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  1. Article ; Online: Upregulation of TCF21 inhibits migration of adrenocortical carcinoma cells.

    Kremer, Jean Lucas / Auricino, Thais Barabba / Dos Santos Passaia, Bárbara / Lotfi, Claudimara Ferini Pacicco

    Discover. Oncology

    2021  Volume 12, Issue 1, Page(s) 23

    Abstract: Background: Adrenocortical carcinomas (ACC) are rare and aggressive cancer. Our previous study has revealed that the transcription factor 21, TCF21, is downregulated in ACC and regulates steroidogenic factor 1 (SF-1) binding to the SF-1 E-box promoter. ... ...

    Abstract Background: Adrenocortical carcinomas (ACC) are rare and aggressive cancer. Our previous study has revealed that the transcription factor 21, TCF21, is downregulated in ACC and regulates steroidogenic factor 1 (SF-1) binding to the SF-1 E-box promoter. In addition, it could be found that TCF21 is a predictor of overall survival (OS) in adult carcinomas.
    Methods: In this study, it was investigated the correlation between TCF21 expression and the promoter methylation status in adrenocortical tumor cells, carcinomas and adenoma. The biological function and potential molecular mechanism of TCF21 restoration in migration and invasion of ACC cells was examined.
    Results: We could be demonstrated a negative correlation between the level of TCF21 expression and methylation of its promoter in adenoma and carcinoma cells indicating the epigenetic control of TCF21 expression. It was also demonstrated that the expression of TCF21 inhibits migration and invasion in the ACC cell line, H295R cells, using plasmid transfection to express TCF21. Furthermore, it could be investigated the TCF21 function as tumor suppressor probably through Kisspeptin 1 (KISS-1) expression and epithelial-mesenchymal transition (EMT) reversion, as well as the modulation of several metalloproteinases in ACC cells.
    Conclusions: Our results suggest that enhancement of TCF21 expression levels may be a potential strategy to revert invasive abilities in adrenocortical carcinomas.
    Language English
    Publishing date 2021-07-23
    Publishing country United States
    Document type Journal Article
    ISSN 2730-6011
    ISSN (online) 2730-6011
    DOI 10.1007/s12672-021-00417-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: The human adrenal cortex: growth control and disorders.

    Lotfi, Claudimara Ferini Pacicco / Kremer, Jean Lucas / Dos Santos Passaia, Barbara / Cavalcante, Isadora Pontes

    Clinics (Sao Paulo, Brazil)

    2018  Volume 73, Issue suppl 1, Page(s) e473s

    Abstract: This review summarizes key knowledge regarding the development, growth, and growth disorders of the adrenal cortex from a molecular perspective. The adrenal gland consists of two distinct regions: the cortex and the medulla. During embryological ... ...

    Abstract This review summarizes key knowledge regarding the development, growth, and growth disorders of the adrenal cortex from a molecular perspective. The adrenal gland consists of two distinct regions: the cortex and the medulla. During embryological development and transition to the adult adrenal gland, the adrenal cortex acquires three different structural and functional zones. Significant progress has been made in understanding the signaling and molecules involved during adrenal cortex zonation. Equally significant is the knowledge obtained regarding the action of peptide factors involved in the maintenance of zonation of the adrenal cortex, such as peptides derived from proopiomelanocortin processing, adrenocorticotropin and N-terminal proopiomelanocortin. Findings regarding the development, maintenance and growth of the adrenal cortex and the molecular factors involved has improved the scientific understanding of disorders that affect adrenal cortex growth. Hypoplasia, hyperplasia and adrenocortical tumors, including adult and pediatric adrenocortical adenomas and carcinomas, are described together with findings regarding molecular and pathway alterations. Comprehensive genomic analyses of adrenocortical tumors have shown gene expression profiles associated with malignancy as well as methylation alterations and the involvement of miRNAs. These findings provide a new perspective on the diagnosis, therapeutic possibilities and prognosis of adrenocortical disorders.
    MeSH term(s) Adrenal Cortex/embryology ; Adrenal Cortex/growth & development ; Adrenal Cortex/physiology ; Adrenal Cortex Diseases/physiopathology ; Embryonic Development/physiology ; Humans
    Language English
    Publishing date 2018-09-06
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2182801-5
    ISSN 1980-5322 ; 1807-5932
    ISSN (online) 1980-5322
    ISSN 1807-5932
    DOI 10.6061/clinics/2018/e473s
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.B 404: Show issues Location:
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  3. Article ; Online: Stathmin 1 is highly expressed and associated with survival outcome in malignant adrenocortical tumours.

    Dos Santos Passaia, Bárbara / Lima, Keli / Kremer, Jean Lucas / da Conceição, Barbara Brito / de Paula Mariani, Beatriz Marinho / da Silva, Jean Carlos Lipreri / Zerbini, Maria Claudia Nogueira / Fragoso, Maria Candida Barisson Villares / Machado-Neto, João Agostinho / Lotfi, Claudimara Ferini Pacicco

    Investigational new drugs

    2019  Volume 38, Issue 3, Page(s) 899–908

    Abstract: Adrenocortical carcinoma (ACC) is an aggressive endocrine cancer with few molecular predictors of malignancy and survival, especially in paediatric patients. Stathmin 1 (STMN1) regulates microtubule dynamics and has been involved in the malignant ... ...

    Abstract Adrenocortical carcinoma (ACC) is an aggressive endocrine cancer with few molecular predictors of malignancy and survival, especially in paediatric patients. Stathmin 1 (STMN1) regulates microtubule dynamics and has been involved in the malignant phenotype of cancer cells. Recently, it was reported that STMN1 is highly expressed in ACC patients, and STMN1 silencing reduces the clonogenicity and migration of ACC cell lines. However, the prognostic significance of STMN1 and its therapeutic potential remain undefined in ACC. In the present study, STMN1 mRNA levels were significantly higher (p < 0.05) in ACC patients, especially in an advanced stage, and correlated with BUB1B and PINK1 expression, the prognostic-related genes in ACC. In paediatric tumours, high STMN1 expression was observed in both adrenocortical carcinoma and adrenocortical adenoma patients. Among the adult malignant tumours, STMN1 level was an independent predictor of survival outcomes (overall survival: hazard ratio = 6.08, p = 0.002; disease-free survival: hazard ratio = 4.65, p < 0.0001). Paclitaxel, a microtubule-stabilizing drug, reduces the activation of STMN1 and significantly decreases cell migration and invasion in ACC cell lines and ACC cells from secondary cell culture (all p < 0.0001). In summary, STMN1 expression may be of great value to clinical and pathological findings in therapeutic trials and deserves future studies in ACC.
    MeSH term(s) Adrenal Cortex Neoplasms/drug therapy ; Adrenal Cortex Neoplasms/genetics ; Adrenal Cortex Neoplasms/mortality ; Adrenocortical Carcinoma/drug therapy ; Adrenocortical Carcinoma/genetics ; Adrenocortical Carcinoma/mortality ; Adrenocortical Carcinoma/pathology ; Adult ; Biomarkers, Tumor/genetics ; Cell Line, Tumor ; Cell Movement/genetics ; Child, Preschool ; Disease-Free Survival ; Female ; Gene Expression Regulation, Neoplastic/drug effects ; Gene Expression Regulation, Neoplastic/genetics ; Humans ; Male ; Paclitaxel/therapeutic use ; Prognosis ; RNA, Messenger/genetics ; Stathmin/genetics
    Chemical Substances Biomarkers, Tumor ; RNA, Messenger ; STMN1 protein, human ; Stathmin ; Paclitaxel (P88XT4IS4D)
    Language English
    Publishing date 2019-08-22
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 604895-x
    ISSN 1573-0646 ; 0167-6997
    ISSN (online) 1573-0646
    ISSN 0167-6997
    DOI 10.1007/s10637-019-00846-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1823: Show issues Location:
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