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  • Xiang, Rong  (4)
  • 2020-2024  (4)
  • 1
    Online Resource
    Online Resource
    A novel isoform of ATOH8 promotes the metastasis of breast cancer by regulating RhoC
    Oxford University Press (OUP) ; 2021
    In:  Journal of Molecular Cell Biology Vol. 13, No. 1 ( 2021-04-10), p. 59-71
    Details
    In: Journal of Molecular Cell Biology, Oxford University Press (OUP), Vol. 13, No. 1 ( 2021-04-10), p. 59-71
    Abstract: Metastases are the main cause of cancer-related mortality in breast cancer. Although significant progress has been made in the field of tumor metastasis, the exact molecular mechanisms involved in tumor metastasis are still unclear. Here, we report that ATOH8-V1, a novel isoform of ATOH8, is highly expressed in breast cancer and is a negative prognostic indicator of survival for patients. Forced expression of ATOH8-V1 dramatically enhances, while silencing of ATOH8-V1 decreases the metastasis of breast cancer cell lines. Moreover, ATOH8-V1 directly binds to the RhoC promoter and stimulates the expression of RhoC, which in turn enhances the metastasis of breast cancer. Altogether, our data demonstrate that ATOH8-V1 is a novel pro-metastatic factor that enhances cancer metastasis, suggesting that ATOH8-V1 is a potential therapeutic target for treatment of metastatic cancers.
    Type of Medium: Online Resource
    ISSN: 1759-4685
    URL: Article
    DOI: 10.1093/jmcb/mjaa050
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2021
    detail.hit.zdb_id: 2500949-7
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  • 2
    Online Resource
    Online Resource
    Abstract 4934: DCBLD2 mediated cisplatin-induced epithelial-to-mesenchymal transition and metastasis in non-small cell lung cancer
    American Association for Cancer Research (AACR) ; 2020
    In:  Cancer Research Vol. 80, No. 16_Supplement ( 2020-08-15), p. 4934-4934
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 80, No. 16_Supplement ( 2020-08-15), p. 4934-4934
    Abstract: In clinical practice, we observed that many patients with solid tumors were diagnosed with early metastasis after chemotherapy, consistent with a large number of preclinical and clinical repots. However, the mechanism how chemotherapy induced tumor metastasis was seldomly reported. In this work, we found that cisplatin promoted epithelial-to-mesenchymal transition (EMT), cell motility and metastasis in non-small cell lung cancer (NSCLC). Moreover, we validated DCBLD2 was a key mediator in cisplatin-induced metastasis in NSCLC through an in vivo, genome-scale CRISPR/Cas9 activation screening. DCBLD2 was abnormally high-expressed in patients with NSCLC, in accordance with the analysis of TCGA database. The expression level of DCBLD2 was negatively correlated with the prognosis of NSCLC patients. Mechanically, DCBLD2 promoted EMT, cell migration in NSCLC cells and metastasis in a mouse xenograft models by binding to cytoskeletal proteins. In addition, we found that cisplatin played an essential role in promoting DCBLD2 expression. The ERK signaling pathway could be activated by cisplatin with phosphorylated, leading to the transcription factor FOS binding to the promoter region of DCBLD2, upregulating the expression of DCBLD2. In conclude, DCBLD2 was a contextual determinant of chemotherapy and metastatic in NSCLC and a potential target for anti-metastasis drugs. Citation Format: Xiaosu Chen, Yajing Lv, Chongbiao Huang, Rong Xiang. DCBLD2 mediated cisplatin-induced epithelial-to-mesenchymal transition and metastasis in non-small cell lung cancer [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 4934.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2020-4934
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2020
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 3
    Online Resource
    Online Resource
    Phosphodiesterase 3A Represents a Therapeutic Target that Drives Stem Cell–like Property and Metastasis in Breast Cancer
    American Association for Cancer Research (AACR) ; 2020
    In:  Molecular Cancer Therapeutics Vol. 19, No. 3 ( 2020-03-01), p. 868-881
    Details
    In: Molecular Cancer Therapeutics, American Association for Cancer Research (AACR), Vol. 19, No. 3 ( 2020-03-01), p. 868-881
    Abstract: Considerable evidence suggests that as breast cancer progresses, genetic and epigenetic mechanisms contribute to the emergence of self-renewing cells (CSC), which may also arise as a consequence of metastasis. Although the molecular pathways that trigger stemness and metastasis are known, key molecular and mechanistic gaps in our understanding of these processes remain unclear. Here, we first screened the inflammation-associated stemness gene phosphodiesterase 3A (PDE3A) using a medium-throughput siRNA library, which was overexpressed in breast tumors and significantly correlated with clinical progression. PDE3A induced the inflammatory nuclear factor NFκB signaling pathway by suppressing cAMP/PKA, which promotes the expression of the stem cell marker OCT4. In addition, PDE3A also promoted the translocation of CCDC88A from the cytoplasm to nuclei, thereby boosting the invasion–metastasis cascade in breast cancer. Most importantly, the PDE3A-selective inhibitor cilostazol dramatically suppressed breast tumor growth and reduced metastasis to the lungs in xenograft breast cancer models, with minimum toxicity. Taken together, we show that PDE3A could predispose patients with breast cancer to metastases by acting as a mediator of cancer stemness. PDE3A is a potential therapeutic target for advanced breast cancer.
    Type of Medium: Online Resource
    ISSN: 1535-7163 , 1538-8514
    URL: Article
    DOI: 10.1158/1535-7163.MCT-18-1233
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2020
    detail.hit.zdb_id: 2062135-8
    SSG: 12
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  • 4
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    Online Resource
    DCBLD2 Mediates Epithelial-Mesenchymal Transition-Induced Metastasis by Cisplatin in Lung Adenocarcinoma
    MDPI AG ; 2021
    In:  Cancers Vol. 13, No. 6 ( 2021-03-19), p. 1403-
    Details
    In: Cancers, MDPI AG, Vol. 13, No. 6 ( 2021-03-19), p. 1403-
    Abstract: Growing evidence suggests that cisplatin and other chemotherapeutic agents promote tumor metastasis while inhibiting tumor growth, which is a critical issue for certain patients in clinical practices. However, the role of chemotherapeutics in promoting tumor metastasis and the molecular mechanism involved are unclear. Here, we investigated the roles of cisplatin in promoting tumor metastasis in lung adenocarcinoma (LUAD). We demonstrated that cisplatin promoted epithelial-mesenchymal transition (EMT), cell motility, and metastasis in vitro and in vivo. The bioinformatic analysis and molecular biology approaches also indicated that DCBLD2 (Discoidin, CUB and LCCL domain containing 2) is a key gene that mediates cisplatin-induced metastasis. DCBLD2 stabilizes β-catenin by phosphorylating GSK3β and transporting accumulated β-catenin to the nucleus to promote the expression of EMT-related transcriptional factors (TFs), ultimately resulting in tumor metastasis. We also identified that cisplatin enhanced DCBLD2 expression by phosphorylating ERK and hence the AP-1-driven transcription of DCBLD2. Furthermore, DCBLD2-specific siRNAs encapsulated by nanocarriers prominently inhibit cisplatin-induced metastasis in vivo. Therefore, DCBLD2 plays a key role in cisplatin-induced metastasis in LUAD and is a potential target for preventing chemotherapy-induced metastasis in vivo.
    Type of Medium: Online Resource
    ISSN: 2072-6694
    URL: Article
    DOI: 10.3390/cancers13061403
    Language: English
    Publisher: MDPI AG
    Publication Date: 2021
    detail.hit.zdb_id: 2527080-1
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