 1, Page(s) 1–12

Abstract: Tight junctions are intercellular junctions adjacent to the apical ends of paracellular spaces. They have two classical functions, the barrier function and the fence function. The former regulates the passage of ions, water and various molecules through ... ...

Abstract	Tight junctions are intercellular junctions adjacent to the apical ends of paracellular spaces. They have two classical functions, the barrier function and the fence function. The former regulates the passage of ions, water and various molecules through paracellular spaces, and is thus related to edema, jaundice, diarrhea and blood-borne metastasis. The latter function maintains cell polarity by forming a fence to prevent intermixing of molecules in the apical membrane with those in the lateral membrane. This function is deeply involved in cancer cell properties in terms of loss of cell polarity. Recently, two novel aspects of tight junctions have been reported. One is their involvement in signal transduction. The other is that fact that tight junctions are considered to be a crucial component of innate immunity. In addition, since some proteins comprising tight junctions work as receptors for viruses and extracellular stimuli, pathogenic bacteria and viruses target and affect the tight junction functions, leading to diseases. In this review, the relationship between tight junctions and human diseases will be described.
MeSH term(s)	Cellular Microenvironment/physiology ; Claudins/metabolism ; Humans ; Immunity, Innate/physiology ; Neoplasms/metabolism ; Neoplasms/pathology ; Occludin/metabolism ; Signal Transduction/physiology ; Tight Junction Proteins/metabolism ; Tight Junctions/pathology ; Tight Junctions/physiology
Chemical Substances	Claudins ; Occludin ; Tight Junction Proteins
Keywords	covid19
Language	English
Publishing date	2013-01-07
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/pin.12021
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Article: Evaluation of the efficacy of

Sawada, Yoko / Sugimoto, Atsushi / Hananouchi, Takehito / Sato, Norimasa / Nagaoka, Isao

Experimental and therapeutic medicine

2017 Volume 14, Issue 5, Page(s) 4561–4571

Abstract: The aim of the present study was to assess the efficacy and safety of the oral administration ... ...

Abstract	The aim of the present study was to assess the efficacy and safety of the oral administration of
Language	English
Publishing date	2017-08-29
Publishing country	Greece
Document type	Journal Article
ZDB-ID	2683844-8
ISSN	1792-1015 ; 1792-0981
ISSN (online)	1792-1015
ISSN	1792-0981
DOI	10.3892/etm.2017.5064
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Article: Retinoic acid-metabolizing enzyme cytochrome P450 26A1 promotes skin carcinogenesis induced by 7,12-dimethylbenz[a]anthracene.

Osanai, Makoto / Takasawa, Akira / Takasawa, Kumi / Murata, Masaki / Sawada, Norimasa

Oncology letters

2018 Volume 15, Issue 6, Page(s) 9987–9993

Abstract: Elevated expression of the retinoic acid-metabolizing enzyme cytochrome P450 26A1 (CYP26A1) has been demonstrated to have an oncogenic function in carcinogenesis. In order to address the oncogenic capacity of ... ...

Abstract	Elevated expression of the retinoic acid-metabolizing enzyme cytochrome P450 26A1 (CYP26A1) has been demonstrated to have an oncogenic function in carcinogenesis. In order to address the oncogenic capacity of CYP26A1
Language	English
Publishing date	2018-04-27
Publishing country	Greece
Document type	Journal Article
ZDB-ID	2573196-8
ISSN	1792-1082 ; 1792-1074
ISSN (online)	1792-1082
ISSN	1792-1074
DOI	10.3892/ol.2018.8599
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Article ; Online: Cholangio-venous reflux of biliary contents through paracellular pathways between hepatocytes in patients with acute cholangitis.

Takada, Tadahiro / Takikawa, Hajime / Sawada, Norimasa / Higuchi, Ryota / Nagamachi, Yukiko / Isaji, Shuji / Yoshida, Masahiro / Yamamoto, Masakazu

Journal of hepato-biliary-pancreatic sciences

2021 Volume 28, Issue 6, Page(s) 508–514

Abstract: Background: We re-analyzed data on cholangio-venous reflux from a clinical study conducted prospectively on 22 patients in 1974.: Method: Direct cholangiography was performed with indocyanine green (ICG) mixed into Urographin: Results: The ... ...

Abstract	Background: We re-analyzed data on cholangio-venous reflux from a clinical study conducted prospectively on 22 patients in 1974. Method: Direct cholangiography was performed with indocyanine green (ICG) mixed into Urographin Results: The intrabiliary pressure of six patients negative for both ICG leakage and signs of infection was approximately 19.5 (median, [range 18-22]) cmH Conclusion: Our findings suggest that the tight junctions sealing the bile canaliculi deteriorated with increasing intrabiliary pressure, resulting in reflux of the biliary contents into the vascular system via paracellular pathways between hepatocytes.
MeSH term(s)	Biliary Tract ; Cholangiography ; Cholangitis/diagnostic imaging ; Hepatocytes ; Humans ; Indocyanine Green
Chemical Substances	Indocyanine Green (IX6J1063HV)
Language	English
Publishing date	2021-04-06
Publishing country	Japan
Document type	Journal Article
ZDB-ID	2536236-7
ISSN	1868-6982 ; 1868-6974
ISSN (online)	1868-6982
ISSN	1868-6974
DOI	10.1002/jhbp.937
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Article ; Online: Claudins in cancer: bench to bedside.

Osanai, Makoto / Takasawa, Akira / Murata, Masaki / Sawada, Norimasa

Pflugers Archiv : European journal of physiology

2017 Volume 469, Issue 1, Page(s) 55–67

Abstract: The claudin family, in mammals, encoded by at least 27 members of a single ancestral gene, CLDN, is the main constituent as integral membrane proteins of tight junctions. It has been shown that the expression levels of claudins are often decreased or ... ...

Abstract	The claudin family, in mammals, encoded by at least 27 members of a single ancestral gene, CLDN, is the main constituent as integral membrane proteins of tight junctions. It has been shown that the expression levels of claudins are often decreased or that their expressions are absent in human neoplasias. These findings are consistent with the well-accepted concept that carcinogenesis is accompanied by the disruption or loss of functional tight junctions. In contrast, accumulating data have showed elevated or aberrant expression of claudins in various cancers, indicating specific roles of claudins in tumorigenesis. Importantly, dysregulated claudins play an oncogenic role or conversely have a tumor-suppressive effect depending on target tissues or cell types, and thus, they contribute to tumor development and progression. Although tight junctions are intercellular structures in epithelial cells, specific roles of claudins in cancer are supported by the evidence that TJs are not simple static constituents for establishing cell adhesion structures but are also cell signaling components that have functions in receiving environmental cues and transmitting signals inside cells. Since the expression profile of claudins is associated with patients' outcome and prognosis in several cancer types, an understanding of the expression pattern and subcellular localization of claudins in various pathologies will lead to the establishment of claudins as useful biomarkers for the detection and diagnosis of cancers.
MeSH term(s)	Animals ; Carcinogenesis/metabolism ; Cell Adhesion/physiology ; Claudins/metabolism ; Epithelial Cells/metabolism ; Humans ; Neoplasms/metabolism ; Tight Junctions/metabolism
Chemical Substances	Claudins
Language	English
Publishing date	2017
Publishing country	Germany
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	6380-0
ISSN	1432-2013 ; 0031-6768
ISSN (online)	1432-2013
ISSN	0031-6768
DOI	10.1007/s00424-016-1877-7
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Article ; Online: Functional Characterization of Acetylcholine Receptors Expressed in Human Neurons Differentiated from Hippocampal Neural Stem/Progenitor Cells.

Fukushima, Kazuyuki / Yamazaki, Kazuto / Miyamoto, Norimasa / Sawada, Kohei

Journal of biomolecular screening

2016 Volume 21, Issue 10, Page(s) 1065–1074

Abstract: Neurotransmission mediated by acetylcholine receptors (AChRs) plays an important role in learning and memory functions in the hippocampus. Impairment of the cholinergic system contributes to Alzheimer's disease (AD), indicating the importance of AChRs as ...

Abstract	Neurotransmission mediated by acetylcholine receptors (AChRs) plays an important role in learning and memory functions in the hippocampus. Impairment of the cholinergic system contributes to Alzheimer's disease (AD), indicating the importance of AChRs as drug targets for AD. To improve the success rates for AD drug development, human cell models that mimic the target brain region are important. Therefore, we characterized the functional expression of nicotinic and muscarinic AChRs (nAChRs and mAChRs, respectively) in human hippocampal neurons differentiated from hippocampal neural stem/progenitor cells (HIP-009 cells). Intracellular calcium flux in 4-week differentiated HIP-009 cells demonstrated that the cells responded to acetylcholine, nicotine, and muscarine in a concentration-dependent manner (EC
Language	English
Publishing date	2016-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	1433680-7
ISSN	1552-454X ; 1087-0571
ISSN (online)	1552-454X
ISSN	1087-0571
DOI	10.1177/1087057116665567
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Zs.A 4911: Show issues

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Article ; Online: Hsp90 inhibitor geldanamycin attenuates the cytotoxicity of sunitinib in cardiomyocytes via inhibition of the autophagy pathway.

Kimura, Takayuki / Uesugi, Mai / Takase, Kazuma / Miyamoto, Norimasa / Sawada, Kohei

Toxicology and applied pharmacology

2017 Volume 329, Page(s) 282–292

Abstract: Sunitinib malate (sunitinib) is an orally available, multitargeted tyrosine kinase inhibitor with antitumor and antiangiogenic activities. Although sunitinib is effective for the treatment of patients with gastrointestinal stromal tumor, advanced renal ... ...

Abstract	Sunitinib malate (sunitinib) is an orally available, multitargeted tyrosine kinase inhibitor with antitumor and antiangiogenic activities. Although sunitinib is effective for the treatment of patients with gastrointestinal stromal tumor, advanced renal cell carcinoma, or pancreatic neuroendocrine tumor, adverse cardiac events associated with sunitinib administration have been reported. Here, we examined the effect of geldanamycin, an inhibitor of heat shock protein (Hsp) 90, on sunitinib-induced cytotoxicity in cardiomyocytes. First, we found that treatment with geldanamycin or other Hsp90 inhibitors (tanespimycin, ganetespib, or BIIB021) significantly attenuated sunitinib-induced cytotoxicity in rat H9c2 cardiomyocytes, suggesting a drug-class effect of Hsp90 inhibitors. We then examined the mechanisms underlying sunitinib-induced cytotoxicity and found that sunitinib induced autophagy in H9c2 cells and that pretreatment with geldanamycin inhibited the induction of autophagy by promoting degradation of the autophagy-related proteins Atg7, Beclin-1, and ULK1. Pharmacological assessment with autophagy inhibitors confirmed that geldanamycin attenuated the cytotoxicity of sunitinib by interfering with autophagy. In addition, we found that the molecular chaperone Hsp70, which is induced by geldanamycin, was not involved in the attenuation of sunitinib-induced cytotoxicity. Finally, to provide more clinically relevant data, we confirmed that geldanamycin attenuated sunitinib-induced cytotoxicity in human induced pluripotent stem cell-derived cardiomyocytes. Together, these data suggest that geldanamycin attenuates sunitinib-induced cytotoxicity in cardiomyocytes by inhibiting the autophagy pathway. Thus, the further investigation of combination or sequential treatment with an Hsp90 inhibitor and sunitinib is warranted as a potential strategy of attenuating the cardiotoxicity associated with sunitinib administration in the clinical setting.
MeSH term(s)	Animals ; Antineoplastic Agents/toxicity ; Autophagy/drug effects ; Autophagy-Related Protein 7/genetics ; Autophagy-Related Protein 7/metabolism ; Autophagy-Related Protein-1 Homolog/genetics ; Autophagy-Related Protein-1 Homolog/metabolism ; Beclin-1/genetics ; Beclin-1/metabolism ; Benzoquinones/pharmacology ; Cardiotoxicity ; Cell Differentiation ; Cell Line ; Cell Lineage ; Cytoprotection ; Dose-Response Relationship, Drug ; HSP70 Heat-Shock Proteins/genetics ; HSP70 Heat-Shock Proteins/metabolism ; HSP90 Heat-Shock Proteins/antagonists & inhibitors ; HSP90 Heat-Shock Proteins/metabolism ; Humans ; Indoles/toxicity ; Induced Pluripotent Stem Cells/drug effects ; Induced Pluripotent Stem Cells/metabolism ; Induced Pluripotent Stem Cells/pathology ; Lactams, Macrocyclic/pharmacology ; Myocytes, Cardiac/drug effects ; Myocytes, Cardiac/metabolism ; Myocytes, Cardiac/pathology ; Protein Kinase Inhibitors/toxicity ; Pyrroles/toxicity ; RNA Interference ; Rats ; Signal Transduction/drug effects ; Transfection
Chemical Substances	Antineoplastic Agents ; Atg7 protein, rat ; Beclin-1 ; Becn1 protein, rat ; Benzoquinones ; HSP70 Heat-Shock Proteins ; HSP90 Heat-Shock Proteins ; Hspa1a protein, rat ; Indoles ; Lactams, Macrocyclic ; Protein Kinase Inhibitors ; Pyrroles ; Autophagy-Related Protein-1 Homolog (EC 2.7.11.1) ; ULK1 protein, rat (EC 2.7.11.1) ; Autophagy-Related Protein 7 (EC 6.2.1.45) ; sunitinib (V99T50803M) ; geldanamycin (Z3K3VJ16KU)
Language	English
Publishing date	2017-08-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	204477-8
ISSN	1096-0333 ; 0041-008X
ISSN (online)	1096-0333
ISSN	0041-008X
DOI	10.1016/j.taap.2017.06.015
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Article ; Online: Regulation of tight junctions in human normal pancreatic duct epithelial cells and cancer cells.

Kojima, Takashi / Sawada, Norimasa

Annals of the New York Academy of Sciences

2012 Volume 1257, Page(s) 85–92

Abstract: To investigate the regulation of tight junction molecules in normal human pancreatic duct epithelial (HPDE) cells and pancreatic cancer cells, we introduced the human telomerase reverse transcriptase (hTERT) gene into HPDE cells in primary culture and ... ...

Abstract	To investigate the regulation of tight junction molecules in normal human pancreatic duct epithelial (HPDE) cells and pancreatic cancer cells, we introduced the human telomerase reverse transcriptase (hTERT) gene into HPDE cells in primary culture and compared them to pancreatic cancer cell lines. The hTERT-transfected HPDE cells were positive for PDE markers and expressed claudin-1, claudin-4, claudin-7, and claudin-18, occludin, tricellulin, marvelD3, JAM-A, zonula occludens (ZO)-1, and ZO-2. The tight junction molecules, including claudin-4 and claudin-18 of normal HPDE cells, were in part regulated via a protein kinase C signal pathway by transcriptional control. In addition, claudin-18 in normal HPDE cells and pancreatic cancer cells was markedly induced by a PKC activator, and claudin-18 in pancreatic cancer cells was also modified by DNA methylation. In the marvel family of normal HPDE cells and pancreatic cancer cells, tricellulin was upregulated via a c-Jun N-terminal kinase pathway, and marvelD3 was downregulated during Snail-induced epithelial-mesenchymal transition.
MeSH term(s)	Carcinoma, Pancreatic Ductal/metabolism ; Cell Line, Tumor ; Claudins/metabolism ; Epithelial Cells/metabolism ; Gene Expression Regulation ; Humans ; JNK Mitogen-Activated Protein Kinases/genetics ; JNK Mitogen-Activated Protein Kinases/metabolism ; MARVEL Domain Containing 2 Protein/metabolism ; Membrane Proteins/metabolism ; Pancreatic Ducts/cytology ; Pancreatic Ducts/metabolism ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/metabolism ; Protein Kinase C/genetics ; Protein Kinase C/metabolism ; Signal Transduction ; Telomerase/genetics ; Telomerase/metabolism ; Tight Junctions/genetics ; Tight Junctions/metabolism
Chemical Substances	Claudins ; MARVEL Domain Containing 2 Protein ; MARVELD2 protein, human ; MARVELD3 protein, human ; Membrane Proteins ; Protein Kinase C (EC 2.7.11.13) ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; TERT protein, human (EC 2.7.7.49) ; Telomerase (EC 2.7.7.49)
Language	English
Publishing date	2012-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	211003-9
ISSN	1749-6632 ; 0077-8923
ISSN (online)	1749-6632
ISSN	0077-8923
DOI	10.1111/j.1749-6632.2012.06579.x
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Article ; Online: Immunoreactivity patterns of tight junction proteins are useful for differential diagnosis of human salivary gland tumors.

Aoyama, Tomoyuki / Takasawa, Akira / Murata, Masaki / Osanai, Makoto / Takano, Kenichi / Hasagawa, Tadashi / Sawada, Norimasa

Medical molecular morphology

2018 Volume 52, Issue 1, Page(s) 23–35

Abstract: The expression pattern of tight junction proteins (TJPs) varies among organs and tumor types. In this study, we examined the immunoreactivity of claudin (CLDN)-1, -4, and -7, and JAM-A in salivary gland tumors (SGTs) by histological types and cell types ... ...

Abstract	The expression pattern of tight junction proteins (TJPs) varies among organs and tumor types. In this study, we examined the immunoreactivity of claudin (CLDN)-1, -4, and -7, and JAM-A in salivary gland tumors (SGTs) by histological types and cell types to estimate their usefulness as differential diagnostic markers. Immunoreactivity of CLDN1 was higher in ductal epithelium cells of SGTs than in non-tumor tissues. Conversely, immunoreactivity of CLDN1 was significantly decreased in basal/myoepithelium cells of SGTs compared with that in non-tumor tissues. There was no significant difference between the immunoreactivity of CLDN1 in benign tumors and that in malignant tumors. Immunoreactivity of CLDN4, CLDN7, and JAM-A in ductal epithelium cells was higher in many SGTs than in non-tumor tissues. There was a difference depending on the histological type of SGT in immunoreactivity of CLDN4, CLDN7, and JAM-A in basaloid/myoepithelial cells. It was possible to classify SGTs by a hierarchical clustering using immunoreactivity of TJPs. The results suggest that an immunohistochemical marker panel including these TJPs may be useful for differential diagnosis of SGTs and that CLDN1 is associated with tumorigenesis of SGTs.
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Cell Adhesion Molecules/analysis ; Cell Adhesion Molecules/immunology ; Claudin-1/analysis ; Claudin-1/immunology ; Claudin-4/analysis ; Claudin-4/immunology ; Claudins/analysis ; Claudins/immunology ; Diagnosis, Differential ; Female ; Humans ; Immunohistochemistry ; Male ; Middle Aged ; Receptors, Cell Surface/analysis ; Receptors, Cell Surface/immunology ; Salivary Gland Neoplasms/diagnosis ; Salivary Gland Neoplasms/metabolism ; Tight Junction Proteins/analysis ; Tight Junction Proteins/immunology ; Young Adult
Chemical Substances	CLDN1 protein, human ; CLDN4 protein, human ; CLDN7 protein, human ; Cell Adhesion Molecules ; Claudin-1 ; Claudin-4 ; Claudins ; F11R protein, human ; Receptors, Cell Surface ; Tight Junction Proteins
Language	English
Publishing date	2018-06-28
Publishing country	Japan
Document type	Journal Article
ZDB-ID	2190059-0
ISSN	1860-1499 ; 1860-1480
ISSN (online)	1860-1499
ISSN	1860-1480
DOI	10.1007/s00795-018-0199-6
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