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| 1 | Association of Fusobacterium nucleatum with immunity andmolecular alterations in colorectal cancer显示文摘The human intestinal microbiome plays a major role in human health and diseases, including colorectal cancer. Colorectal carcinogenesis represents a heterogeneous process with a differing set of somatic molecular alterations, influenced by diet, environmental and microbial exposures, and host immunity. Fusobacterium species are part of the human oral and intestinal microbiota. Metagenomic analyses have shown an enrichment of Fusobacterium nucleatum(F. nucleatum) in colorectal carcinoma tissue. Using 511 colorectal carcinomas from Japanese patients, we assessed the presence of F. nucleatum. Our results showed that the frequency of F. nucleatum positivity in the Japanese colorectal cancer was 8.6%(44/511), which was lower than that in United States cohort studies(13%). Similar to the United States studies, F. nucleatum positivityin Japanese colorectal cancers was significantly associated with microsatellite instability(MSI)-high status. Regarding the immune response in colorectal cancer, high levels of infiltrating T-cell subsets(i.e., CD3+, CD8+, CD45RO+, and FOXP3+ cells) have been associated with better patient prognosis. There is also evidence to indicate that molecular features of colorectal cancer, especially MSI, influence T-cell-mediated adaptive immunity. Concerning the association between the gut microbiome and immunity, F. nucleatum has been shown to expand myeloid-derived immune cells, which inhibit T-cell proliferation and induce T-cell apoptosis in colorectal cancer. This finding indicates that F. nucleatum possesses immunosuppressive activities by inhibiting human T-cell responses. Certain micro RNAs are induced during the macrophage inflammatory response and have the ability to regulate host-cell responses to pathogens. Micro RNA-21 increases the levels of IL-10 and prostaglandin E2, which suppress antitumor T-cell-mediated adaptive immunity through the inhibition of the antigen-presenting capacities of dendritic cells and T-cell proliferation in colorectal cancer cells. Thus, emerging evidence may provide insights for strategies to target microbiota, immune cells and tumor molecular alterations for colorectal cancer prevention and treatment. Further investigation is needed to clarify the association of Fusobacterium with T-cells and micro RNA expressions in colorectal cancer. | Katsuhiko Nosho Yasutaka Sukawa Yasushi Adachi Miki Ito Kei Mitsuhashi Hiroyoshi Kurihara Shinichi Kanno Itaru Yamamoto Keisuke Ishigami Hisayoshi Igarashi Reo Maruyama Kohzoh Imai Hiroyuki Yamamoto Yasuhisa Shinomura | 2016 | World Journal of Gastroenterology2016，22，2： | 44 |
| 2 | Biological significance of the CpG island methylator phenotype显示文摘 | Hiromu Suzuki Eiichiro Yamamoto Reo Maruyama Takeshi Niinuma Masahiro Kai | 2014 | Biochemical and Biophysical Research Communications2014，，： | 1 |
| 3 | DNA methylation and microRNA dysregulation in cancer显示文摘 | Hiromu Suzuki Reo Maruyama Eiichiro Yamamoto Masahiro Kai | 2012 | Molecular Oncology2012，，6： | 1 |
| 4 | The JAK2/STAT3 signaling pathway is required for growth of CD44^sup +^CD24^sup -^ stem cell-like breast cancer cells in human tumors显示文摘 | Marotta Lauren L C Almendro Vanessa Marusyk Andriy Shipitsin Michail Schemme Janina Walker Sarah R Bloushtain-Qimron Noga Kim Jessica J Choudhury Sibgat A Maruyama Reo Wu Zhenhua G?nen Mithat Mulvey Laura A Bessarabova Marina O Huh Sung Jin | 2011 | Journal of Clinical Investigation2011，，： | 1 |
| 5 | Molecular Dissection of Premalignant Colorectal Lesions Reveals Early Onset of the CpG Island Methylator Phenotype显示文摘 | Eiichiro Yamamoto Hiromu Suzuki Hiro-o Yamano Reo Maruyama Masanori Nojima Seiko Kamimae Takeshi Sawada Masami Ashida Kenjiro Yoshikawa Tomoaki Kimura Ryo Takagi Taku Harada Ryo Suzuki Akiko Sato Masahiro Kai Yasushi Sasaki Takashi Tokino Tamotsu Sugai Ko | 2012 | The American Journal of Pathology2012，，5： | 1 |
| 6 | Aberrant methylation of microRNA-34b/c is a predictive marker of metachronous gastric cancer risk显示文摘 | Ryo Suzuki Eiichiro Yamamoto Masanori Nojima Reo Maruyama Hiro-o Yamano Kenjiro Yoshikawa Tomoaki Kimura Taku Harada Masami Ashida Takeshi Niinuma Akiko Sato Katsuhiko Nosho Hiroyuki Yamamoto Masahiro Kai Tamotsu Sugai Kohzoh Imai Hiromu Suzuki Yasuhisa S | 2014 | Journal of Gastroenterology2014，，7： | 1 |
| 7 | Association of Fusobacterium nucleatum with clinical and molecular features in colorectal serrated pathway显示文摘 | Miki Ito Shinichi Kanno Katsuhiko Nosho Yasutaka Sukawa Kei Mitsuhashi Hiroyoshi Kurihara Hisayoshi Igarashi Taiga Takahashi Mami Tachibana Hiroaki Takahashi Shinji Yoshii Toshinao Takenouchi Tadashi Hasegawa Kenji Okita Koichi Hirata Reo Maruyama Hiromu | 2015 | Int. J. Cancer2015，，6： | 1 |
| 8 | Colorectal Carcinomas with CpG Island Methylator Phenotype 1 Frequently Contain Mutations in Chromatin Regulators显示文摘 | Tomomitsu Tahara Eiichiro Yamamoto Priyanka Madireddi Hiromu Suzuki Reo Maruyama Woonbok Chung Judith Garriga Jaroslav Jelinek Hiro-o Yamano Tamotsu Sugai Yutaka Kondo Minoru Toyota Jean-Pierre J. Issa Marcos R.H. Estécio | 2013 | Gastroenterology2013，，： | 1 |
| 9 | Two target gene activation pathways for orphan ERR nuclear receptors显示文摘Estrogen-related receptors(ERRα/β/γ)are orphan nuclear receptors that function in energy-demanding physiological processes,as well as in development and stem cell maintenance,but mechanisms underlying target gene activation by ERRs are largely unknown.Here,reconstituted biochemical assays that manifest ERR-dependent transcription have revealed two complementary mechanisms.On DNA templates,ERRs activate transcription with just the normal complement of general initiation factors through an interaction of the ERR DNA-binding domain with the p52 subunit of initiation factor TFIIH.On chromatin templates,activation by ERRs is dependent on AF2 domain interactions with the cell-specific coactivator PGC-1α,which in turn recruits the ubiquitous p300 and MED1/Mediator coactivators.This role of PGC-1αmay also be fulfilled by other AF2-interacting coactivators like NCOA3,which is shown to recruit Mediator selectively to ERRβand ERRγ.Importantly,combined genetic and RNA-seq analyses establish that both the TFIIH and the AF2 interaction-dependent pathways are essential for ERRβ/γ-selective gene expression and pluripotency maintenance in embryonic stem cells in which NCOA3 is a critical coactivator. | Tomoyoshi Nakadai Miho Shimada Keiichi Ito Murat Alper Cevher Chi-Shuen Chu Kohei Kumegawa Reo Maruyama Sohail Malik Robert G Roeder | 2023 | Cell Research2023，33，2： | 0 |
| 10 | IGF2 differentially methylated region hypomethylation in relation to pathological and molecular features of serrated lesions显示文摘AIM:To investigate insulin-like growth factor 2(IGF2)differentially methylated region(DMR)0 hypomethylation in relation to clinicopathological and molecular features in colorectal serrated lesions.METHODS:To accurately analyze the association between the histological types and molecular features of each type of serrated lesion,we consecutively collected1386 formalin-fixed paraffin-embedded tissue specimens that comprised all histological types[hyperplastic polyps(HPs,n=121),sessile serrated adenomas(SSAs,n=132),traditional serrated adenomas(TSAs,n=111),non-serrated adenomas(n=195),and colorectal cancers(n=827)].We evaluated the methylation levels of IGF2 DMR0 and long interspersed nucleotide element-1(LINE-1)in HPs(n=115),SSAs(n=120),SSAs with cytological dysplasia(n=10),TSAs(n=91),TSAs with high-grade dysplasia(HGD)(n=15),non-serrated adenomas(n=80),non-serrated adenomas with HGD(n=105),and CRCs(n=794).For the accurate quantification of the relative methylation levels(scale 0%-100%)of IGF2 DMR0 and LINE-1,we used bisulfite pyrosequencing method.Tumor specimens were analyzed for microsatellite instability,KRAS(codons 12 and 13),BRAF(V600E),and PIK3CA(exons 9and 20)mutations;MLH1 and MGMT methylation;and IGF2 expression by immunohistochemistry.RESULTS:The distribution of the IGF2 DMR0 methylation level in 351 serrated lesions and 185 non-serrated adenomas(with or without HGD)was as follows:mean61.7,median 62.5,SD 18.0,range 5.0-99.0,interquartile range 49.5-74.4.The IGF2 DMR0 methylation level was divided into quartiles(Q1≥74.5,Q2 62.6-74.4,Q3 49.6-62.5,Q4≤49.5)for further analysis.With regard to the histological type,the IGF2 DMR0 methylation levels of SSAs(mean±SD,73.1±12.3)were significantly higher than those of HPs(61.9±20.5),TSAs(61.6±19.6),and non-serrated adenomas(59.0±15.8)(P<0.0001).The IGF2 DMR0 methylation level was inversely correlated with the IGF2 expression level(r=-0.21,P=0.0051).IGF2 DMR0 hypomethylation was less frequently detected in SSAs compared with HPs,TSAs,and non-serrated adenomas(P<0.0001).Multivariate logistic regression analysis also showed that IGF2 DMR0 hypomethylation was inversely associated with SSAs(P<0.0001).The methylation levels of IGF2 DMR0 and LINE-1 in TSAs with HGD(50.2±18.7and 55.7±5.4,respectively)were significantly lower than those in TSAs(61.6±19.6 and 58.8±4.7,respectively)(IGF2 DMR0,P=0.038;LINE-1,P=0.024).CONCLUSION:IGF2 DMR0 hypomethylation may be an infrequent epigenetic alteration in the SSA pathway.Hypomethylation of IGF2 DMR0 and LINE-1 may play a role in TSA pathway progression. | Takafumi Naito Katsuhiko Nosho Miki Ito Hisayoshi Igarashi Kei Mitsuhashi Shinji Yoshii Hironori Aoki Masafumi Nomura Yasutaka Sukawa Eiichiro Yamamoto Yasushi Adachi Hiroaki Takahashi Masao Hosokawa Masahiro Fujita Toshinao Takenouchi Reo Maruyama Hiromu Suzuki Yoshifumi Baba Kohzoh Imai Hiroyuki Yamamoto Shuji Ogino Yasuhisa Shinomura | 2014 | World Journal of Gastroenterology2014，20，29： | 0 |
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