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  1. Article ; Online: Increased SLC7A3 Expression inhibits Tumor Cell Proliferation and Predicts a Favorable Prognosis in Breast Cancer.

    He, Lifang / Xu, Yue / Lin, Jiediao / Lin, Stanley / Cui, Yukun

    Recent patents on anti-cancer drug discovery

    2024  

    Abstract: Background: Arginine plays significant and contrasting roles in breast cancer growth and survival. However, the factors governing arginine balance remain poorly characterized.: Objective: We aimed to identify the molecule that governs arginine ... ...

    Abstract Background: Arginine plays significant and contrasting roles in breast cancer growth and survival. However, the factors governing arginine balance remain poorly characterized.
    Objective: We aimed to identify the molecule that governs arginine metabolism in breast cancer and to elucidate its significance.
    Methods: We analyzed the correlation between the expression of solute carrier family 7 member 3 (SLC7A3), the major arginine transporter, and breast cancer survival in various databases, including GEPIA, UALCAN, Metascape, String, Oncomine, KM-plotter, CBioPortal and Prognosis. Additionally, we validated our findings through bioinformatic analyses and experimental investigations, including colony formation, wound healing, transwell, and mammosphere formation assays.
    Results: Our analysis revealed a significant reduction in SLC7A3 expression in all breast cancer subtypes compared to adjacent breast tissues. Kaplan-Meier survival analyses demonstrated that high SLC7A3 expression was positively associated with decreased nodal metastasis (HR=0.70, 95% CI [0.55, 0.89]), ER positivity (HR=0.79, 95% CI [0.65, 0.95]), and HER2 negativity (HR=0.69, 95% CI [0.58, 0.82]), and increased recurrence-free survival. Moreover, low SLC7A3 expression predicted poor prognosis in breast cancer patients for overall survival. Additionally, the knockdown of SLC7A3 in MCF-7 and MDA-MB-231 cells resulted in increased cell proliferation and invasion in vitro.
    Conclusion: Our findings indicate a downregulation of SLC7A3 expression in breast cancer tissues compared to adjacent breast tissues. High SLC7A3 expression could serve as a prognostic indicator for favorable outcomes in breast cancer patients due to its inhibitory effects on breast cancer cell proliferation and invasion.
    Language English
    Publishing date 2024-01-08
    Publishing country United Arab Emirates
    Document type Journal Article
    ZDB-ID 2250820-X
    ISSN 2212-3970 ; 1574-8928
    ISSN (online) 2212-3970
    ISSN 1574-8928
    DOI 10.2174/0115748928279007231130070056
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6393: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  2. Article: IGFBP5, as a Prognostic Indicator Promotes Tumor Progression and Correlates with Immune Microenvironment in Glioma.

    Lin, Jiediao / Huang, Guowei / Zeng, Qianru / Zhang, Rendong / Lin, Yun / Li, Yaochen / Huang, Baohua / Pan, Hongchao

    Journal of Cancer

    2024  Volume 15, Issue 1, Page(s) 232–250

    Abstract: Background: ...

    Abstract Background:
    Language English
    Publishing date 2024-01-01
    Publishing country Australia
    Document type Journal Article
    ZDB-ID 2573318-7
    ISSN 1837-9664
    ISSN 1837-9664
    DOI 10.7150/jca.87733
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Reciprocal regulation of forkhead box C1 and L1 cell adhesion molecule contributes to triple-negative breast cancer progression.

    Zhang, Fan / Xu, Yue / Lin, Jiediao / Pan, Hongchao / Giuliano, Armando E / Cui, Xiaojiang / Cui, Yukun

    Breast cancer research and treatment

    2024  Volume 204, Issue 3, Page(s) 465–474

    Abstract: Purpose: The potential of targeting forkhead box C1 (FOXC1) as a therapeutic approach for triple-negative breast cancer (TNBC) is promising. However, a comprehensive understanding of FOXC1 regulation, particularly upstream factors, remains elusive. ... ...

    Abstract Purpose: The potential of targeting forkhead box C1 (FOXC1) as a therapeutic approach for triple-negative breast cancer (TNBC) is promising. However, a comprehensive understanding of FOXC1 regulation, particularly upstream factors, remains elusive. Expression of the L1 cell adhesion molecule (L1CAM), a transmembrane glycoprotein associated with brain metastasis, was observed to be positively associated with FOXC1 transcripts. Thus, this study aims to investigate their relationship in TNBC progression.
    Methods: Publicly available FOXC1 and L1CAM transcriptomic data were obtained, and their corresponding proteins were analyzed in four TNBC cell lines. In BT549 cells, FOXC1 and L1CAM were individually silenced, while L1CAM was overexpressed in BT549-shFOXC1, MDA-MB-231, and HCC1937 cells. CCK-8, transwell, and wound healing assays were performed in these cell lines, and immunohistochemical staining was conducted in tumor samples.
    Results: A positive correlation between L1CAM and FOXC1 transcripts was observed in publicly available datasets. In BT549 cells, knockdown of FOXC1 led to reduced L1CAM expression at both the transcriptional and protein levels, and conversely, silencing of L1CAM decreased FOXC1 protein levels, but interestingly, FOXC1 transcripts remained largely unaffected. Overexpressing L1CAM resulted in increased FOXC1 protein expression without significant changes in FOXC1 mRNA levels. This trend was also observed in BT549-shFOXC1, MDA-MB-231-L1CAM, and HCC1937-L1CAM cells. Notably, alterations in FOXC1 or L1CAM levels corresponded to changes in cell proliferation, migration, and invasion capacities. Furthermore, a positive correlation between L1CAM and FOXC1 protein expression was detected in human TNBC tumors.
    Conclusion: FOXC1 and L1CAM exhibit co-regulation at the protein level, with FOXC1 regulating at the transcriptional level and L1CAM regulating at the post-transcriptional level, and together they positively influence cell proliferation, migration, and invasion in TNBC.
    MeSH term(s) Humans ; Cell Line, Tumor ; Cell Movement/genetics ; Cell Proliferation/genetics ; Forkhead Transcription Factors/genetics ; Gene Expression Regulation, Neoplastic ; Neural Cell Adhesion Molecule L1/genetics ; Neural Cell Adhesion Molecule L1/metabolism ; Neural Cell Adhesion Molecule L1/therapeutic use ; Triple Negative Breast Neoplasms/pathology
    Chemical Substances Forkhead Transcription Factors ; Neural Cell Adhesion Molecule L1 ; L1CAM protein, human ; FOXC1 protein, human
    Language English
    Publishing date 2024-01-06
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 604563-7
    ISSN 1573-7217 ; 0167-6806
    ISSN (online) 1573-7217
    ISSN 0167-6806
    DOI 10.1007/s10549-023-07177-7
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1655: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  4. Article ; Online: Forkhead box C1 boosts triple-negative breast cancer metastasis through activating the transcription of chemokine receptor-4.

    Pan, Hongchao / Peng, Zhilan / Lin, Jiediao / Ren, Xiaosha / Zhang, Guojun / Cui, Yukun

    Cancer science

    2018  Volume 109, Issue 12, Page(s) 3794–3804

    Abstract: The transcription factor forkhead box C1 (FOXC1) has recently been proposed as a crucial regulator of triple-negative breast cancer (TNBC) and associated with TNBC metastasis. However, the mechanism of FOXC1 in TNBC development and metastasis is elusive. ...

    Abstract The transcription factor forkhead box C1 (FOXC1) has recently been proposed as a crucial regulator of triple-negative breast cancer (TNBC) and associated with TNBC metastasis. However, the mechanism of FOXC1 in TNBC development and metastasis is elusive. In this study, overexpression of FOXC1 in MDA-MB-231 cells significantly enhanced, whereas knockdown of FOXC1 in BT549 cells significantly reduced, the capabilities of TNBC cell invasion and motility in vitro and metastasis to the lung in vivo, when compared to their respective control cells. Mechanistic studies revealed that FOXC1 increased the expression of CXC chemokine receptor-4 (CXCR4), probably through transcriptional activation. AMD3100, an inhibitor of CXCR4, could block cell migration. In a zebrafish tumor model, AMD3100 could suppress cell invasion and metastasis. In addition, overexpressing CXCR4 in FOXC1-knockdown BT549 cells increased the capabilities of TNBC cell invasion and motility. In contrast, inhibition of CXCR4 with either AMD3100 or siRNA in MDA-MB-231 cells overexpressing FOXC1 reduced the capabilities of invasion and motility. Taken together, our results reveal a potential mechanism for FOXC1-induced TNBC metastasis.
    MeSH term(s) Animals ; Cell Line, Tumor ; Cell Movement/drug effects ; Female ; Forkhead Transcription Factors/genetics ; Forkhead Transcription Factors/metabolism ; Heterocyclic Compounds/pharmacology ; Humans ; Lung Neoplasms/genetics ; Lung Neoplasms/metabolism ; Lung Neoplasms/secondary ; Mice ; Neoplasm Transplantation ; Receptors, CXCR4/genetics ; Receptors, CXCR4/metabolism ; Transcriptional Activation/drug effects ; Triple Negative Breast Neoplasms/genetics ; Triple Negative Breast Neoplasms/metabolism ; Zebrafish
    Chemical Substances CXCR4 protein, human ; FOXC1 protein, human ; Forkhead Transcription Factors ; Heterocyclic Compounds ; Receptors, CXCR4 ; plerixafor (S915P5499N)
    Language English
    Publishing date 2018-11-18
    Publishing country England
    Document type Journal Article
    ZDB-ID 2115647-5
    ISSN 1349-7006 ; 1347-9032
    ISSN (online) 1349-7006
    ISSN 1347-9032
    DOI 10.1111/cas.13823
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: Elevated transcriptional levels of aldolase A (ALDOA) associates with cell cycle-related genes in patients with NSCLC and several solid tumors.

    Zhang, Fan / Lin, Jie-Diao / Zuo, Xiao-Yu / Zhuang, Yi-Xuan / Hong, Chao-Qun / Zhang, Guo-Jun / Cui, Xiao-Jiang / Cui, Yu-Kun

    BioData mining

    2017  Volume 10, Page(s) 6

    Abstract: Background: Aldolase A (ALDOA) is one of the glycolytic enzymes primarily found in the developing embryo and adult muscle. Recently, a new role of ALDOA in several cancers has been proposed. However, the underlying mechanism remains obscure and ... ...

    Abstract Background: Aldolase A (ALDOA) is one of the glycolytic enzymes primarily found in the developing embryo and adult muscle. Recently, a new role of ALDOA in several cancers has been proposed. However, the underlying mechanism remains obscure and inconsistent. In this study, we tried to investigate ALDOA-associated (AA) genes using available microarray datasets to help elucidating the role of ALDOA in cancer.
    Results: In the dataset of patients with non-small-cell lung cancer (NSCLC, E-GEOD-19188), 3448 differentially expressed genes (DEGs) including ALDOA were identified, in which 710 AA genes were found to be positively associated with ALDOA. Then according to correlation coefficients between each pair of AA genes, ALDOA-associated gene co-expression network (GCN) was constructed including 182 nodes and 1619 edges. 11 clusters out of GCN were detected by ClusterOne plugin in Cytoscape, and only 3 of them have more than three nodes. These three clusters were functionally enriched. A great number of genes (43/79, 54.4%) in the biggest cluster (Cluster 1) primarily involved in biological process like cell cycle process (
    Conclusions: ALDOA could contribute to the progress of cancer, at least partially through its association with genes relevant to cell cycle independent of glycolysis. AA genes plus ALDOA represent a potential new signature for development and prognosis in several cancers.
    Language English
    Publishing date 2017-02-07
    Publishing country England
    Document type Journal Article
    ZDB-ID 2438773-3
    ISSN 1756-0381
    ISSN 1756-0381
    DOI 10.1186/s13040-016-0122-4
    Database MEDical Literature Analysis and Retrieval System OnLINE

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