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View article: Abstract 2788 Chemokine Switching via ARF6-AMAP1: A Key Mechanism of Immune Evasion in Pancreatic Cancer
Abstract 2788 Chemokine Switching via ARF6-AMAP1: A Key Mechanism of Immune Evasion in Pancreatic Cancer Open
View article: Plasticity and Tumor Microenvironment in Pancreatic Cancer: Genetic, Metabolic, and Immune Perspectives
Plasticity and Tumor Microenvironment in Pancreatic Cancer: Genetic, Metabolic, and Immune Perspectives Open
Cancer has long been believed to be a genetic disease caused by the accumulation of mutations in key genes involved in cellular processes. However, recent advances in sequencing technology have demonstrated that cells with cancer driver mu…
View article: MitoNEET reduces the mitochondrial oxidative phosphorylation during epithelial-mesenchymal transition
MitoNEET reduces the mitochondrial oxidative phosphorylation during epithelial-mesenchymal transition Open
Mitochondrial functions range from catabolic to anabolic, which are tightly coordinated to meet cellular demands for proliferation and motility. MitoNEET is a mitochondrial outer membrane protein with a CDGSH domain and is involved in mito…
View article: p53 ensures the normal behavior and modification of G1/S-specific histone H3.1 in the nucleus
p53 ensures the normal behavior and modification of G1/S-specific histone H3.1 in the nucleus Open
H3.1 histone is predominantly synthesized and enters the nucleus during the G1/S phase of the cell cycle, as a new component of duplicating nucleosomes. Here, we found that p53 is necessary to secure the normal behavior and modification of…
View article: Correction to: Computer model of IL-6-dependent rheumatoid arthritis in F759 mice
Correction to: Computer model of IL-6-dependent rheumatoid arthritis in F759 mice Open
View article: ADP-Ribosylation Factor 6 Pathway Acts as a Key Executor of Mesenchymal Tumor Plasticity
ADP-Ribosylation Factor 6 Pathway Acts as a Key Executor of Mesenchymal Tumor Plasticity Open
Despite the “big data” on cancer from recent breakthroughs in high-throughput technology and the development of new therapeutic modalities, it remains unclear as to how intra-tumor heterogeneity and phenotypic plasticity created by various…
View article: p53 secures the normal behavior of H3.1 histone in the nucleus by regulating nuclear phosphatidic acid and EZH2 during the G1/S phase
p53 secures the normal behavior of H3.1 histone in the nucleus by regulating nuclear phosphatidic acid and EZH2 during the G1/S phase Open
Histones are key molecules of epigenetic regulation and inheritance, and are thought to be chaperoned and transported into the nucleus appropriately prior to being integrated into nucleosomes. H3.1 histone is predominantly synthesized and …
View article: Data from Arid5a Promotes Immune Evasion by Augmenting Tryptophan Metabolism and Chemokine Expression
Data from Arid5a Promotes Immune Evasion by Augmenting Tryptophan Metabolism and Chemokine Expression Open
The acquisition of mesenchymal traits leads to immune evasion in various cancers, but the underlying molecular mechanisms remain unclear. In this study, we found that the expression levels of AT-rich interaction domain-containing protein 5…
View article: Supplementary Figures and Tables from Arid5a Promotes Immune Evasion by Augmenting Tryptophan Metabolism and Chemokine Expression
Supplementary Figures and Tables from Arid5a Promotes Immune Evasion by Augmenting Tryptophan Metabolism and Chemokine Expression Open
Supplementary Figures 1-8 and Tables 1-3
View article: Data from Arid5a Promotes Immune Evasion by Augmenting Tryptophan Metabolism and Chemokine Expression
Data from Arid5a Promotes Immune Evasion by Augmenting Tryptophan Metabolism and Chemokine Expression Open
The acquisition of mesenchymal traits leads to immune evasion in various cancers, but the underlying molecular mechanisms remain unclear. In this study, we found that the expression levels of AT-rich interaction domain-containing protein 5…
View article: Supplementary Figures and Tables from Arid5a Promotes Immune Evasion by Augmenting Tryptophan Metabolism and Chemokine Expression
Supplementary Figures and Tables from Arid5a Promotes Immune Evasion by Augmenting Tryptophan Metabolism and Chemokine Expression Open
Supplementary Figures 1-8 and Tables 1-3
View article: A peptide derived from adaptor protein STAP-2 inhibits tumor progression by downregulating epidermal growth factor receptor signaling
A peptide derived from adaptor protein STAP-2 inhibits tumor progression by downregulating epidermal growth factor receptor signaling Open
View article: Orchestration of mesenchymal plasticity and immune evasiveness via rewiring of the metabolic program in pancreatic ductal adenocarcinoma
Orchestration of mesenchymal plasticity and immune evasiveness via rewiring of the metabolic program in pancreatic ductal adenocarcinoma Open
Pancreatic ductal adenocarcinoma (PDAC) is the most fatal cancer in humans, due to its difficulty of early detection and its high metastatic ability. The occurrence of epithelial to mesenchymal transition in preinvasive pancreatic lesions …
View article: Tumor-derived interleukin-34 creates an immunosuppressive and chemoresistant tumor microenvironment by modulating myeloid-derived suppressor cells in triple-negative breast cancer
Tumor-derived interleukin-34 creates an immunosuppressive and chemoresistant tumor microenvironment by modulating myeloid-derived suppressor cells in triple-negative breast cancer Open
View article: Central Roles of STAT3-Mediated Signals in Onset and Development of Cancers: Tumorigenesis and Immunosurveillance
Central Roles of STAT3-Mediated Signals in Onset and Development of Cancers: Tumorigenesis and Immunosurveillance Open
Since the time of Rudolf Virchow in the 19th century, it has been well-known that cancer-associated inflammation contributes to tumor initiation and progression. However, it remains unclear whether a collapse of the balance between the ant…
View article: ARF6-AMAP1 pathway induces pancreatic cancer cells to express immunosuppressive chemokines
ARF6-AMAP1 pathway induces pancreatic cancer cells to express immunosuppressive chemokines Open
Aim: The tumor microenvironment (TME) of pancreatic ductal adenocarcinoma (PDAC) is highly immune suppressive with modest T-cell infiltration, and only rarely responds to immune checkpoint inhibition (ICI) therapy. Our aim was to clarify t…
View article: Arid5a Promotes Immune Evasion by Augmenting Tryptophan Metabolism and Chemokine Expression
Arid5a Promotes Immune Evasion by Augmenting Tryptophan Metabolism and Chemokine Expression Open
The acquisition of mesenchymal traits leads to immune evasion in various cancers, but the underlying molecular mechanisms remain unclear. In this study, we found that the expression levels of AT-rich interaction domain-containing protein 5…
View article: Inhibition of mutant KRAS-driven overexpression of ARF6 and MYC by an eIF4A inhibitor drug improves the effects of anti-PD-1 immunotherapy for pancreatic cancer
Inhibition of mutant KRAS-driven overexpression of ARF6 and MYC by an eIF4A inhibitor drug improves the effects of anti-PD-1 immunotherapy for pancreatic cancer Open
View article: High expression of AMAP1, an ARF6 effector, is associated with elevated levels of PD-L1 and fibrosis of pancreatic cancer
High expression of AMAP1, an ARF6 effector, is associated with elevated levels of PD-L1 and fibrosis of pancreatic cancer Open
View article: ARF6 and AMAP1 are major targets of <i>KRAS</i> and <i>TP53</i> mutations to promote invasion, PD-L1 dynamics, and immune evasion of pancreatic cancer
ARF6 and AMAP1 are major targets of <i>KRAS</i> and <i>TP53</i> mutations to promote invasion, PD-L1 dynamics, and immune evasion of pancreatic cancer Open
Significance Pancreatic ductal carcinomas (PDACs) have been extensively studied regarding their genomic alterations, microenvironmental intercommunication, and metabolic reprogramming. However, identification of the protein machinery of tu…
View article: Endothelin type B receptor interacts with the 78‐<scp>kD</scp>a glucose‐regulated protein
Endothelin type B receptor interacts with the 78‐<span>kD</span>a glucose‐regulated protein Open
Endothelin ( ET )‐1 is involved in the vascular system, cell proliferation and apoptosis. ET receptors consist of ET type A receptor ( ET A R ) and ET type B receptor ( ET B R ). ET A R and ET B R generally exhibit opposite responses, alth…
View article: GRP78 promotes ERK activation through endothelin type B receptor
GRP78 promotes ERK activation through endothelin type B receptor Open
Endothelin (ET)-1 is involved in various diseases, including cancer, hypertension, atherosclerosis, diabetes, and fibrotic diseases, although ET-1 is originally identified as endothelium-derived vasocontractile peptide. ET receptors belong…
View article: Epithelial-specific histone modification of the miR-96/182 locus targeting AMAP1 mRNA predisposes p53 to suppress cell invasion in epithelial cells
Epithelial-specific histone modification of the miR-96/182 locus targeting AMAP1 mRNA predisposes p53 to suppress cell invasion in epithelial cells Open
Histone modifications of certain miRNA loci, such as the miR-183-96-182 cistron, are different between epithelial cells and non-epithelial cells. Such epithelial-specific miRNA regulation appears to provide the molecular basis for the epit…
View article: Frequent overexpression of AMAP1, an Arf6 effector in cell invasion, is characteristic of the MMTV-PyMT rather than the MMTV-Neu human breast cancer model
Frequent overexpression of AMAP1, an Arf6 effector in cell invasion, is characteristic of the MMTV-PyMT rather than the MMTV-Neu human breast cancer model Open
View article: Additional file 2: of Epithelial-specific histone modification of the miR-96/182 locus targeting AMAP1 mRNA predisposes p53 to suppress cell invasion in epithelial cells
Additional file 2: of Epithelial-specific histone modification of the miR-96/182 locus targeting AMAP1 mRNA predisposes p53 to suppress cell invasion in epithelial cells Open
Figure S2. Epigenome status of each miRNA. The ENCODE data of miRNAs in Fig. 2a are shown by the UCSC Genome Browser. Definitions of the colors are given at the top of Fig. 3c. (ZIP 21369â kb)
View article: High expression of EPB41L5, an integral component of the Arf6-driven mesenchymal program, correlates with poor prognosis of squamous cell carcinoma of the tongue
High expression of EPB41L5, an integral component of the Arf6-driven mesenchymal program, correlates with poor prognosis of squamous cell carcinoma of the tongue Open
View article: Arf6 and its ZEB1-EPB41L5 mesenchymal axis are required for both mesenchymal- and amoeboid-type invasion of cancer cells
Arf6 and its ZEB1-EPB41L5 mesenchymal axis are required for both mesenchymal- and amoeboid-type invasion of cancer cells Open
Modes of cancer invasion interchange between the mesenchymal type and amoeboid type in response to the microenvironment, in which RhoA and Rac1 are selectively required to perform different modes of actin-cytoskeletal remodeling. Membrane …
View article: ZEB1 induces EPB41L5 in the cancer mesenchymal program that drives ARF6-based invasion, metastasis and drug resistance
ZEB1 induces EPB41L5 in the cancer mesenchymal program that drives ARF6-based invasion, metastasis and drug resistance Open
View article: Tumor responsiveness to statins requires overexpression of the ARF6 pathway
Tumor responsiveness to statins requires overexpression of the ARF6 pathway Open
The mevalonate pathway results in the prenylation of small GTPases, which are pivotal for oncogenesis and cancer malignancies. However, inhibitors of this pathway, such as statins, have not necessarily produced favorable results in clinica…
View article: P53- and mevalonate pathway–driven malignancies require Arf6 for metastasis and drug resistance
P53- and mevalonate pathway–driven malignancies require Arf6 for metastasis and drug resistance Open
Drug resistance, metastasis, and a mesenchymal transcriptional program are central features of aggressive breast tumors. The GTPase Arf6, often overexpressed in tumors, is critical to promote epithelial–mesenchymal transition and invasiven…