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Article ; Online: Integrative analysis reveals early epigenetic alterations in high-grade serous ovarian carcinomas.

Machino, Hidenori / Dozen, Ai / Konaka, Mariko / Komatsu, Masaaki / Nakamura, Kohei / Ikawa, Noriko / Shozu, Kanto / Asada, Ken / Kaneko, Syuzo / Yoshida, Hiroshi / Kato, Tomoyasu / Nakayama, Kentaro / Saloura, Vassiliki / Kyo, Satoru / Hamamoto, Ryuji

Experimental & molecular medicine

2023 Volume 55, Issue 10, Page(s) 2205–2219

Abstract: High-grade serous ovarian carcinoma (HGSOC) is the most lethal gynecological malignancy. To date, the profiles of gene mutations and copy number alterations in HGSOC have been well characterized. However, the patterns of epigenetic alterations and ... ...

Abstract	High-grade serous ovarian carcinoma (HGSOC) is the most lethal gynecological malignancy. To date, the profiles of gene mutations and copy number alterations in HGSOC have been well characterized. However, the patterns of epigenetic alterations and transcription factor dysregulation in HGSOC have not yet been fully elucidated. In this study, we performed integrative omics analyses of a series of stepwise HGSOC model cells originating from human fallopian tube secretory epithelial cells (HFTSECs) to investigate early epigenetic alterations in HGSOC tumorigenesis. Assay for transposase-accessible chromatin using sequencing (ATAC-seq), chromatin immunoprecipitation sequencing (ChIP-seq), and RNA sequencing (RNA-seq) methods were used to analyze HGSOC samples. Additionally, protein expression changes in target genes were confirmed using normal HFTSECs, serous tubal intraepithelial carcinomas (STICs), and HGSOC tissues. Transcription factor motif analysis revealed that the DNA-binding activity of the AP-1 complex and GATA family proteins was dysregulated during early tumorigenesis. The protein expression levels of JUN and FOSL2 were increased, and those of GATA6 and DAB2 were decreased in STIC lesions, which were associated with epithelial-mesenchymal transition (EMT) and proteasome downregulation. The genomic region around the FRA16D site, containing a cadherin cluster region, was epigenetically suppressed by oncogenic signaling. Proteasome inhibition caused the upregulation of chemokine genes, which may facilitate immune evasion during HGSOC tumorigenesis. Importantly, MEK inhibitor treatment reversed these oncogenic alterations, indicating its clinical effectiveness in a subgroup of patients with HGSOC. This result suggests that MEK inhibitor therapy may be an effective treatment option for chemotherapy-resistant HGSOC.
MeSH term(s)	Female ; Humans ; Ovarian Neoplasms/metabolism ; Proteasome Endopeptidase Complex/metabolism ; Cystadenocarcinoma, Serous/genetics ; Cystadenocarcinoma, Serous/metabolism ; Cystadenocarcinoma, Serous/pathology ; Carcinogenesis/genetics ; Transcription Factors/metabolism ; Epigenesis, Genetic ; Mitogen-Activated Protein Kinase Kinases/metabolism
Chemical Substances	Proteasome Endopeptidase Complex (EC 3.4.25.1) ; Transcription Factors ; Mitogen-Activated Protein Kinase Kinases (EC 2.7.12.2)
Language	English
Publishing date	2023-10-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1328915-9
ISSN	2092-6413 ; 1226-3613 ; 0378-8512
ISSN (online)	2092-6413
ISSN	1226-3613 ; 0378-8512
DOI	10.1038/s12276-023-01090-1
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Article ; Online: Downregulation of METTL6 mitigates cell progression, migration, invasion and adhesion in hepatocellular carcinoma by inhibiting cell adhesion molecules.

Bolatkan, Amina / Asada, Ken / Kaneko, Syuzo / Suvarna, Kruthi / Ikawa, Noriko / Machino, Hidenori / Komatsu, Masaaki / Shiina, Shuichiro / Hamamoto, Ryuji

International journal of oncology

2021 Volume 60, Issue 1

Abstract: RNA modifications have attracted increasing interest in recent years because they have been frequently implicated in various human diseases, including cancer, highlighting the importance of dynamic post‑transcriptional modifications. Methyltransferase‑ ... ...

Abstract	RNA modifications have attracted increasing interest in recent years because they have been frequently implicated in various human diseases, including cancer, highlighting the importance of dynamic post‑transcriptional modifications. Methyltransferase‑like 6 (METTL6) is a member of the RNA methyltransferase family that has been identified in many cancers; however, little is known about its specific role or mechanism of action. In the present study, we aimed to study the expression levels and functional role of METTL6 in hepatocellular carcinoma (HCC), and further investigate the relevant pathways. To this end, we systematically conducted bioinformatics analysis of METTL6 in HCC using gene expression data and clinical information from a publicly available dataset. The mRNA expression levels of
MeSH term(s)	Carcinoma, Hepatocellular/genetics ; Carcinoma, Hepatocellular/physiopathology ; Cell Adhesion Molecules/adverse effects ; Cell Adhesion Molecules/therapeutic use ; Cell Line ; Cell Movement/genetics ; Cell Movement/physiology ; Cell Proliferation/genetics ; Cell Proliferation/physiology ; Down-Regulation/genetics ; Humans ; Liver Neoplasms/genetics ; Liver Neoplasms/physiopathology ; tRNA Methyltransferases/adverse effects ; tRNA Methyltransferases/metabolism
Chemical Substances	Cell Adhesion Molecules ; METTL6 protein, human (EC 2.1.1.-) ; tRNA Methyltransferases (EC 2.1.1.-)
Language	English
Publishing date	2021-12-16
Publishing country	Greece
Document type	Journal Article
ZDB-ID	1154403-x
ISSN	1791-2423 ; 1019-6439
ISSN (online)	1791-2423
ISSN	1019-6439
DOI	10.3892/ijo.2021.5294
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Article: Tumor Suppressive Role of the

Dozen, Ai / Shozu, Kanto / Shinkai, Norio / Ikawa, Noriko / Aoyama, Rina / Machino, Hidenori / Asada, Ken / Yoshida, Hiroshi / Kato, Tomoyasu / Hamamoto, Ryuji / Kaneko, Syuzo / Komatsu, Masaaki

Journal of personalized medicine

2022 Volume 12, Issue 12

Abstract: Ovarian clear cell carcinoma (OCCC) has a poor prognosis, and its therapeutic strategy has not been established. PRELP is a leucine-rich repeat protein in the extracellular matrix of connective tissues. Although PRELP anchors the basement membrane to the ...

Abstract	Ovarian clear cell carcinoma (OCCC) has a poor prognosis, and its therapeutic strategy has not been established. PRELP is a leucine-rich repeat protein in the extracellular matrix of connective tissues. Although PRELP anchors the basement membrane to the connective tissue and is absent in most epithelial cancers, much remains unknown regarding its function as a regulator of ligand-mediated signaling pathways. Here, we obtained sets of differentially expressed genes by PRELP expression using OCCC cell lines. We found that more than 1000 genes were significantly altered by PRELP expression, particularly affecting the expression of a group of genes involved in the PI3K-AKT signaling pathway. Furthermore, we revealed the loss of active histone marks on the loci of the
Language	English
Publishing date	2022-12-02
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2662248-8
ISSN	2075-4426
ISSN	2075-4426
DOI	10.3390/jpm12121999
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Article ; Online: The metabolic stress-activated checkpoint LKB1-MARK3 axis acts as a tumor suppressor in high-grade serous ovarian carcinoma.

Machino, Hidenori / Kaneko, Syuzo / Komatsu, Masaaki / Ikawa, Noriko / Asada, Ken / Nakato, Ryuichiro / Shozu, Kanto / Dozen, Ai / Sone, Kenbun / Yoshida, Hiroshi / Kato, Tomoyasu / Oda, Katsutoshi / Osuga, Yutaka / Fujii, Tomoyuki / von Keudell, Gottfried / Saloura, Vassiliki / Hamamoto, Ryuji

Communications biology

2022 Volume 5, Issue 1, Page(s) 39

Abstract: High-grade serous ovarian carcinoma (HGSOC) is the most aggressive gynecological malignancy, resulting in approximately 70% of ovarian cancer deaths. However, it is still unclear how genetic dysregulations and biological processes generate the malignant ... ...

Abstract	High-grade serous ovarian carcinoma (HGSOC) is the most aggressive gynecological malignancy, resulting in approximately 70% of ovarian cancer deaths. However, it is still unclear how genetic dysregulations and biological processes generate the malignant subtype of HGSOC. Here we show that expression levels of microtubule affinity-regulating kinase 3 (MARK3) are downregulated in HGSOC, and that its downregulation significantly correlates with poor prognosis in HGSOC patients. MARK3 overexpression suppresses cell proliferation and angiogenesis of ovarian cancer cells. The LKB1-MARK3 axis is activated by metabolic stress, which leads to the phosphorylation of CDC25B and CDC25C, followed by induction of G2/M phase arrest. RNA-seq and ATAC-seq analyses indicate that MARK3 attenuates cell cycle progression and angiogenesis partly through downregulation of AP-1 and Hippo signaling target genes. The synthetic lethal therapy using metabolic stress inducers may be a promising therapeutic choice to treat the LKB1-MARK3 axis-dysregulated HGSOCs.
MeSH term(s)	AMP-Activated Protein Kinase Kinases/genetics ; Biomarkers, Tumor/genetics ; Cell Line, Tumor ; Cell Proliferation/genetics ; Down-Regulation/genetics ; Epigenesis, Genetic/genetics ; Female ; Genes, Tumor Suppressor ; Humans ; Ovarian Neoplasms/genetics ; Ovarian Neoplasms/pathology ; Protein Serine-Threonine Kinases/genetics ; Stress, Physiological/genetics
Chemical Substances	Biomarkers, Tumor ; MARK3 protein, human (EC 2.7.1.-) ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; STK11 protein, human (EC 2.7.11.1) ; AMP-Activated Protein Kinase Kinases (EC 2.7.11.3)
Language	English
Publishing date	2022-01-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2399-3642
ISSN (online)	2399-3642
DOI	10.1038/s42003-021-02992-4
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Article ; Online: Deregulation of the Histone Lysine-Specific Demethylase 1 Is Involved in Human Hepatocellular Carcinoma.

Kim, Sangchul / Bolatkan, Amina / Kaneko, Syuzo / Ikawa, Noriko / Asada, Ken / Komatsu, Masaaki / Hayami, Shinya / Ojima, Hidenori / Abe, Nobutsugu / Yamaue, Hiroki / Hamamoto, Ryuji

Biomolecules

2019 Volume 9, Issue 12

Abstract: Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer and is a leading cause of cancer-related death worldwide. Given that the standard-of-care for advanced liver cancer is limited, there is an urgent need to develop a novel ... ...

Abstract	Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer and is a leading cause of cancer-related death worldwide. Given that the standard-of-care for advanced liver cancer is limited, there is an urgent need to develop a novel molecular targeted therapy to improve therapeutic outcomes for HCC. In order to tackle this issue, we conducted functional analysis of the histone lysine-specific demethylase (LSD1) to explore the possibility that this enzyme acts as a therapeutic target in HCC. According to immunohistochemical analysis, 232 of 303 (77%) HCC cases showed positive staining of LSD1 protein, and its expression was correlated with several clinicopathological characteristics, such as female gender, AFP (alpha-fetoprotein) levels, and HCV (hepatitis C virus) infectious. The survival curves for HCC using the Kaplan-Meier method and the log-rank test indicate that positive LSD1 protein expression was significantly associated with decreased rates of overall survival (OS) and disease-free survival (DFS); the multivariate analysis indicates that LSD1 expression was an independent prognostic factor for both OS and DFS in patients with HCC. In addition, knockout of LSD1 using the CRISPR/Cas9 system showed a significantly lower number of colony formation units (CFUs) and growth rate in both SNU-423 and SNU-475 HCC cell lines compared to the corresponding control cells. Moreover, LSD1 knockout decreased cells in S phase of SNU-423 and SNU-475 cells with increased levels of H3K4me1/2 and H3K9me1/2. Finally, we identified the signaling pathways regulated by LSD1 in HCC, including the retinoic acid (RA) pathway. Our findings imply that deregulation of LSD1 can be involved in HCC; further studies may explore the usefulness of LSD1 as a therapeutic target of HCC.
MeSH term(s)	Aged ; Carcinoma, Hepatocellular/genetics ; Carcinoma, Hepatocellular/metabolism ; Cell Cycle ; Cell Line, Tumor ; Cell Proliferation ; Female ; Gene Expression Profiling ; Histone Demethylases/genetics ; Histone Demethylases/metabolism ; Humans ; Liver Neoplasms/genetics ; Liver Neoplasms/metabolism ; Male ; Middle Aged ; Prognosis ; Signal Transduction
Chemical Substances	Histone Demethylases (EC 1.14.11.-) ; KDM1A protein, human (EC 1.5.-)
Language	English
Publishing date	2019-12-01
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2701262-1
ISSN	2218-273X ; 2218-273X
ISSN (online)	2218-273X
ISSN	2218-273X
DOI	10.3390/biom9120810
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Article: Genome-Wide Chromatin Analysis of FFPE Tissues Using a Dual-Arm Robot with Clinical Potential.

Cancers

2021 Volume 13, Issue 9

Abstract: Although chromatin immunoprecipitation and next-generation sequencing (ChIP-seq) using formalin-fixed paraffin-embedded tissue (FFPE) has been reported, it remained elusive whether they retained accurate transcription factor binding. Here, we developed a ...

Abstract	Although chromatin immunoprecipitation and next-generation sequencing (ChIP-seq) using formalin-fixed paraffin-embedded tissue (FFPE) has been reported, it remained elusive whether they retained accurate transcription factor binding. Here, we developed a method to identify the binding sites of the insulator transcription factor CTCF and the genome-wide distribution of histone modifications involved in transcriptional activation. Importantly, we provide evidence that the ChIP-seq datasets obtained from FFPE samples are similar to or even better than the data for corresponding fresh-frozen samples, indicating that FFPE samples are compatible with ChIP-seq analysis. H3K27ac ChIP-seq analyses of 69 FFPE samples using a dual-arm robot revealed that driver mutations in EGFR were distinguishable from pan-negative cases and were relatively homogeneous as a group in lung adenocarcinomas. Thus, our results demonstrate that FFPE samples are an important source for epigenomic research, enabling the study of histone modifications, nuclear chromatin structure, and clinical data.
Language	English
Publishing date	2021-04-28
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers13092126
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Article ; Online: Enhanced HSP70 lysine methylation promotes proliferation of cancer cells through activation of Aurora kinase B.

Cho, Hyun-Soo / Shimazu, Tadahiro / Toyokawa, Gouji / Daigo, Yataro / Maehara, Yoshihiko / Hayami, Shinya / Ito, Akihiro / Masuda, Ken / Ikawa, Noriko / Field, Helen I / Tsuchiya, Eiju / Ohnuma, Shin-ichi / Ponder, Bruce A J / Yoshida, Minoru / Nakamura, Yusuke / Hamamoto, Ryuji

Nature communications

2012 Volume 3, Page(s) 1072

Abstract: Although heat-shock protein 70 (HSP70), an evolutionarily highly conserved molecular chaperone, is known to be post-translationally modified in various ways such as phosphorylation, ubiquitination and glycosylation, physiological significance of lysine ... ...

Abstract	Although heat-shock protein 70 (HSP70), an evolutionarily highly conserved molecular chaperone, is known to be post-translationally modified in various ways such as phosphorylation, ubiquitination and glycosylation, physiological significance of lysine methylation has never been elucidated. Here we identify dimethylation of HSP70 at Lys-561 by SETD1A. Enhanced HSP70 methylation was detected in various types of human cancer by immunohistochemical analysis, although the methylation was barely detectable in corresponding non-neoplastic tissues. Interestingly, methylated HSP70 predominantly localizes to the nucleus of cancer cells, whereas most of the HSP70 protein locates to the cytoplasm. Nuclear HSP70 directly interacts with Aurora kinase B (AURKB) in a methylation-dependent manner and promotes AURKB activity in vitro and in vivo. We also find that methylated HSP70 has a growth-promoting effect in cancer cells. Our findings demonstrate a crucial role of HSP70 methylation in human carcinogenesis.
MeSH term(s)	Animals ; Aurora Kinase B ; Aurora Kinases ; Blotting, Western ; COS Cells ; Cell Line, Tumor ; Cell Proliferation ; Chlorocebus aethiops ; HSP70 Heat-Shock Proteins/metabolism ; Humans ; Immunohistochemistry ; Immunoprecipitation ; Lysine ; Methylation ; Protein Binding ; Protein Serine-Threonine Kinases/metabolism ; Tissue Array Analysis
Chemical Substances	HSP70 Heat-Shock Proteins ; AURKB protein, human (EC 2.7.11.1) ; Aurora Kinase B (EC 2.7.11.1) ; Aurora Kinases (EC 2.7.11.1) ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Lysine (K3Z4F929H6)
Language	English
Publishing date	2012-09-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/ncomms2074
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Article ; Online: Determination of splice-site mutations in Lynch syndrome (hereditary non-polyposis colorectal cancer) patients using functional splicing assay.

Naruse, Hiromu / Ikawa, Noriko / Yamaguchi, Kiyoshi / Nakamura, Yusuke / Arai, Masami / Ishioka, Chikashi / Sugano, Kokichi / Tamura, Kazuo / Tomita, Naohiro / Matsubara, Nagahide / Yoshida, Teruhiko / Moriya, Yoshihiro / Furukawa, Yoichi

Familial cancer

2009 Volume 8, Issue 4, Page(s) 509–517

Abstract: Lynch syndrome (hereditary non-polyposis colorectal cancer) is an inherited disease caused by germ-line mutation in mismatch repair genes such as MLH1, MSH2, and MSH6. The mutations include missense and nonsense mutations, small insertions and deletions, ...

Abstract	Lynch syndrome (hereditary non-polyposis colorectal cancer) is an inherited disease caused by germ-line mutation in mismatch repair genes such as MLH1, MSH2, and MSH6. The mutations include missense and nonsense mutations, small insertions and deletions, and gross genetic alterations including large deletions and duplications. In addition to these genetic changes, mutations in introns are also involved in the pathogenesis. However, it is sometimes difficult to interpret correctly the pathogenicity of variants in exons as well as introns. To evaluate the effect of splice-site mutations in two Lynch syndrome patients, we carried out a functional splicing assay using minigenes. Consequently, this assay showed that the mutation of c.1731+5G>A in MLH1 led to exon15 skipping, and that the mutation of c.211+1G>C in MSH2 created an activated cryptic splice-site 17-nucleotides upstream in exon1. These aberrant splicing patterns were not observed when wild type sequence was used for the assay. We also obtained concordant results by RT-PCR experiments with transcripts from the patients. Furthermore, additional functional splicing assays using two different intronic mutations described in earlier studies revealed splicing alterations that were in complete agreement with the reports. Therefore, functional splicing assay is helpful for evaluating the effects of genetic variants on splicing.
MeSH term(s)	Adaptor Proteins, Signal Transducing/genetics ; Adult ; Base Sequence ; Colorectal Neoplasms, Hereditary Nonpolyposis/genetics ; DNA-Binding Proteins/genetics ; Female ; Genetic Predisposition to Disease ; Genetic Techniques ; Humans ; Male ; Middle Aged ; MutL Protein Homolog 1 ; MutS Homolog 2 Protein/genetics ; Mutation ; Nuclear Proteins/genetics ; RNA Splice Sites/genetics ; Reverse Transcriptase Polymerase Chain Reaction
Chemical Substances	Adaptor Proteins, Signal Transducing ; DNA-Binding Proteins ; G-T mismatch-binding protein ; MLH1 protein, human ; Nuclear Proteins ; RNA Splice Sites ; MSH2 protein, human (EC 3.6.1.3) ; MutL Protein Homolog 1 (EC 3.6.1.3) ; MutS Homolog 2 Protein (EC 3.6.1.3)
Language	English
Publishing date	2009-08-15
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1502496-9
ISSN	1573-7292 ; 1389-9600
ISSN (online)	1573-7292
ISSN	1389-9600
DOI	10.1007/s10689-009-9280-6
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Zs.A 6099: Show issues

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Article ; Online: The JmjC domain-containing histone demethylase KDM3A is a positive regulator of the G1/S transition in cancer cells via transcriptional regulation of the HOXA1 gene.

Cho, Hyun-Soo / Toyokawa, Gouji / Daigo, Yataro / Hayami, Shinya / Masuda, Ken / Ikawa, Noriko / Yamane, Yuka / Maejima, Kazuhiro / Tsunoda, Tatsuhiko / Field, Helen I / Kelly, John D / Neal, David E / Ponder, Bruce A J / Maehara, Yoshihiko / Nakamura, Yusuke / Hamamoto, Ryuji

International journal of cancer

2011 Volume 131, Issue 3, Page(s) E179–89

Abstract: A number of histone demethylases have been identified and biochemically characterized, yet their biological functions largely remain uncharacterized, particularly in the context of human diseases such as cancer. In this study, we describe important roles ...

Abstract	A number of histone demethylases have been identified and biochemically characterized, yet their biological functions largely remain uncharacterized, particularly in the context of human diseases such as cancer. In this study, we describe important roles for the histone demethylase KDM3A, also known as JMJD1A, in human carcinogenesis. Expression levels of KDM3A were significantly elevated in human bladder carcinomas compared with nonneoplastic bladder tissues (p < 0.0001), when assessed by real-time PCR. We confirmed that some other cancers including lung cancer also overexpressed KDM3A, using cDNA microarray analysis. Treatment of cancer cell lines with small interfering RNA targeting KDM3A significantly knocked down its expression and resulted in the suppression of proliferation. Importantly, we found that KDM3A activates transcription of the HOXA1 gene through demethylating histone H3 at lysine 9 di-methylation by binding to its promoter region. Indeed, expression levels of KDM3A and HOXA1 in several types of cancer cell lines and bladder cancer samples were statistically correlated. We observed the down-regulation of HOXA1 as well as CCND1 after treatment with KDM3A siRNA, indicating G(1) arrest of cancer cells. Together, our results suggest that elevated expression of KDM3A plays a critical role in the growth of cancer cells, and further studies may reveal a cancer therapeutic potential in KDM3A inhibition.
MeSH term(s)	Cell Line, Tumor ; Cell Proliferation ; Cyclin D1/biosynthesis ; G1 Phase Cell Cycle Checkpoints ; Gene Expression Regulation, Neoplastic ; Histones/metabolism ; Homeodomain Proteins/genetics ; Humans ; Jumonji Domain-Containing Histone Demethylases/genetics ; Jumonji Domain-Containing Histone Demethylases/metabolism ; Lung Neoplasms/genetics ; Lung Neoplasms/metabolism ; Lung Neoplasms/pathology ; Methylation ; Oligonucleotide Array Sequence Analysis ; RNA Interference ; RNA, Small Interfering ; Transcription Factors/genetics ; Transcription, Genetic ; Urinary Bladder Neoplasms/genetics ; Urinary Bladder Neoplasms/metabolism ; Urinary Bladder Neoplasms/pathology
Chemical Substances	CCND1 protein, human ; Histones ; Homeodomain Proteins ; RNA, Small Interfering ; Transcription Factors ; homeobox A1 protein ; Cyclin D1 (136601-57-5) ; Jumonji Domain-Containing Histone Demethylases (EC 1.14.11.-) ; KDM3A protein, human (EC 1.14.11.-)
Language	English
Publishing date	2011-12-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	218257-9
ISSN	1097-0215 ; 0020-7136
ISSN (online)	1097-0215
ISSN	0020-7136
DOI	10.1002/ijc.26501
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