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  1. Artikel ; Online: p27kip1: a target for tumor therapies?

    Nickeleit, Irina / Zender, Steffen / Kossatz, Uta / Malek, Nisar P

    Cell division

    2007  Band 2, Seite(n) 13

    Abstract: ... which highlight the potential use of p27 as a target for oncological therapies. ... The cyclin kinase inhibitor p27kip1 acts as a potent tumor supressor protein in a variety of human ... to other tumor suppressor proteins p27 expression levels in tumor cells are frequently regulated by ubiquitin dependent proteolysis ...

    Abstract The cyclin kinase inhibitor p27kip1 acts as a potent tumor supressor protein in a variety of human cancers. Its expression levels correlate closely with the overall prognosis of the affected patient and often predict the outcome to different treatment modalities. In contrast to other tumor suppressor proteins p27 expression levels in tumor cells are frequently regulated by ubiquitin dependent proteolysis. Re-expression of p27 in cancer cells therefore does not require gene therapy but can be achieved by interfering with the protein turnover machinery. In this review we will summarize experimental results which highlight the potential use of p27 as a target for oncological therapies.
    Sprache Englisch
    Erscheinungsdatum 2007-05-09
    Erscheinungsland England
    Dokumenttyp Journal Article
    ZDB-ID 2236097-9
    ISSN 1747-1028 ; 1747-1028
    ISSN (online) 1747-1028
    ISSN 1747-1028
    DOI 10.1186/1747-1028-2-13
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: p27 kip1

    Kossatz Uta / Zender Steffen / Nickeleit Irina / Malek Nisar P

    Cell Division, Vol 2, Iss 1, p

    a target for tumor therapies?

    2007  Band 13

    Abstract: ... which highlight the potential use of p27 as a target for oncological therapies. ... Abstract The cyclin kinase inhibitor p27 kip1 acts as a potent tumor supressor protein in a variety ... to other tumor suppressor proteins p27 expression levels in tumor cells are frequently regulated by ubiquitin dependent proteolysis ...

    Abstract Abstract The cyclin kinase inhibitor p27 kip1 acts as a potent tumor supressor protein in a variety of human cancers. Its expression levels correlate closely with the overall prognosis of the affected patient and often predict the outcome to different treatment modalities. In contrast to other tumor suppressor proteins p27 expression levels in tumor cells are frequently regulated by ubiquitin dependent proteolysis. Re-expression of p27 in cancer cells therefore does not require gene therapy but can be achieved by interfering with the protein turnover machinery. In this review we will summarize experimental results which highlight the potential use of p27 as a target for oncological therapies.
    Schlagwörter Cytology ; QH573-671 ; Biology (General) ; QH301-705.5 ; Science ; Q ; DOAJ:Cytology ; DOAJ:Biology ; DOAJ:Biology and Life Sciences
    Sprache Englisch
    Erscheinungsdatum 2007-05-01T00:00:00Z
    Verlag BioMed Central
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  3. Artikel ; Online: RNF4 promotes tumorigenesis, therapy resistance of cholangiocarcinoma and affects cell cycle by regulating the ubiquitination degradation of p27kip1 in the nucleus.

    Huang, Jie / Yang, Wei / Jiang, Kainian / Liu, Yan / Tan, Xiaolong / Luo, Jian

    Experimental cell research

    2022  Band 419, Heft 1, Seite(n) 113295

    Abstract: ... our research group found that as a key tumor suppressor, nuclear dysfunction of p27kip1 is closely related ... showed that p27kip1 was a target protein for SUMOylation and high expression of RNF4 decreased the levels ... driven tumors were strongly dependent on the SUMO pathway. RNF4, as the SUMO-targeted ubiquitin ligase ...

    Abstract Among the hallmarks of cholangiocarcinoma (CCA) progression and unresponsiveness to therapy is impaired ubiquitin-dependent degradation of nuclear tumor suppressor protein. In the previous stage, our research group found that as a key tumor suppressor, nuclear dysfunction of p27kip1 is closely related to chemotherapy resistance of CCA, but the specific mechanism is unclear. It was recently shown that p27kip1-driven tumors were strongly dependent on the SUMO pathway. RNF4, as the SUMO-targeted ubiquitin ligase (STUbL), identifies SUMOylated proteins as a substrate through sumo-interacting motifs (SIM) and causes its degradation via the ubiquitin proteasome pathway. Here we described that the expression of RNF4 was upregulated in CCA tissues and related to malignant features. Silencing RNF4 arrested human CCA cells at the G1 phase, which was associated with the upregulation of p27kip1 and the downregulation of its downstream cycle-related proteins. Silencing RNF4 inhibited cell proliferation and migration, increased cell apoptosis, and sensitized CCA cells to treatment of chemotherapeutic drugs in vitro. Immunofluorescence showed that p27kip1 and RNF4 were mainly co-located in the nucleus. Immunoprecipitation and Western blot showed that p27kip1 was a target protein for SUMOylation and high expression of RNF4 decreased the levels of nuclear p27kip1, enhanced the levels of ubiquitinated and SUMOylated p27kip1, indicating that RNF4 could regulate cell cycle progression via recognizing SUMOylated p27kip1 and facilitating its ubiquitination degradation. These data indicate that RNF4-mediated ubiquitination degradation of SUMOylated proteins is a novel regulatory mechanism of p27kip1 dysfunction and CCA tumorigenesis, which provides a potential option for therapeutic intervention of CCA.
    Mesh-Begriff(e) Carcinogenesis ; Cell Cycle ; Cholangiocarcinoma ; Cyclin-Dependent Kinase Inhibitor p27/metabolism ; Humans ; Nuclear Proteins/metabolism ; Sumoylation ; Transcription Factors/metabolism ; Ubiquitin ; Ubiquitination
    Chemische Substanzen CDKN1B protein, human ; Nuclear Proteins ; RNF4 protein, human ; Transcription Factors ; Ubiquitin ; Cyclin-Dependent Kinase Inhibitor p27 (147604-94-2)
    Sprache Englisch
    Erscheinungsdatum 2022-08-02
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1493-x
    ISSN 1090-2422 ; 0014-4827
    ISSN (online) 1090-2422
    ISSN 0014-4827
    DOI 10.1016/j.yexcr.2022.113295
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel: Heparanase modulates the prognosis and development of BRAF V600E-mutant colorectal cancer by regulating AKT/p27Kip1/Cyclin E2 pathway.

    Liu, Mengling / Xu, Xiaojing / Peng, Ke / Hou, Pengcong / Yuan, Yitao / Li, Suyao / Sun, Xun / Shi, Zhongyi / Zhang, Jiayu / Dong, Yu / Liu, Qing / Ai, Luoyan / Liang, Li / Gan, Lu / Huang, Qihong / Yu, Yiyi / Liu, Tianshu

    Oncogenesis

    2022  Band 11, Heft 1, Seite(n) 58

    Abstract: ... which suggests it holds great promise as a prognostic biomarker and a potential therapeutic target ... regression models. Cell models and xenografts were utilized to investigate the effect of HPSE on tumor ... knockdown impeded tumor proliferation of BRAF V600E-mutant CRC cells in vitro and in vivo. Mechanistically ...

    Abstract BRAF V600E-mutant colorectal cancer (CRC) is a rare subtype of colorectal cancer with poor prognosis. Compelling evidence indicates that the heparanase (HPSE) gene has multiple functions in cancer, however, its role in BRAF V600E-mutant CRC remains elusive. Differentially expressed genes between BRAF V600E-mutant and wild-type patients were explored by analyzing public data from The Cancer Genome Atlas and the Gene Expression Omnibus. Clinical samples of 172 patients with BRAF V600E-mutant CRC diagnosed at Zhongshan Hospital Fudan University were collected. Overall survival was analyzed using Kaplan-Meier curves and Cox regression models. Cell models and xenografts were utilized to investigate the effect of HPSE on tumor proliferation. HPSE was significantly highly expressed in the BRAF V600E-mutant group. High HPSE expression level was independently associated with inferior survival in the BRAF V600E-mutant cohort. HPSE knockdown impeded tumor proliferation of BRAF V600E-mutant CRC cells in vitro and in vivo. Mechanistically, HPSE silencing arrested cell cycle in G0/G1 phase by downregulating Cyclin E2 expression via the AKT/p27Kip1 pathway. These findings support a role for HPSE in promoting BRAF V600E-mutant CRC progression, which suggests it holds great promise as a prognostic biomarker and a potential therapeutic target for the aggressive CRC subtype.
    Sprache Englisch
    Erscheinungsdatum 2022-09-21
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 2674437-5
    ISSN 2157-9024
    ISSN 2157-9024
    DOI 10.1038/s41389-022-00428-0
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; Online: HMGA2 drives the IGFBP1/AKT pathway to counteract the increase in P27KIP1 protein levels in mtDNA/RNA-less cancer cells.

    Maruyama, Tsuyoshi / Saito, Koji / Higurashi, Masato / Ishikawa, Fumihiro / Kohno, Yohko / Mori, Kazunori / Shibanuma, Motoko

    Cancer science

    2022  

    Abstract: ... as a vulnerability of cancer cells or target for tumor-agnostic therapy inducing irreversible cell proliferation ... inhibitor (CKI), P27KIP1, and facilitates its ubiquitin-mediated degradation. Accordingly, intervention ... in the HMGA2 function by RNAi resulted in an increase in P27KIP1 levels and an induction of senescence-like ...

    Abstract Recent comprehensive analyses of mtDNA and orthogonal RNA-sequencing data revealed that in numerous human cancers, mtDNA copy numbers and mtRNA amounts are significantly reduced, followed by low respiratory gene expression. Under such conditions (called mt-Low), cells encounter severe cell proliferation defects; therefore, they must acquire countermeasures against this fatal disadvantage during malignant transformation. This study elucidated a countermeasure against the mt-Low condition-induced antiproliferative effects in hepatocellular carcinoma (HCC) cells. The mechanism relied on the architectural transcriptional regulator HMGA2, which was preferably expressed in HCC cells of the mt-Low type in vitro and in vivo. Detailed in vitro analyses suggest that HMGA2 regulates insulin-like growth factor binding protein 1 (IGFBP1) expression, leading to AKT activation, which then phosphorylates the cyclin-dependent kinase inhibitor (CKI), P27KIP1, and facilitates its ubiquitin-mediated degradation. Accordingly, intervention in the HMGA2 function by RNAi resulted in an increase in P27KIP1 levels and an induction of senescence-like cell proliferation inhibition in mt-Low-type HCC cells. Conclusively, the HMGA2/IGFBP1/AKT axis has emerged as a countermeasure against P27KIP1 CKI upregulation under mt-Low conditions, thereby circumventing cell proliferation inhibition and supporting the tumorigenic state. Notably, similar to in vitro cell lines, HMGA2 was likely to regulate IGFBP1 expression in HCC in vivo, thereby contributing to poor patient prognosis. Considering the significant number of cases under mt-Low or the threat of CKI upregulation cancer-wide, the axis is noteworthy as a vulnerability of cancer cells or target for tumor-agnostic therapy inducing irreversible cell proliferation inhibition via CKI upregulation in a large population with cancer.
    Sprache Englisch
    Erscheinungsdatum 2022-09-14
    Erscheinungsland England
    Dokumenttyp Journal Article
    ZDB-ID 2115647-5
    ISSN 1349-7006 ; 1349-7006
    ISSN (online) 1349-7006
    ISSN 1349-7006
    DOI 10.1111/cas.15582
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel: ANO1 Expression Orchestrates p27Kip1/MCL1-Mediated Signaling in Head and Neck Squamous Cell Carcinoma.

    Filippou, Artemis / Pehkonen, Henna / Karhemo, Piia-Riitta / Väänänen, Juho / Nieminen, Anni I / Klefström, Juha / Grénman, Reidar / Mäkitie, Antti A / Joensuu, Heikki / Monni, Outi

    Cancers

    2021  Band 13, Heft 5

    Abstract: ... targeted-therapies and biomarkers towards patients' stratification are caveats in the disease treatment ... Head and neck squamous cell carcinoma (HNSCC) is a heterogeneous group of tumors that derive ...

    Abstract Head and neck squamous cell carcinoma (HNSCC) is a heterogeneous group of tumors that derive from the mucosal epithelium of the upper aerodigestive tract and present high mortality rate. Lack of efficient targeted-therapies and biomarkers towards patients' stratification are caveats in the disease treatment. Anoctamin 1 (
    Sprache Englisch
    Erscheinungsdatum 2021-03-09
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers13051170
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  7. Artikel ; Online: Prognostic significance of LAPTM4B and p27kip1 expression in triple-negative breast cancer.

    Li, Xuelu / Song, Chen / Wang, Kainan / Li, Ning / Sun, Siwen / Li, Na / Zhao, Zuowei / Li, Man

    Cancer biomarkers : section A of Disease markers

    2019  Band 25, Heft 1, Seite(n) 19–27

    Abstract: ... poor prognosis, and the lack of druggable markers leads to the unavailability of targeted therapies ... prognostic marker and candidate target for therapeutic intervention of triple-negative breast cancer. ... In this study, we aimed to explore the expression of LAPTM4B and p27kip1 in triple-negative breast cancer, and ...

    Abstract Backgroud: Triple-negative breast cancer (TNBC) is associated with an aggressive phenotype and poor prognosis, and the lack of druggable markers leads to the unavailability of targeted therapies. Thus, there is an urgent need to identify potential targets for triple-negative breast cancer.
    Objective: In this study, we aimed to explore the expression of LAPTM4B and p27kip1 in triple-negative breast cancer, and its clinical significance.
    Methods: We analyzed the expression and association of LAPTM4B and p27kip1 in human breast cancer databases. To analyze the role of LAPTM4B in the aggressiveness of the human triple-negative breast cancer, the expressions of LAPTM4B were knocked down in MDA-MB-231 and HCC1187 cell lines. Then, cell proliferation, migration and apoptosis were assessed in vitro. Furthermore, the immunohistochemistry examinations of LAPTM4B and p27kip1 expression were performed using surgical specimens from 188 primary triple-negative breast cancer patients.
    Results: Through analyses of several independent breast cancer cohorts, we found the correlation of the LAPTM4B and p27kip1 expression. Remarkably, the knockdown of LAPTM4B restored p27kip1 expression and inhibited the aggressiveness of breast cancer cells. Meanwhile, the knockdown of p27kip1 relieved the suppression of cell migration. Consistent with the analyses of human breast cancer cohorts, the immunohistochemistry results showed that the expression levels of LAPTM4B and p27kip1 were correlated in 188 triple-negative breast cancer samples (p= 0.019). We also validated that the higher LAPTM4B expression, the lower p27kip1 expression (p= 0.0001), and the LAPTM4B+/p27kip1- subgroup (p< 0.0001) were poor prognostic indicators, as well as the higher histologic grade (p= 0.0001). In the multivariate Cox regression, p27kip1 expression was considered as an independent predictor of survival (p< 0.001).
    Conclusions: The overexpression of LAPTM4B and the loss of p27kip1 expression are correlated. Meanwhile, the up-regulated expression of LAPTM4B together with the down-regulated expression of p27kip1 could classified a group of breast cancer patients with poor prognosis, consequently considered as a potentially prognostic marker and candidate target for therapeutic intervention of triple-negative breast cancer.
    Mesh-Begriff(e) Biomarkers, Tumor/genetics ; Biomarkers, Tumor/metabolism ; Cell Line, Tumor ; Cell Movement ; Cyclin-Dependent Kinase Inhibitor p27/genetics ; Cyclin-Dependent Kinase Inhibitor p27/metabolism ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Immunohistochemistry ; Lymphatic Metastasis ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Middle Aged ; Oncogene Proteins/genetics ; Oncogene Proteins/metabolism ; Prognosis ; Survival Rate ; Triple Negative Breast Neoplasms/diagnosis ; Triple Negative Breast Neoplasms/genetics ; Triple Negative Breast Neoplasms/metabolism ; Triple Negative Breast Neoplasms/pathology
    Chemische Substanzen Biomarkers, Tumor ; CDKN1B protein, human ; LAPTM4B protein, human ; Membrane Proteins ; Oncogene Proteins ; Cyclin-Dependent Kinase Inhibitor p27 (147604-94-2)
    Sprache Englisch
    Erscheinungsdatum 2019-05-26
    Erscheinungsland Netherlands
    Dokumenttyp Journal Article
    ZDB-ID 2203517-5
    ISSN 1875-8592 ; 1574-0153 ; 1875-8592
    ISSN (online) 1875-8592 ; 1574-0153
    ISSN 1875-8592
    DOI 10.3233/CBM-182094
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  8. Artikel ; Online: 11‐Cl‐BBQ, a select modulator of AhR‐regulated transcription, suppresses lung cancer cell growth via activation of p53 and p27Kip1

    Nguyen, Bach D. / Stevens, Brenna L. / Elson, Daniel J. / Finlay, Darren / Gamble, John T. / Kopparapu, Prasad R. / Tanguay, Robyn L. / Buermeyer, Andrew B. / Kerkvliet, Nancy I. / Kolluri, Siva K.

    The FEBS Journal. 2023 Apr., v. 290, no. 8, p.2064-2084

    2023  , Seite(n) 2064–2084

    Abstract: ... Cl‐BBQ as a potential lung cancer therapeutic, highlight the feasibility of targeting AhR and provide ... as a tumour suppressor in different cancer models. In the present study, we report detailed characterization ... regulated transcription (SMAhRT) with anti‐cancer actions. Treatment of lung cancer cells with 11‐Cl‐BBQ ...

    Abstract Aryl hydrocarbon receptor (AhR) is a ligand‐activated transcription factor and functions as a tumour suppressor in different cancer models. In the present study, we report detailed characterization of 11‐chloro‐7H‐benzimidazo[2,1‐a]benzo[de]iso‐quinolin‐7‐one (11‐Cl‐BBQ) as a select modulator of AhR‐regulated transcription (SMAhRT) with anti‐cancer actions. Treatment of lung cancer cells with 11‐Cl‐BBQ induced potent and sustained AhR‐dependent anti‐proliferative effects by promoting G1 phase cell cycle arrest. Investigation of 11‐Cl‐BBQ‐induced transcription in H460 cells with or without the AhR expression by RNA‐sequencing revealed activation of p53 signalling. In addition, 11‐Cl‐BBQ suppressed multiple pathways involved in DNA replication and increased expression of cyclin‐dependent kinase inhibitors, including p27ᴷⁱᵖ¹, in an AhR‐dependent manner. CRISPR/Cas9 knockout of individual genes revealed the requirement for both p53 and p27ᴷⁱᵖ¹ for the AhR‐mediated anti‐proliferative effects. Our results identify 11‐Cl‐BBQ as a potential lung cancer therapeutic, highlight the feasibility of targeting AhR and provide important mechanistic insights into AhR‐mediated‐anticancer actions.
    Schlagwörter CRISPR-Cas systems ; DNA replication ; aryl hydrocarbon receptors ; cell cycle checkpoints ; cell growth ; cyclin-dependent kinase ; interphase ; lung neoplasms ; neoplasm cells ; sequence analysis ; therapeutics
    Sprache Englisch
    Erscheinungsverlauf 2023-04
    Umfang p. 2064-2084
    Erscheinungsort John Wiley & Sons, Ltd
    Dokumenttyp Artikel ; Online
    Anmerkung JOURNAL ARTICLE
    ZDB-ID 2173655-8
    ISSN 1742-4658 ; 1742-464X
    ISSN (online) 1742-4658
    ISSN 1742-464X
    DOI 10.1111/febs.16683
    Datenquelle NAL Katalog (AGRICOLA)

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  9. Artikel ; Online: p27Kip1 and Ser10-phosphorylated p27Kip1 in breast cancer

    Song W / Xie RL / Zhu AY / Xu YM / Shi YQ / Shen Y / Zhang WW / Yang F / Guan XX

    OncoTargets and Therapy, Vol 2015, Iss default, Pp 1863-

    clinical significance and expression

    2015  Band 1869

    Abstract: ... invasive ductal carcinomas and analyzed the relationship of these biomarkers and tumor characteristics ... Results: Of the 107 tumor samples, 38.3% (41 of 107) overexpressed p27 and 64.5% (69 of 107) overexpressed ... significantly higher in malignant tumors than in adjacent tissues, while p27 showed the opposite trend. Also ...

    Abstract Wei Song,1* Ruilian Xie,2* Aiyu Zhu,1 Yumei Xu,1 Yaqin Shi,3 Yan Shen,3 Wenwen Zhang,3 Fang Yang,3 Xiaoxiang Guan1,3 1Department of Medical Oncology, Jinling Hospital, Southern Medical University, Guangzhou, 2Department of Medical Oncology, The First Affiliated Hospital of Gannan Medical College, Ganzhou, 3Department of Medical Oncology, Jinling Hospital, Medical School of Nanjing University, Nanjing, People’s Republic of China *These authors contributed equally to this work Background: The protein p27 (p27Kip1) is a member of the cyclin-dependent kinase inhibitor family, which negatively regulates cell cycle progression, and the phosphorylation of p27 has been proven to affect its stability and nuclear export. Clinical studies on the relation between p27 and phosphorylated p27 (p-p27Ser10) in breast invasive ductal carcinomas are still scarce. Methods: We examined the expression of p27 and p-p27Ser10 using immunohistochemistry in 107 breast invasive ductal carcinomas and analyzed the relationship of these biomarkers and tumor characteristics. Results: Of the 107 tumor samples, 38.3% (41 of 107) overexpressed p27 and 64.5% (69 of 107) overexpressed p-p27Ser10. Analysis of correlation with clinical characteristics showed that high expression level of p-p27Ser10 was linked to poor differentiation, advanced disease stage, and lymph node metastasis, whereas a contrary trend was observed for p27 (all P<0.05). In addition, the expression of p-p27Ser10 was significantly higher in malignant tumors than in adjacent tissues, while p27 showed the opposite trend. Also, there were different levels of p27 and p-p27Ser10 in different types of breast cancer. Conclusion: p27 and p-p27Ser10 are involved in the development of invasive ductal carcinoma and are potential indicators to judge the degree of malignancy as well as recurrence and metastasis. Keywords: breast cancer, p27, p-p27Ser10, Ki67, ERα, PR, Her2
    Schlagwörter Neoplasms. Tumors. Oncology. Including cancer and carcinogens ; RC254-282 ; Internal medicine ; RC31-1245 ; Medicine ; R
    Thema/Rubrik (Code) 616 ; 610
    Sprache Englisch
    Erscheinungsdatum 2015-07-01T00:00:00Z
    Verlag Dove Medical Press
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  10. Artikel ; Online: TMIGD1 acts as a tumor suppressor through regulation of p21Cip1/p27Kip1 in renal cancer.

    Meyer, Rosana D / Zou, Xueqing / Ali, Marwa / Ersoy, Esma / Bondzie, Philip Apraku / Lavaei, Mehrdad / Alexandrov, Ilya / Henderson, Joel / Rahimi, Nader

    Oncotarget

    2018  Band 9, Heft 11, Seite(n) 9672–9684

    Abstract: Renal cell carcinoma (RCC) is a high-risk metastasizing tumor with a poor prognosis and poorly ... TMIGD1) is a novel tumor suppressor that is highly expressed in normal renal tubular epithelial cells ... TMIGD1 promoter activity and expression of TMIGD1. Re-introduction of TMIGD1 into renal tumor cells ...

    Abstract Renal cell carcinoma (RCC) is a high-risk metastasizing tumor with a poor prognosis and poorly understood mechanism. In this study, we demonstrate that transmembrane and immunoglobulin domain-containing 1 (TMIGD1) is a novel tumor suppressor that is highly expressed in normal renal tubular epithelial cells, but it is downregulated in human renal cancer. We have identified CCAAT/enhancer-binding proteinβ (C/EBPβ, also called LAP) as a key transcriptional regulator of TMIGD1, whose loss of expression is responsible for downregulation of TMIGD1 in RCC. Transcriptionally active C/EBPβ/LAP physically interacted with and increased TMIGD1 promoter activity and expression of TMIGD1. Re-introduction of TMIGD1 into renal tumor cells significantly inhibited tumor growth and metastatic behaviors such as morphogenic branching and cell migration. Restoring TMIGD1 expression in renal tumor cells stimulated phosphorylation of p38MAK, induced expression of p21CIP1 (cyclin-dependent kinase inhibitor 1), and p27KIP1 (cyclin-dependent kinase inhibitor 1B) expression, key cell cycle inhibitor proteins involved in regulation of the cell cycle. The present study identifies TMIGD1 as a novel candidate tumor suppressor gene and provides important insight into pathobiology of RCC that could lead to a better diagnosis and possible novel therapy for RCC.
    Sprache Englisch
    Erscheinungsdatum 2018-02-09
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 2560162-3
    ISSN 1949-2553 ; 1949-2553
    ISSN (online) 1949-2553
    ISSN 1949-2553
    DOI 10.18632/oncotarget.23822
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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