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Auteur : Grafiati
Publié le 10 mars 2023

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1

Wang, Yanhong, Ying Song, Lijie Zhou, Mengxi Wang, Dong Wang, Jing Bai, Songbin Fu et Jingcui Yu. « The Overexpression of TOB1 Induces Autophagy in Gastric Cancer Cells by Secreting Exosomes ». Disease Markers 2022 (12 avril 2022) : 1–10. http://dx.doi.org/10.1155/2022/7925097.

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We previously confirmed that transducer of ERBB2, 1 (TOB1) gene, can induce autophagy in gastric cancer cells. Studies have shown the biogenesis of exosomes overlaps with different autophagy processes, which helps to maintain the self-renewal and homeostasis of body cells. This study is aimed at verifying whether overexpressing TOB1 induces autophagy by secreting exosomes in gastric cancer cells and its underlying mechanisms. Differential ultracentrifugation was used to extracted the exosomes from the culture medium of gastric cancer cell line AGS-TOB1 ectopically overexpressing TOB1 (exo-AGS-TOB1, experimental group) and AGS-empty-vector cell line with low expression of endogenous TOB1 (exo-AGS-Vector, control group). Exosomal markers CD9 and TSG101 were determined in both the cell supernatants of exo-AGS-TOB1 and exo-AGS-Vector by Western blot. Under the transmission electron microscope (TEM), the exosomes were round and saucer-like vesicles with double-layer membrane structure, and the vesicles showed different translucency due to different contents. The peak size of exosomes detected by nanoparticle tracking analysis (NTA) was about 100 nm. When the exosomes of exo-AGS-TOB1 and exo-AGS-Vector were cocultured with TOB1 knockdown gastric cancer cell line HGC-27-TOB1-6E12 for 48 hours, the conversion of autophagy-related protein LC3-I to LC3-II in HGC-27-TOB1-6E12 gastric cancer cells cocultured with exo-AGS-TOB1 was significantly higher than that in the control group, and the ratio of LC3-II/LC3-I was statistically different ( P < 0.05 ). More autophagosomes in HGC-27-TOB1-6E12 cells cocultured with exo-AGS-TOB1 for 48 hours were observed under TEM, while fewer autophagosomes were found in the control group. Lastly, miRNAs were differentially expressed by cell supernatant-exosomal whole transcriptome sequencing. Thus, our results provide new insights into TOB1-induced autophagy in gastric cancer.
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Gao, Yulei, Yinquan Zhang, Yanghu Lu, Yi Wang, Xingrui Kou, Yi Lou et Yifan Kang. « TOB1 Deficiency Enhances the Effect of Bone Marrow-Derived Mesenchymal Stem Cells on Tendon-Bone Healing in a Rat Rotator Cuff Repair Model ». Cellular Physiology and Biochemistry 38, no 1 (2016) : 319–29. http://dx.doi.org/10.1159/000438632.

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Background/Aims: This study investigated the effect of silencing TOB1 (Transducer of ERBB2, 1) expression in bone marrow-derived mesenchymal stem cells (MSCs) on MSC-facilitated tendon-bone healing in a rat supraspinatus repair model. Methods: Rat MSCs were transduced with a recombinant lentivirus encoding short hairpin RNA (shRNA) against TOB1. MSC cell proliferation was analyzed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays. The effect of MSCs with TOB1 deficiency on tendon-bone healing in a rat rotator cuff repair model was evaluated by biomechanical testing, histological analysis and collagen type I and II gene expression. An upstream regulator (miR-218) of TOB1 was determined in MSCs. Results: We found that knockdown of TOB1 significantly increased the proliferative activity of rat MSCs in vitro. When MSCs with TOB1 deficiency were injected into injured rat supraspinatus tendon-bone junctions, the effect on tendon-bone healing was enhanced compared to treatment with control MSCs with normal TOB1 expression, as evidenced by elevated levels of ultimate load to failure and stiffness, increased amount of fibrocartilage and augmented expression of collagen type I and type II genes. In addition, we found that the TOB1 3′ untranslated region is a direct target of miR-218. Similar to the effect of TOB1 deficiency, overexpression of miR-218 effectively promoted tendon-bone healing in rat. Conclusion: These results suggest that TOB1 may play a negative role in the effect of MSCs on tendon-bone healing, and imply that expression of TOB1 may be regulated by miR-218.
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Ho, Karen J., Nhue L. Do, Hasan H. Otu, Martin J. Dib, Xianghui Ren, Keiichi Enjyoji, Simon C. Robson, Ernest F. Terwilliger et Seth J. Karp. « Tob1 is a constitutively expressed repressor of liver regeneration ». Journal of Experimental Medicine 207, no 6 (31 mai 2010) : 1197–208. http://dx.doi.org/10.1084/jem.20092434.

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How proliferative and inhibitory signals integrate to control liver regeneration remains poorly understood. A screen for antiproliferative factors repressed after liver injury identified transducer of ErbB2.1 (Tob1), a member of the PC3/BTG1 family of mito-inhibitory molecules as a target for further evaluation. Tob1 protein decreases after 2/3 hepatectomy in mice secondary to posttranscriptional mechanisms. Deletion of Tob1 increases hepatocyte proliferation and accelerates restoration of liver mass after hepatectomy. Down-regulation of Tob1 is required for normal liver regeneration, and Tob1 controls hepatocyte proliferation in a dose-dependent fashion. Tob1 associates directly with both Caf1 and cyclin-dependent kinase (Cdk) 1 and modulates Cdk1 kinase activity. In addition, Tob1 has significant effects on the transcription of critical cell cycle components, including E2F target genes and genes involved in p53 signaling. We provide direct evidence that levels of an inhibitory factor control the rate of liver regeneration, and we identify Tob1 as a crucial check point molecule that modulates the expression and activity of cell cycle proteins.
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Schulze-Topphoff, Ulf, Simona Casazza, Michel Varrin-Doyer, Kara Pekarek, Raymond A. Sobel, Stephen L. Hauser, Jorge R. Oksenberg, Scott S. Zamvil et Sergio E. Baranzini. « Tob1 plays a critical role in the activation of encephalitogenic T cells in CNS autoimmunity ». Journal of Experimental Medicine 210, no 7 (24 juin 2013) : 1301–9. http://dx.doi.org/10.1084/jem.20121611.

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Reliable biomarkers corresponding to disease progression or therapeutic responsiveness in multiple sclerosis (MS) have not been yet identified. We previously reported that low expression of the antiproliferative gene TOB1 in CD4+ T cells of individuals presenting with an initial central nervous system (CNS) demyelinating event (a clinically isolated syndrome), correlated with high risk for progression to MS. We report that experimental autoimmune encephalomyelitis (EAE) in Tob1−/− mice was associated with augmented CNS inflammation, increased infiltrating CD4+ and CD8+ T cell counts, and increased myelin-reactive Th1 and Th17 cells, with reduced numbers of regulatory T cells. Reconstitution of Rag1−/− mice with Tob1−/− CD4+ T cells recapitulated the aggressive EAE phenotype observed in Tob1−/− mice. Furthermore, severe spontaneous EAE was observed when Tob1−/− mice were crossed to myelin oligodendrocyte glycoprotein–specific T cell receptor transgenic (2D2) mice. Collectively, our results reveal a critical role for Tob1 in adaptive T cell immune responses that drive development of EAE, thus providing support for the development of Tob1 as a biomarker for demyelinating disease activity.
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Wang, Dong, Yunlong Li, Shuning Sui, Mengdi Cai, Kexian Dong, Ping Wang, Xiao Liang, Songbin Fu et Jingcui Yu. « Involvement of TOB1 on autophagy in gastric cancer AGS cells via decreasing the activation of AKT/mTOR signaling pathway ». PeerJ 10 (4 février 2022) : e12904. http://dx.doi.org/10.7717/peerj.12904.

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Background We previously identified the tumor suppressor gene TOB1 as related to gastric cancer. The purpose of this study was to explore whether TOB1 induces autophagy through the AKT/mTOR signaling pathway in gastric cancer. Methods Western blotting was used to detect the protein levels of TOB1, LC3, AKT, mTOR, phosphorylated (p) AKT, and p-mTOR. A double fluorescent GFP-RFP-LC3 fusion protein was used to trace autophagy by laser confocal microscopy. Autophagosomes were observed by transmission electron microscopy. Results The conversion of LC3-I to LC3-II and the LC3-II/LC3-I ratio were significantly increased in AGS cells overexpressing TOB1 compared with control cells. Fluorescence imaging showed LC3 puncta at 48 h, and these puncta increased significantly at 72 h after TOB1 transfection compared with control tumor cells. The presence of autophagosomes in AGS cells was observed at 72 h after TOB1 transfection by transmission electron microscopy, and no autophagosomes were found in the control cells. Moreover, the levels of p-AKT and p -mTOR were lower in AGS cells than in control cancer cells. Conclusion Our results provide novel insight that TOB1 might suppress gastric cancer by inducing autophagy, possibly through decreasing phosphorylation and the subsequent activation of the AKT/mTOR signaling pathway.
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Mascarenhas, Cintia Do Couto, Anderson Ferreira Cunha, Ana Flavia Brugnerotto, Sheley Gambero, Joao Machado-Neto, Adriana S. S. Duarte, Katia B. Pagnano, Fernando Ferreira Costa et Carmino Antonio De Souza. « The Relationship Between the Regulation of TOB1 Gene with Cell Proliferation, Apoptosis and Cell Cycle in BCR-ABL Positive Cells ». Blood 120, no 21 (16 novembre 2012) : 5125. http://dx.doi.org/10.1182/blood.v120.21.5125.5125.

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Abstract Abstract 5125 The TOB1 gene is a transcription factor responsible for the transduction of the gene ERBB2. It is a member of a family of cell suppressor proliferation proteins called TOB/BTG1 family; also, this gene operates on the inhibition of neoplastic transformation. The TOB1 gene presents a decreased expression in several types of cancer such as lung, breast, thyroid and stomach cancer. However, the function of this gene in chronic myeloid leukemia (CML) remains unknown. Aiming to evaluate the inhibition of gene TOB1 into BCR-ABL positive cells and trying to elucidate the molecular mechanisms associated with the inhibition of this gene in the CML we proceed to a more detailed study of this gene. The inhibition of this gene in K562 cells was performed using specific lentivirus. The effect of silencing TOB1 in the proliferation of K562 cells was assessed by the MTT assay after 48 hours of culture; in shTOB1 the proliferation was increased in comparison with shControl cells. To evaluate the synergistic effect between the inhibition of kinase tyrosine activity of BCR-ABL and the inhibition of TOB1 we performed a treatment with different concentrations of imatinib (0. 1, 0. 5 and 1μM), but we observed the decrease in cell proliferation of shTOB1 cells to similar levels of shControl cells only at the 1μM concentration. Therefore, the TOB1 silencing increased the proliferation of K562 cells without an additional effect of a treatment with Imatinib. To analyze the clonogenicity, we performed a formation of colonies assay, in methylcellulose, to determine whether silencing TOB1 could cause a change in the clonal growth of positive BCR-ABL cells. There was no significant change in the number of colonies that grew in cell culture shTOB1 compared to shControl cells. These results suggest that silencing TOB1 in K562 cells may not change the clonogenicity. In the assessment of cell cycle, the flow cytometry analysis revealed a significant accumulation of K562 cells in S phase, with consequent reduction of cells in the G2 phase of the cell cycle in cells shTOB1 compared to cells shControl. The TOB1 gene silencing in K562 cells kept the cells in the S phase and prevented the entry of cells in the G2 phase showing that the inhibition of gene TOB1 induced an increase in proliferation of K562 BCR-ABL cells. The level of apoptosis was assessed by flow cytometry after labeling the cells with anexin-V/PI. The Imatinib treatment presented dose-response in the induction of apoptosis as expected. However, a cumulative effect with TOB1 silencing was not observed. Furthermore, the apoptosis was also assessed by assays of caspases 3, 8 and 9, which showed an increase of the caspase activity of shControl cells in relation of the shTOB1 cells, showing that inhibition of this gene also changes the level of apoptosis. These results corroborate the literature data that report the relationship of this tumour suppressor gene in signalling pathways related to angiogenesis, carcinogenesis, apoptosis and metastasis. When we relate the results obtained with the LMC, we can consider the possibility of TOB1 regulation changes be related to modification of important signalling pathways such as AKT, PI3K, STAT3 and STAT5, among others. Furthermore, the inhibition of TOB1 may be related with an increase on the number of BCR-ABL positive cells and subsequent disease progression. In conclusion, this study confirmed literature data showing that TOB1 gene works as a tumour suppressor protein in cells of many types of cancer. From this work we can infer that in CML the expression of this gene is transformed, resulting in changing of the capacity of induction of apoptosis, decrease tumour necrosis and increase cell proliferation. This work was supported by FAPESP and INCT. Disclosures: No relevant conflicts of interest to declare.
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Guan, Rongwei, Lei Peng, Dong Wang, Hongjie He, Dexu Wang, Rui Zhang, Hui Wang et al. « Decreased TOB1 expression and increased phosphorylation of nuclear TOB1 promotes gastric cancer ». Oncotarget 8, no 43 (8 septembre 2017) : 75243–53. http://dx.doi.org/10.18632/oncotarget.20749.

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Guo, Gang. « MicroRNA-25 promotes gastric cancer migration, invasion and proliferation by directly targeting transducer of ERBB2, 1, and predicts poor patient survival (TUM2P.882) ». Journal of Immunology 192, no 1_Supplement (1 mai 2014) : 71.6. http://dx.doi.org/10.4049/jimmunol.192.supp.71.6.

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Abstract Gastric cancer (GC) is the most common tumors and the molecular mechanism underlying tumor metastasis is still largely unclear. Here, we show that miR-25 was overexpressed in plasma and primary tumor tissues of GC patients with TNM stage (III or IV) or lymph node metastasis. MiR-25 inhibition significantly decreased the metastasis, invasion and proliferation potential of GC cells in vitro, and reduced their capacity to develop distal pulmonary metastases and peritoneal dissemination in vivo. Furthermore, miR-25 repressed transducer of ERBB2, 1 (TOB1) expression by directly binding to the 3’-UTR, and the inverse correlation was observed between the expressions of miR-25 and TOB1 mRNA in primary GC tissues. Moreover, the loss of TOB1 increased the metastasis, invasion and proliferation of GC cells, and the restoration of TOB1 led to the metastasis, invasion and proliferation suppression. The receiver operating characteristics (ROC) analysis yielded an area under the curve (AUC) value of 0.7325 in distinguishing the GC patients with death from those with living. The analysis of optimal cutoff value revealed significant difference of patients’ survival between GC patients with high plasma concentrations of miR-25 (&gt; 0.2333 amol/μL) and those with low (&lt; 0.2333 amol/μL). Taken together, miR-25 promotes GC progress by directly down-regulating TOB1 expression, and the high concentrations of miR-25 in plasma of GC patients predict poor patient survival.
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Hiramatsu, Yoshihiro, Kyoko Kitagawa, Toru Suzuki, Chiharu Uchida, Takayuki Hattori, Hirotoshi Kikuchi, Toshiaki Oda et al. « Degradation of Tob1 Mediated by SCFSkp2-Dependent Ubiquitination ». Cancer Research 66, no 17 (1 septembre 2006) : 8477–83. http://dx.doi.org/10.1158/0008-5472.can-06-1603.

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Thomas, D. K. « On a subclass of Bazilevič functions ». International Journal of Mathematics and Mathematical Sciences 8, no 4 (1985) : 779–83. http://dx.doi.org/10.1155/s0161171285000850.

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LetB(α)be the class of normalised Bazilevič functions of typeα>0with respect to the starlike functiong. LetB1(α)be the subclass ofB(α)wheng(z)≡z. Distortion theorems and coefficient estimates are obtained for functions belonging toB1(α).
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Yuan, Jing, Ji-Yue Cao, Zhong-Lin Tang, Ning Wang et Kui Li. « Molecular Characterization of Tob1 in Muscle Development in Pigs ». International Journal of Molecular Sciences 12, no 7 (4 juillet 2011) : 4315–26. http://dx.doi.org/10.3390/ijms12074315.

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Ho, Karen J., Nhue L. Do, Hasan H. Otu, Martin J. Dib, Xianghui Ren, Keiichi Enjyoji, Simon C. Robson, Ernest F. Terwilliger et Seth J. Karp. « Tob1 is a constitutively expressed repressor of liver regeneration ». Journal of Cell Biology 189, no 6 (14 juin 2010) : i14. http://dx.doi.org/10.1083/jcb1896oia14.

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Bora, K., et R. L. Jaffe. « Double-scattering contribution tob1(x,Q2)in the deuteron ». Physical Review D 57, no 11 (1 juin 1998) : 6906–11. http://dx.doi.org/10.1103/physrevd.57.6906.

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Chen, Yuanfan, Chenchen Wang, Jenny Wu et Lingsong Li. « BTG/Tob family members Tob1 and Tob2 inhibit proliferation of mouse embryonic stem cells via Id3 mRNA degradation ». Biochemical and Biophysical Research Communications 462, no 3 (juillet 2015) : 208–14. http://dx.doi.org/10.1016/j.bbrc.2015.04.117.

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Bai, Yuru, Lu Qiao, Ning Xie, Yan Li, Yongzhan Nie, Yan Pan, Yupeng Shi, Jinhai Wang et Na Liu. « TOB1 suppresses proliferation in K‐Ras wild‐type pancreatic cancer ». Cancer Medicine 9, no 4 (31 décembre 2019) : 1503–14. http://dx.doi.org/10.1002/cam4.2756.

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Lee, Hun, Juthika Kundu, Ryong Kim et Young Shin. « Transducer of ERBB2.1 (TOB1) as a Tumor Suppressor : A Mechanistic Perspective ». International Journal of Molecular Sciences 16, no 12 (15 décembre 2015) : 29815–28. http://dx.doi.org/10.3390/ijms161226203.

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Nakamura, Rina, Motomi Konishi, Masanari Taniguchi, Yusuke Hatakawa et Toshifumi Akizawa. « The discovery of shorter synthetic proteolytic peptides derived from Tob1 protein ». Peptides 116 (juin 2019) : 71–77. http://dx.doi.org/10.1016/j.peptides.2019.03.005.

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Bista, Pradeep, Deanna A. Mele, Diana Velez Baez et Brigitte T. Huber. « Lymphocyte quiescence factor Dpp2 is transcriptionally activated by KLF2 and TOB1 ». Molecular Immunology 45, no 13 (août 2008) : 3618–23. http://dx.doi.org/10.1016/j.molimm.2008.05.001.

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Guo, Hai, Fuzhi Ji, Xiaofeng Zhao, Xiaozhong Yang, Jingdong He, Lingling Huang et Yuanyuan Zhang. « MicroRNA-371a-3p promotes progression of gastric cancer by targeting TOB1 ». Cancer Letters 443 (février 2019) : 179–88. http://dx.doi.org/10.1016/j.canlet.2018.11.021.

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Rudnytska, O. « GRAPHENE OXIDE AFFECT THE EXPRESSION OF PROLIFERATION RELATED GENES AND microRNA IN NORMAL HUMAN ASTROCYTES ». Biotechnologia Acta 15, no 2 (avril 2022) : 68–69. http://dx.doi.org/10.15407/biotech15.02.068.

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Aim. In this study we investigate the impact of low doses of graphene oxide on the expression of key regulatory genes which control cell proliferation as well as microRNAs in normal human astrocytes. Methods. The expression level of genes related to cell proliferation was studied by real-time qPCR in normal human astrocytes line NHA/TS (Cambrex Bio Science, Walkersville, MD, USA) using SYBRGreen Mix and specific for each mRNA forward and reverse primers. These astrocytes were treated with graphene oxide (1 and 4 ng/ml of medium) for 24 hrs. Graphene oxide (2 mg/ml, dispersion in water) was received from Sigma-Aldrich Chemie GmbH, Germany. Total RNA was extracted using TRIZOL reagent. For reverse transcription of mRNAs we used Thermo Scientific Verso cDNA Synthesis Kit (Germany). The values of mRNA expressions were normalized to the level of ACTB mRNA and represented as percent of control (100 %). For polyadenylation and reverse transcription of miRNAs we used Mir-X miRNA First-Strand Synthesis Kit (Takara, Japan). The expression level of microRNAs was studied by real-time qPCR using SYBRGreen Mix and specific for each miRNA forward primers and universal reverse primer. For normalization of microRNA expressions the level of U6 RNA expression was used. Results. It was shown that the expression level of TOB1, HSPA5, EDEM1, MYBL1, and MYBL2 significantly increased in normal human astrocytes line NHA/TS, which were treated with graphene oxide (1 and 4 ng/ml of medium) for 24 hrs. Up-regulation of these genes expression was dose-dependent: bigger dose of graphene oxide (4 ng/ml of medium) introduced more significant changes in the expression of all these genes. Furthermore, bioinformatics analysis of 3′-untranslated regions of mRNA allowed identifying binding sites of microRNA: miR-19a for MYBL1, miR-143 for MYBL2 and miR-182 for TOB1. It was also shown that the expression of all these microRNA significantly down-regulated by graphene oxide, supporting the idea of both post-transcriptional and transcriptional regulation of MYBL1, MYBL2 and TOB1 gene expressions. Conclusions. Graphene oxide significantly disturbs genome stability by up-regulation of the expression of key regulatory genes and down-regulation of microRNA.
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Nieto, Leandro, Mariana Fuertes, Josefina Rosmino, Sergio Senin et Eduardo Arzt. « Crosstalk of BMP-4 and RA signaling pathways on Pomc gene regulation in corticotrophs ». Journal of Molecular Endocrinology 63, no 3 (octobre 2019) : 161–74. http://dx.doi.org/10.1530/jme-19-0059.

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Retinoic acid (RA), an active metabolite of Vitamin A, and bone morphogenetic protein 4 (BMP-4) pathways control the transcription of pro-opiomelanocortin (Pomc), the precursor of ACTH. We describe a novel mechanism by which RA and BMP-4 act together in the context of pituitary corticotroph tumoral cells to regulate Pomc transcription. BMP-4 and RA exert a potentiated inhibition on Pomc gene expression. This potentiation of the inhibitory action on Pomc transcription was blocked by the inhibitory SMADs of the BMP-4 pathway (SMAD6 and SMAD7), a negative regulator of BMP-4 signaling (TOB1) and a blocker of RA pathway (COUP-TFI). AtT-20 corticotrophinoma cells express RA receptors (RARB, RXRA and RXRG) which associate with factors of BMP-4 (SMAD4 and SMAD1) signaling cascade in transcriptional complexes that block Pomc transcription. COUP-TFI and TOB1 disrupt these complexes. Deletions and mutations of the Pomc promoter and a specific DNA-binding assay show that the complexes bind to the RARE site in the Pomc promoter. The enhanced inhibitory interaction between RA and BMP-4 pathways occurs also in another relevant corticotroph gene promoter, the corticotropin-releasing hormone receptor 1 (Crh-r1). The understanding of the molecules that participate in the control of corticotroph gene expression contribute to define more precise targets for the treatment of corticotrophinomas.
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JIAO, Yang, Chun-min GE, Qing-hui MENG, Jian-ping CAO, Jian TONG et Sai-jun FAN. « Adenovirus-mediated expression of Tob1 sensitizes breast cancer cells to ionizing radiation1 ». Acta Pharmacologica Sinica 28, no 10 (octobre 2007) : 1628–36. http://dx.doi.org/10.1111/j.1745-7254.2007.00647.x.

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LIN, SHEYU, QINGFENG ZHU, YANG XU, HUI LIU, JUNYU ZHANG, JIAWEI XU, HONGLIAN WANG, QING SANG, QINGHE XING et JIA FAN. « The role of the TOB1 gene in growth suppression of hepatocellular carcinoma ». Oncology Letters 4, no 5 (16 août 2012) : 981–87. http://dx.doi.org/10.3892/ol.2012.864.

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Jiang, Yaling, Xinhua Yuan, Bing Li, Mingxing Liu, Yu Shi, Jianhuai Feng, Hua Zhou, Miaoxian Ou et Xiaozhen Huang. « TOB1 modulates the decidualization of human endometrial stromal cells via the Notch pathway ». Journal of Assisted Reproduction and Genetics 38, no 10 (octobre 2021) : 2641–50. http://dx.doi.org/10.1007/s10815-021-02277-z.

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Zhang, Y.-W., R. E. Nasto, R. Varghese, S. A. Jablonski, I. G. Serebriiskii, R. Surana, V. S. Calvert et al. « Acquisition of estrogen independence induces TOB1-related mechanisms supporting breast cancer cell proliferation ». Oncogene 35, no 13 (13 juillet 2015) : 1643–56. http://dx.doi.org/10.1038/onc.2015.226.

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Casazza, Simona, Jean-Christophe Corvol, Di Wu, Jorge Oksenberg et Sergio Baranzini. « S.110. Tob1 Deficient Mice Experience Early EAE Onset and Present Immunological Abnormalities ». Clinical Immunology 131 (2009) : S162. http://dx.doi.org/10.1016/j.clim.2009.03.480.

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Wu, Dapeng, Weijie Zhou, Shunchang Wang, Zhenyu Zhou, Sheng Wang et Lei Chen. « Tob1 enhances radiosensitivity of breast cancer cells involving the JNK and p38 pathways ». Cell Biology International 39, no 12 (28 septembre 2015) : 1425–30. http://dx.doi.org/10.1002/cbin.10545.

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CHE, JUN, YAN-WEI LU, KE-KANG SUN, CHAN FENG, AI-JING DONG et YANG JIAO. « Overexpression of TOB1 confers radioprotection to bronchial epithelial cells through the MAPK/ERK pathway ». Oncology Reports 30, no 2 (11 juin 2013) : 637–42. http://dx.doi.org/10.3892/or.2013.2536.

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May, Sarah L., Qing Zhou, Mitzi Lewellen, Cristan M. Carter, David Coffey, Steven L. Highfill, Christoph M. Bucher et al. « Nfatc2 and Tob1 Have Non-Overlapping Function in T Cell Negative Regulation and Tumorigenesis ». PLoS ONE 9, no 6 (19 juin 2014) : e100629. http://dx.doi.org/10.1371/journal.pone.0100629.

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Xiong, Bo, Yanning Rui, Min Zhang, Kehui Shi, Shunji Jia, Tian Tian, Kun Yin et al. « Tob1 Controls Dorsal Development of Zebrafish Embryos by Antagonizing Maternal β-Catenin Transcriptional Activity ». Developmental Cell 11, no 2 (août 2006) : 225–38. http://dx.doi.org/10.1016/j.devcel.2006.06.012.

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Schick, Fritz, Jürgen Forster, Jürgen Machann, Peter Huppert et Claus D. Claussen. « Highly selective water and fat imaging applying multislice sequences without sensitivity toB1 field inhomogeneities ». Magnetic Resonance in Medicine 38, no 2 (août 1997) : 269–74. http://dx.doi.org/10.1002/mrm.1910380216.

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Perrotte, Paul, Nadia Benachenou, Pierre I. Karakiewicz, Myriam Senay et Fred Saad. « 951 : TOB1 and ID-1 Two Novel Genes Implicated in Bladder Cancer Progression and Prognosis ». Journal of Urology 171, no 4S (avril 2004) : 252. http://dx.doi.org/10.1016/s0022-5347(18)38188-6.

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Salerno, Fiamma, René A. W. van Lier et Monika C. Wolkers. « Better safe than sorry : TOB1 employs multiple parallel regulatory pathways to keep Th17 cells quiet ». European Journal of Immunology 44, no 3 (19 février 2014) : 646–49. http://dx.doi.org/10.1002/eji.201444465.

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Hosokawa, Kohei, Sachiko Kajigaya, Keyvan Keyvanfar, Qiao Wangmin, Yanling Xie, Olga Rios, Barbara Weinstein et al. « T Cell Transcriptomes from Paroxysmal Nocturnal Hemoglobinuria Patients Reveal Novel Signaling Pathways ». Blood 128, no 22 (2 décembre 2016) : 1042. http://dx.doi.org/10.1182/blood.v128.22.1042.1042.

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Abstract Background. Paroxysmal nocturnal hemoglobinuria (PNH) is a rare acquired blood disease, characterized by hemolytic anemia, bone marrow (BM) failure, and venous thrombosis. The etiology of PNH is a somatic mutation in the phosphatidylinositol glycan class A gene (PIG-A) on the X chromosome, which causes deficiency in glycosyl phosphatidylinositol-anchored proteins (GPI-APs). The involvement of T cells in PNH is strongly supported by clinical overlap between PNH and aplastic anemia (AA); the presence of GPI-AP deficient cells in AA associated with favorable response to immunosuppressive therapy; and an oligoclonal T cell repertoire in PNH patients. However, the molecular mechanisms responsible for the aberrant immune responses in PNH patients are not well understood. To identify aberrant molecular mechanisms involved in immune targeting of hematopoietic stem cells in BM, RNA sequencing (RNA-seq) was applied to examine the transcriptome of T cell subsets from PNH patients and healthy controls. Method. Blood samples were obtained after informed consent from 15 PNH patients and 15 age-matched healthy controls. For RNA extraction, freshly isolated peripheral blood mononuclear cells were sorted on the same day of blood draw to obtain four different T cell (CD3+ CD14- CD19- ViViD-) populations [CD4+ naïve (CD45RA+ CD45RO-), CD4+ memory (CD45RA- CD45RO+), CD8+ naïve (CD45RA+ CD45RO-), and CD8+ memory (CD45RA- CD45RO+) T cells] by fluorescence-activated cell sorter . RNA-Seq analysis from three PNH and three healthy controls was performed using the Illumina HiSeq™ 2000 platform. The Ingenuity® Pathway Analysis and Gene set enrichment analysis (GSEA) were employed to elucidate transcriptional pathways. RNA-seq data were validated by flow cytometry and quantitative real-time RT-PCR (RT-qPCR). Results and Discussion . Differentially expressed gene analysis of four T cell subsets showed distinct gene expression signatures in individual T cell subsets. In CD4+ naïve T cells, 11 gene expression levels were significantly different: five upregulated (including SRRM2 and TNFSF8) and six downregulated genes (including GIMAP6) (> 2 fold change, false discovery rate [FDR] < 0.05). In CD4+ memory T cells, 25 gene expression levels were significantly different: 15 upregulated (including JUND and TOB1) and 10 downregulated genes (including GIMAP4). In CD8+ naive T cells, only two gene expression levels were significantly different: upregulated CTSW and downregulated RPL9. In CD8+ memory T cells, seven gene expression levels were significantly different: two upregulated (CTSW and DPP4) and five downregulated genes (including SLC12A7). Further, differentially expressed gene analysis was performed by combining CD4+ naïve, CD4+ memory, CD8+ naïve, and CD8+ memory T cells from PNH or healthy controls, respectively. Out of 55 gene expression levels that were significantly different, 41 were upregulated (including TNFAIP3, JUN, JUND, TOB1, TNFSF8, and CD69) and 14 downregulated (including GIMAP4). By canonical pathways analysis, putative gene network interactions of differentially expressed genes were significantly enriched for canonical pathways of TNFR1, TNFR2, IL-17A, and CD27 signaling. By GSEA, the most significantly upregulated gene sets in CD4+ naïve, CD4+ memory, CD8+ naïve, and CD8+ memory T cells from PNH patients displayed gene signatures related to the "IGF1 pathway", "Pre-NOTCH expression and processing", "AP-1 pathway", and "ATF2 pathway", respectively. For validation of the RNA-seq data, we chose seven genes (TNFAIP3, JUN, JUND, TOB1, TNFSF8, CD69, and CTSW) because these are important mediators involved in regulation for T cells and dysregulation of these genes is associated with autoimmune diseases. Differential expression levels of TNFAIP3, JUN, and TOB1 were validated by RT-qPCR. By flow cytometry, higher expression of CD69 and TNFSF8 was confirmed in CD4+ and CD8+T cells from PNH compared to healthy controls. Conclusion. Using RNA-seq, we identified novel molecular mechanisms and pathways which may underlie the aberrant T cell immune status in PNH. Specific dysregulation of T cell intracellular signaling may contribute to BM failure and the inflammatory environment in PNH. Understanding these pathways may provide new therapeutic strategies to modulate T cell immune responses in BM failure. Disclosures Hosokawa: Aplastic Anemia and MDS International Foundation: Research Funding. Rios:GSK/Novartis: Research Funding. Weinstein:GSK/Novartis: Research Funding. Townsley:GSK/Novartis: Research Funding.
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Liang, Hong, Yumei Tang, Hui Zhang et Chao Zhang. « MiR-32-5p Regulates Radiosensitization, Migration And Invasion Of Colorectal Cancer Cells By Targeting TOB1 Gene ». OncoTargets and Therapy Volume 12 (novembre 2019) : 9651–61. http://dx.doi.org/10.2147/ott.s228995.

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Wang, Jianguang, Shuaijun Dong, Jianfeng Zhang, Dongshuai Jing, Wenqiang Wang, Lujia Dong et Yuanzhen Zhao. « LncRNA NR2F1-AS1 Regulates miR-371a-3p/TOB1 Axis to Suppress Proliferation of Colorectal Cancer Cells ». Cancer Biotherapy and Radiopharmaceuticals 35, no 10 (1 décembre 2020) : 760–64. http://dx.doi.org/10.1089/cbr.2019.3237.

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Ma, Caiyun, Wenjing Yang, Liang Chen et Zhanju Liu. « TOB1 Deficiency Promotes Intestinal Mucosal Inflammation through Induction of Th1/Th17 Cell Immune Responses in IBD ». Gastroenterology 152, no 5 (avril 2017) : S756. http://dx.doi.org/10.1016/s0016-5085(17)32625-2.

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Liu, Qing, Qing Gao, Yu Zhang, Zhibao Li et Xiaoxue Mei. « MicroRNA-590 promotes pathogenic Th17 cell differentiation through targeting Tob1 and is associated with multiple sclerosis ». Biochemical and Biophysical Research Communications 493, no 2 (novembre 2017) : 901–8. http://dx.doi.org/10.1016/j.bbrc.2017.09.123.

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SUN, KE-KANG, NING ZHONG, YANG YANG, LIN ZHAO et YANG JIAO. « Enhanced radiosensitivity of NSCLC cells by transducer of erbB2.1 (TOB1) through modulation of the MAPK/ERK pathway ». Oncology Reports 29, no 6 (12 avril 2013) : 2385–91. http://dx.doi.org/10.3892/or.2013.2403.

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Zhu, Lingyu, Suisui Zhang, Songda Chen, Huijie Wu, Mengjie Jiang et Aiqun Liu. « Exosomal miR-552-5p promotes tumorigenesis and disease progression via the PTEN/TOB1 axis in gastric cancer ». Journal of Cancer 13, no 3 (2022) : 890–905. http://dx.doi.org/10.7150/jca.66903.

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Shapouri, Farnaz, Shaghayegh Saeidi, Robb U. de Iongh, Franca Casagranda, Patrick S. Western, Eileen A. McLaughlin, Jessie M. Sutherland, Gary R. Hime et Mary Familari. « Tob1 is expressed in developing and adult gonads and is associated with the P-body marker, Dcp2 ». Cell and Tissue Research 364, no 2 (11 décembre 2015) : 443–51. http://dx.doi.org/10.1007/s00441-015-2328-z.

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Lin, Ritian, Caiyun Ma, Leilei Fang, Chunjin Xu, Cui Zhang, Xiaohan Wu, Wei Wu, Ruixin Zhu, Yingzi Cong et Zhanju Liu. « TOB1 Blocks Intestinal Mucosal Inflammation Through Inducing ID2-Mediated Suppression of Th1/Th17 Cell Immune Responses in IBD ». Cellular and Molecular Gastroenterology and Hepatology 13, no 4 (2022) : 1201–21. http://dx.doi.org/10.1016/j.jcmgh.2021.12.007.

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Jiao, Yang, Ke-kang Sun, Lin Zhao, Jia-ying Xu, Li-li Wang et Sai-jun Fan. « Suppression of human lung cancer cell proliferation and metastasis in vitro by the transducer of ErbB-2.1 (TOB1) ». Acta Pharmacologica Sinica 33, no 2 (12 décembre 2011) : 250–60. http://dx.doi.org/10.1038/aps.2011.163.

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Ma, Caiyun, Cui Zhang, Wei Wu, Mingming Sun et Zhanju Liu. « 377 - Critical Role of TOB1 in Controlling Intestinal Mucosal Inflammation by Inhibitiing Th1/Th17 Immune Responses in IBD ». Gastroenterology 154, no 6 (mai 2018) : S—89. http://dx.doi.org/10.1016/s0016-5085(18)30745-5.

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Başoğlu Köseahmet, Fulya, Candan Eker, Musa Öztürk, Şebnem Özdemir, Ayhan Köksal, Savim Baybaş et Tuba Günel. « The Role of rs4626 and rs7221352 Polymorphisms on the TOB1 Gene in Turkish Relapsing-Remitting Multiple Sclerosis Patients ». European Journal of Biology 81, no 2 (30 décembre 2022) : 197–205. http://dx.doi.org/10.26650/eurjbiol.2022.1191215.

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Ikeda, Yuka, Kurumi Taniguchi, Sayuri Yoshikawa, Haruka Sawamura, Ai Tsuji et Satoru Matsuda. « A budding concept with certain microbiota, anti-proliferative family proteins, and engram theory for the innovative treatment of colon cancer ». Exploration of Medicine 2, no 3 (27 octobre 2022) : 468–78. http://dx.doi.org/10.37349/emed.2022.00108.

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Inflammatory bowel disease (IBD) is a multifactorial chronic disease. Patients with IBD have an increased risk of developing colorectal cancer which has become a major health concern. IBD might exert a role of engrams for making the condition of specific inflammation in the gut. Dysregulation of immune cells induced by the command of engrams might be crucial in the pathogenesis of damages in gut epithelium. The anti-proliferative (APRO) family of anti-proliferative proteins characterized by immediate early responsive gene-products that might be involved in the machinery of the carcinogenesis in IBD. Herein, it is suggested that some probiotics with specific bacteria could prevent the development and/or progression of the IBD related tumors. In addition, consideration regarding the application of studying APRO family proteins for the comprehension of IBD related tumors has been presented. It is hypothesized that overexpression of Tob1, a member of APRO family proteins, in the epithelium of IBD could suppress the function of adjacent cytotoxic immune cells possibly via the paracrine signaling.
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Dehghanzad, Reyhaneh, Majid Pahlevan Kakhki, Asieh Alikhah, Mohammad Ali Sahraian et Mehrdad Behmanesh. « The Putative Association of TOB1-AS1 Long Non-coding RNA with Immune Tolerance : A Study on Multiple Sclerosis Patients ». NeuroMolecular Medicine 22, no 1 (3 septembre 2019) : 100–110. http://dx.doi.org/10.1007/s12017-019-08567-1.

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Guo, Haonan, Rui Zhang, Justice Afrifa, Yuanyuan Wang et Jingcui Yu. « Decreased expression levels of DAL-1 and TOB1 are associated with clinicopathological features and poor prognosis in gastric cancer ». Pathology - Research and Practice 215, no 6 (juin 2019) : 152403. http://dx.doi.org/10.1016/j.prp.2019.03.031.

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Wang, Hui, Huiting Hao, Haonan Guo, Yuanyuan Wang, Xuelong Zhang, Lidan Xu et Jingcui Yu. « Association between the SNPs of the TOB1 gene and gastric cancer risk in the Chinese Han population of northeast China ». Journal of Cancer 9, no 8 (2018) : 1371–78. http://dx.doi.org/10.7150/jca.23805.

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Chen, Jie, Mao Liu, Xiao Luo, Lihui Peng, Zixia Zhao, Chengsong He et Yue He. « Exosomal miRNA-486-5p derived from rheumatoid arthritis fibroblast-like synoviocytes induces osteoblast differentiation through the Tob1/BMP/Smad pathway ». Biomaterials Science 8, no 12 (2020) : 3430–42. http://dx.doi.org/10.1039/c9bm01761e.

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