Atsushi Nara
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Atsushi Nara has a total of 34 co-authors. Here are the top co-authors by number of shared publications:
- Atsushi Kamachi
Department of Molecular Oncology, Graduate School of Medicine, Institute of Science Tokyo, Tokyo, Japan; Division of Gastroenterological, Hepato-Biliary-Pancreatic, Transplantation and Pediatric Surgery, Department of Surgery, Shinshu University School of Medicine, Matsumoto, Japan
25 shared publications - Koya Yasukawa
Department of Molecular Oncology, Graduate School of Medicine, Institute of Science Tokyo, Tokyo, Japan; Division of Gastroenterological, Hepato-Biliary-Pancreatic, Transplantation and Pediatric Surgery, Department of Surgery, Shinshu University School of Medicine, Matsumoto, Japan
25 shared publications - Masahiro Yamane
Department of Molecular Oncology, Graduate School of Medicine, Institute of Science Tokyo, Tokyo, Japan; Department of Hepatobiliary and Pancreatic Surgery, Graduate School of Medicine, Institute of Science Tokyo, Tokyo, Japan
25 shared publications - Shinji Tanaka
Department of Molecular Oncology, Graduate School of Medicine, Institute of Science Tokyo, Tokyo, Japan
25 shared publications - Shu Shimada
Department of Molecular Oncology, Graduate School of Medicine, Institute of Science Tokyo, Tokyo, Japan
25 shared publications - Yoshiaki Tanji
Department of Molecular Oncology, Graduate School of Medicine, Institute of Science Tokyo, Tokyo, Japan; Department of Surgery, The Jikei University School of Medicine, Tokyo, Japan
25 shared publications
Latest Publications
- Open Access
- 17 February 2026
- Published by Elsevier in JHEP Reports
- Vol. 8 (5) , 101786
H4K5 lactylation - ENO2 loop drives glycolysis and HCC progression
- 17 February 2026
- Published by Elsevier in JHEP Reports
- Vol. 8 (5) , 101786
Open AccessH4K5 lactylation - ENO2 loop drives glycolysis and HCC progression
- Open Access
- 2 October 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S10 from PAD2-Mediated Histone Citrullination Drives Tumor Progression by Enhancing Cell Proliferation and Modifying the Microenvironment in Pancreatic Cancer
Transcriptome-based correlation of PAD2 and PRUNE1 and prognostic significance of PRUNE1 and CD206 in PDAC
- 2 October 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S10 from PAD2-Mediated Histone Citrullination Drives Tumor Progression by Enhancing Cell Proliferation and Modifying the Microenvironment in Pancreatic Cancer
Transcriptome-based correlation of PAD2 and PRUNE1 and prognostic significance of PRUNE1 and CD206 in PDAC
- Open Access
- 2 October 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S3 from PAD2-Mediated Histone Citrullination Drives Tumor Progression by Enhancing Cell Proliferation and Modifying the Microenvironment in Pancreatic Cancer
Expression of PAD family in normal pancreatic ductal cells and PDAC cell lines
- 2 October 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S3 from PAD2-Mediated Histone Citrullination Drives Tumor Progression by Enhancing Cell Proliferation and Modifying the Microenvironment in Pancreatic Cancer
Expression of PAD family in normal pancreatic ductal cells and PDAC cell lines
- Open Access
- 2 October 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S6 from PAD2-Mediated Histone Citrullination Drives Tumor Progression by Enhancing Cell Proliferation and Modifying the Microenvironment in Pancreatic Cancer
Effects of PRUNE1 knockdown and macrophage depletion
- 2 October 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S6 from PAD2-Mediated Histone Citrullination Drives Tumor Progression by Enhancing Cell Proliferation and Modifying the Microenvironment in Pancreatic Cancer
Effects of PRUNE1 knockdown and macrophage depletion
- Open Access
- 2 October 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S7 from PAD2-Mediated Histone Citrullination Drives Tumor Progression by Enhancing Cell Proliferation and Modifying the Microenvironment in Pancreatic Cancer
Flow cytometric analysis of macrophage polarization
- 2 October 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S7 from PAD2-Mediated Histone Citrullination Drives Tumor Progression by Enhancing Cell Proliferation and Modifying the Microenvironment in Pancreatic Cancer
Flow cytometric analysis of macrophage polarization
- Open Access
- 2 October 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Table S3 from PAD2-Mediated Histone Citrullination Drives Tumor Progression by Enhancing Cell Proliferation and Modifying the Microenvironment in Pancreatic Cancer
Clinicopathological backgrounds of 109 PDAC cases, comparing PAD2-high and -low groups
- 2 October 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S3 from PAD2-Mediated Histone Citrullination Drives Tumor Progression by Enhancing Cell Proliferation and Modifying the Microenvironment in Pancreatic Cancer
Clinicopathological backgrounds of 109 PDAC cases, comparing PAD2-high and -low groups
- Open Access
- 2 October 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Table S8 from PAD2-Mediated Histone Citrullination Drives Tumor Progression by Enhancing Cell Proliferation and Modifying the Microenvironment in Pancreatic Cancer
Clinicopathological backgrounds of 104 PDAC cases, comparing CD206-high and -low groups
- 2 October 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S8 from PAD2-Mediated Histone Citrullination Drives Tumor Progression by Enhancing Cell Proliferation and Modifying the Microenvironment in Pancreatic Cancer
Clinicopathological backgrounds of 104 PDAC cases, comparing CD206-high and -low groups
- Open Access
- 2 October 2025
- Published by American Association for Cancer Research (AACR)
Data from PAD2-Mediated Histone Citrullination Drives Tumor Progression by Enhancing Cell Proliferation and Modifying the Microenvironment in Pancreatic Cancer
Histone citrullination is catalyzed by peptidyl-arginine deiminases (PAD) that play a role in gene regulation, and several specific inhibitors have been developed. However, the clinical significance, molecular mechanisms of histone citrullination and PADs, and effects of PAD inhibitors in pancreatic ductal adenocarcinoma (PDAC) remain unclear. This study aimed to investigate the role and potential molecular mechanisms of PADs in PDAC. Histone citrullination was upregulated and strongly associated with the nuclear expression of PAD2, one of the PAD family, in human PDAC tissues, correlating with aggressiveness and poor prognosis. PAD2 overexpression increased PDAC cell proliferation, whereas its knockdown had the opposite effect in vitro. PAD2 was recruited to the promoter regions of PRUNE1 and E2F1, resulting in the activation of their mRNA expression via increased histone citrullination and chromatin accessibility. PAD2 overexpression enhanced tumorigenicity and increased PRUNE1 expression and M2 tumor–associated macrophage (M2 TAM) infiltration in vivo. PAD2 inhibitor suppressed the growth and tumorigenicity of PAD2-expressing PDAC mouse models by reducing PRUNE1 expression and M2 macrophage infiltration. Pad2 knockdown and PAD inhibitor treatment showed similar effects in syngeneic mouse models. The triple-high expression of nuclear PAD2, PRUNE1, and the M2 TAM marker CD206 may serve as independent adverse prognostic factors for human PDAC. Conclusively, PAD2-mediated histone citrullination drives PDAC progression by epigenetically regulating downstream target genes and influencing the tumor microenvironment. The PAD2–PRUNE1–M2 TAM axis presents a promising therapeutic target and prognostic indicator for PDAC.Implications:Elevated PAD2 expression promotes PDAC progression by epigenetically activating PRUNE1 and enhancing M2 macrophage polarization.
- 2 October 2025
- Published by American Association for Cancer Research (AACR)
Open AccessData from PAD2-Mediated Histone Citrullination Drives Tumor Progression by Enhancing Cell Proliferation and Modifying the Microenvironment in Pancreatic Cancer
Histone citrullination is catalyzed by peptidyl-arginine deiminases (PAD) that play a role in gene regulation, and several specific inhibitors have been developed. However, the clinical significance, molecular mechanisms of histone citrullination and PADs, and effects of PAD inhibitors in pancreatic ductal adenocarcinoma (PDAC) remain unclear. This study aimed to investigate the role and potential molecular mechanisms of PADs in PDAC. Histone citrullination was upregulated and strongly associated with the nuclear expression of PAD2, one of the PAD family, in human PDAC tissues, correlating with aggressiveness and poor prognosis. PAD2 overexpression increased PDAC cell proliferation, whereas its knockdown had the opposite effect in vitro. PAD2 was recruited to the promoter regions of PRUNE1 and E2F1, resulting in the activation of their mRNA expression via increased histone citrullination and chromatin accessibility. PAD2 overexpression enhanced tumorigenicity and increased PRUNE1 expression and M2 tumor–associated macrophage (M2 TAM) infiltration in vivo. PAD2 inhibitor suppressed the growth and tumorigenicity of PAD2-expressing PDAC mouse models by reducing PRUNE1 expression and M2 macrophage infiltration. Pad2 knockdown and PAD inhibitor treatment showed similar effects in syngeneic mouse models. The triple-high expression of nuclear PAD2, PRUNE1, and the M2 TAM marker CD206 may serve as independent adverse prognostic factors for human PDAC. Conclusively, PAD2-mediated histone citrullination drives PDAC progression by epigenetically regulating downstream target genes and influencing the tumor microenvironment. The PAD2–PRUNE1–M2 TAM axis presents a promising therapeutic target and prognostic indicator for PDAC.Implications:Elevated PAD2 expression promotes PDAC progression by epigenetically activating PRUNE1 and enhancing M2 macrophage polarization.
- Open Access
- 2 October 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S8 from PAD2-Mediated Histone Citrullination Drives Tumor Progression by Enhancing Cell Proliferation and Modifying the Microenvironment in Pancreatic Cancer
PAD inhibitor and macrophage depletion experiments
- 2 October 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S8 from PAD2-Mediated Histone Citrullination Drives Tumor Progression by Enhancing Cell Proliferation and Modifying the Microenvironment in Pancreatic Cancer
PAD inhibitor and macrophage depletion experiments
- Open Access
- 2 October 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S4 from PAD2-Mediated Histone Citrullination Drives Tumor Progression by Enhancing Cell Proliferation and Modifying the Microenvironment in Pancreatic Cancer
Effect of PAD2 on PDAC cell proliferation in vitro
- 2 October 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S4 from PAD2-Mediated Histone Citrullination Drives Tumor Progression by Enhancing Cell Proliferation and Modifying the Microenvironment in Pancreatic Cancer
Effect of PAD2 on PDAC cell proliferation in vitro