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  1. Article ; Online: Ets1 Promotes the Differentiation of Post-Selected iNKT Cells through Regulation of the Expression of Vα14Jα18 T Cell Receptor and PLZF.

    Chuang, Ya-Ting / Chuang, Wan-Chu / Liu, Chih-Chun / Liu, Chia-Wei / Huang, Yu-Wen / Yang, Huang-Yu / Ho, I-Cheng / Tai, Tzong-Shyuan

    International journal of molecular sciences

    2021  Volume 22, Issue 22

    Abstract: The transcription factor Ets1 is essential for the development/differentiation of invariant Natural Killer T (iNKT) cells at multiple stages. However, its mechanisms of action and target genes in iNKT cells are still elusive. Here, we show that Ets1 is ... ...

    Abstract The transcription factor Ets1 is essential for the development/differentiation of invariant Natural Killer T (iNKT) cells at multiple stages. However, its mechanisms of action and target genes in iNKT cells are still elusive. Here, we show that Ets1 is required for the optimal expression of the Vα14Jα18 T cell receptor (TCR) in post-selected thymic iNKT cells and their immediate differentiation. Ets1 is also critical for maintaining the peripheral homeostasis of iNKT cells, which is a role independent of the expression of the Vα14Jα18 TCR. Genome-wide transcriptomic analyses of post-selected iNKT cells further reveal that Ets1 controls leukocytes activation, proliferation differentiation, and leukocyte-mediated immunity. In addition, Ets1 regulates the expression of ICOS and PLZF in iNKT cells. More importantly, restoring the expression of PLZF and the Vα14Jα18 TCR partially rescues the differentiation of iNKT cells in the absence of Ets1. Taken together, our results establish a detailed molecular picture of how Ets1 regulates the stepwise differentiation of iNKT cells.
    MeSH term(s) Animals ; Cell Differentiation/genetics ; Cell Differentiation/immunology ; Gene Expression Regulation/immunology ; Mice ; Mice, Knockout ; Natural Killer T-Cells/immunology ; Promyelocytic Leukemia Zinc Finger Protein/genetics ; Promyelocytic Leukemia Zinc Finger Protein/immunology ; Proto-Oncogene Protein c-ets-1/genetics ; Proto-Oncogene Protein c-ets-1/immunology ; Receptors, Antigen, T-Cell, alpha-beta/genetics ; Receptors, Antigen, T-Cell, alpha-beta/immunology
    Chemical Substances Ets1 protein, mouse ; Promyelocytic Leukemia Zinc Finger Protein ; Proto-Oncogene Protein c-ets-1 ; Receptors, Antigen, T-Cell, alpha-beta ; Zbtb16 protein, mouse
    Language English
    Publishing date 2021-11-11
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms222212199
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Ets1 regulates the differentiation and function of iNKT cells through both Pointed domain-dependent and domain-independent mechanisms.

    Tai, Tzong-Shyuan / Tsao, Hsiao-Wei / Chuang, Wan-Chu / Liu, Chih-Chun / Huang, Yu-Wen / Oettgen, Peter / Chuang, Ya-Ting / Ho, I-Cheng

    Cellular & molecular immunology

    2020  Volume 17, Issue 11, Page(s) 1198–1200

    MeSH term(s) Animals ; Cell Differentiation ; Integrases/metabolism ; Mice, Transgenic ; Natural Killer T-Cells/cytology ; Natural Killer T-Cells/metabolism ; Protein Domains ; Proto-Oncogene Protein c-ets-1/chemistry ; Proto-Oncogene Protein c-ets-1/metabolism ; Structure-Activity Relationship
    Chemical Substances Proto-Oncogene Protein c-ets-1 ; Cre recombinase (EC 2.7.7.-) ; Integrases (EC 2.7.7.-)
    Language English
    Publishing date 2020-03-05
    Publishing country China
    Document type Letter ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2435097-7
    ISSN 2042-0226 ; 1672-7681
    ISSN (online) 2042-0226
    ISSN 1672-7681
    DOI 10.1038/s41423-020-0382-2
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: FLJ10540 is associated with tumor progression in nasopharyngeal carcinomas and contributes to nasopharyngeal cell proliferation, and metastasis via osteopontin/CD44 pathway

    Chen Chang-Han / Shiu Li-Yen / Su Li-Jen / Huang Chi-Ying F / Huang Shun-Chen / Huang Chao-Cheng / Yin Yu-Fang / Wang Wei-Sheng / Tsai Hsin-Ting / Fang Fu-Min / Chuang Wan-Chu / Kang Hong-Chang / Hwang Chung-Feng

    Journal of Translational Medicine, Vol 10, Iss 1, p

    2012  Volume 93

    Abstract: Abstract Background Nasopharyngeal carcinoma (NPC) is well-known for its highly metastatic characteristics, but little is known of its molecular mechanisms. New biomarkers that predict clinical outcome, in particular the ability of the primary tumor to ... ...

    Abstract Abstract Background Nasopharyngeal carcinoma (NPC) is well-known for its highly metastatic characteristics, but little is known of its molecular mechanisms. New biomarkers that predict clinical outcome, in particular the ability of the primary tumor to develop metastatic tumors are urgently needed. The aim of this study is to investigate the role of FLJ10540 in human NPC development. Methods A bioinformatics approach was used to explore the potentially important regulatory genes involved in the growth/metastasis control of NPC. FLJ10540 was chosen for this study. Two co-expression strategies from NPC microarray were employed to identify the relationship between FLJ10540 and osteopontin. Quantitative-RT-PCR, immunoblotting, and immunohistochemistry analysis were used to investigate the mRNA and protein expression profiles of FLJ10540 and osteopontin in the normal and NPC tissues to confirm microarray results. TW01 and Hone1 NPC cells with overexpression FLJ10540 or siRNA to repress endogenous FLJ10540 were generated by stable transfection to further elucidate the molecular mechanisms of FLJ10540-elicited cell growth and metastasis under osteopontin stimulation. Results We found that osteopontin expression exhibited a positive correlation with FLJ10540 in NPC microarray. We also demonstrated comprehensively that FLJ10540 and osteopontin were not only overexpressed in NPC specimens, but also significantly correlated with advanced tumor and lymph node-metastasis stages, and had a poor 5-year survival rate, respectively. Stimulation of NPC parental cells with osteopontin results in an increase in FLJ10540 mRNA and protein expressions. Functionally, FLJ10540 transfectant alone, or stimulated with osteopontin, exhibited fast growth and increased metastasis as compared to vehicle control with or without osteopontin stimulation. Conversely, knockdown of FLJ10540 by siRNA results in the suppression of NPC cell growth and motility. Treatment with anti-CD44 antibodies in NPC parental cells not only resulted in a decrease of ...
    Keywords Nasopharyngeal carcinoma ; FLJ10540 ; Osteopontin ; CD44 ; Medicine ; R
    Subject code 610
    Language English
    Publishing date 2012-05-01T00:00:00Z
    Publisher BMC
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: FLJ10540 is associated with tumor progression in nasopharyngeal carcinomas and contributes to nasopharyngeal cell proliferation, and metastasis via osteopontin/CD44 pathway.

    Chen, Chang-Han / Shiu, Li-Yen / Su, Li-Jen / Huang, Chi-Ying F / Huang, Shun-Chen / Huang, Chao-Cheng / Yin, Yu-Fang / Wang, Wei-Sheng / Tsai, Hsin-Ting / Fang, Fu-Min / Chuang, Wan-Chu / Kang, Hong-Chang / Hwang, Chung-Feng

    Journal of translational medicine

    2012  Volume 10, Page(s) 93

    Abstract: Background: Nasopharyngeal carcinoma (NPC) is well-known for its highly metastatic characteristics, but little is known of its molecular mechanisms. New biomarkers that predict clinical outcome, in particular the ability of the primary tumor to develop ... ...

    Abstract Background: Nasopharyngeal carcinoma (NPC) is well-known for its highly metastatic characteristics, but little is known of its molecular mechanisms. New biomarkers that predict clinical outcome, in particular the ability of the primary tumor to develop metastatic tumors are urgently needed. The aim of this study is to investigate the role of FLJ10540 in human NPC development.
    Methods: A bioinformatics approach was used to explore the potentially important regulatory genes involved in the growth/metastasis control of NPC. FLJ10540 was chosen for this study. Two co-expression strategies from NPC microarray were employed to identify the relationship between FLJ10540 and osteopontin. Quantitative-RT-PCR, immunoblotting, and immunohistochemistry analysis were used to investigate the mRNA and protein expression profiles of FLJ10540 and osteopontin in the normal and NPC tissues to confirm microarray results. TW01 and Hone1 NPC cells with overexpression FLJ10540 or siRNA to repress endogenous FLJ10540 were generated by stable transfection to further elucidate the molecular mechanisms of FLJ10540-elicited cell growth and metastasis under osteopontin stimulation.
    Results: We found that osteopontin expression exhibited a positive correlation with FLJ10540 in NPC microarray. We also demonstrated comprehensively that FLJ10540 and osteopontin were not only overexpressed in NPC specimens, but also significantly correlated with advanced tumor and lymph node-metastasis stages, and had a poor 5-year survival rate, respectively. Stimulation of NPC parental cells with osteopontin results in an increase in FLJ10540 mRNA and protein expressions. Functionally, FLJ10540 transfectant alone, or stimulated with osteopontin, exhibited fast growth and increased metastasis as compared to vehicle control with or without osteopontin stimulation. Conversely, knockdown of FLJ10540 by siRNA results in the suppression of NPC cell growth and motility. Treatment with anti-CD44 antibodies in NPC parental cells not only resulted in a decrease of FLJ10540 protein, but also affected the abilities of FLJ10540-elicited cell growth and motility in osteopontin stimulated-NPC cells.
    Conclusions: These findings suggest that FLJ10540 may be critical regulator of disease progression in NPC, and the underlying mechanism may involve in the osteopontin/CD44 pathway.
    MeSH term(s) Carcinoma ; Cell Cycle Proteins/genetics ; Cell Cycle Proteins/metabolism ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Chi-Square Distribution ; Disease Progression ; Down-Regulation/genetics ; Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; Genes, Neoplasm/genetics ; Humans ; Immunohistochemistry ; Nasopharyngeal Carcinoma ; Nasopharyngeal Neoplasms/genetics ; Nasopharyngeal Neoplasms/pathology ; Nasopharynx/metabolism ; Nasopharynx/pathology ; Neoplasm Invasiveness ; Neoplasm Metastasis ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Osteopontin/genetics ; Osteopontin/metabolism ; Prognosis ; Proportional Hazards Models ; RNA, Small Interfering/metabolism ; Signal Transduction/genetics ; Survival Analysis ; Transfection ; Up-Regulation/genetics
    Chemical Substances Cell Cycle Proteins ; Cep55 protein, human ; Nuclear Proteins ; RNA, Small Interfering ; Osteopontin (106441-73-0)
    Language English
    Publishing date 2012-05-16
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1479-5876
    ISSN (online) 1479-5876
    DOI 10.1186/1479-5876-10-93
    Database MEDical Literature Analysis and Retrieval System OnLINE

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