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  • Wiley  (3)
  • Wang, Yan  (3)
  • Wu, Qingnan  (3)
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  • Wiley  (3)
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  • 1
    Online Resource
    Online Resource
    FAM135B sustains the reservoir of Tip60‐ATM assembly to promote DNA damage response
    Wiley ; 2022
    In:  Clinical and Translational Medicine Vol. 12, No. 8 ( 2022-08)
    Details
    In: Clinical and Translational Medicine, Wiley, Vol. 12, No. 8 ( 2022-08)
    Abstract: Recently, the mechanism by which cells adapt to intrinsic and extrinsic stresses has received considerable attention. Tat‐interactive protein 60‐kDa/ataxia–telangiectasia‐mutated (TIP60/ATM) axis‐mediated DNA damage response (DDR) is vital for maintaining genomic integrity. Methods Protein levels were detected by western blot, protein colocalisation was examined by immunofluorescence (IF) and protein interactions were measured by co‐immunoprecipitation, proximity ligation assay and GST pull‐down assays. Flow cytometry, comet assay and IF assays were used to explore the biological functions of sequence similarity 135 family member B (FAM135B) in DDR. Xenograft tumour, FAM135B transgenic mouse models and immunohistochemistry were utilised to confirm in vitro observations. Results We identified a novel DDR regulator FAM135B which could protect cancer cells from genotoxic stress in vitro and in vivo. The overexpression of FAM135B promoted the removal of γH2AX and 53BP1 foci, whereas the elimination of FAM135B attenuated these effects. Consistently, our findings revealed that FAM135B could promote homologous recombination and non‐homologous end‐joining repairs. Further study demonstrated that FAM135B physically bound to the chromodomain of TIP60 and improved its histone acetyltransferase activity. Moreover, FAM135B enhanced the interactions between TIP60 and ATM under resting conditions. Intriguingly, the protein levels of FAM135B dramatically decreased following DNA damage stress but gradually increased during the DNA repair period. Thus, we proposed a potential DDR mechanism where FAM135B sustains a reservoir of pre‐existing TIP60‐ATM assemblies under resting conditions. Once cancer cells suffer DNA damage, FAM135B is released from TIP60, and the functioning pre‐assembled TIP60‐ATM complex participates in DDR. Conclusions : We characterised FAM135B as a novel DDR regulator and further elucidated the role of the TIP60‐ATM axis in response to DNA damage, which suggests that targeting FAM135B in combination with radiation therapy or chemotherapy could be a potentially effective approach for cancer treatment.
    Type of Medium: Online Resource
    ISSN: 2001-1326 , 2001-1326
    URL: Issue
    URL: Article
    DOI: 10.1002/ctm2.v12.8
    DOI: 10.1002/ctm2.945
    Language: English
    Publisher: Wiley
    Publication Date: 2022
    detail.hit.zdb_id: 2697013-2
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  • 2
    Online Resource
    Online Resource
    BAALC‐AS1/G3BP2/c‐Myc feedback loop promotes cell proliferation in esophageal squamous cell carcinoma
    Wiley ; 2021
    In:  Cancer Communications Vol. 41, No. 3 ( 2021-03), p. 240-257
    Details
    In: Cancer Communications, Wiley, Vol. 41, No. 3 ( 2021-03), p. 240-257
    Abstract: Long non‐coding RNAs (lncRNAs) have been found to be involved in the development of many cancers. In this study, we aimed to identify the molecular mechanisms of lncRNA BAALC antisense RNA 1 (BAALC‐AS1) in regulating the malignancy of esophageal squamous cell carcinoma (ESCC). Methods The expression of BAALC‐AS1 in cancer patients was analyzed using a tissue microarray. The protein and RNA levels of BAALC‐AS1 were determined by Western blotting analysis and quantitative reverse transcription‐PCR (RT‐qPCR), respectively. The cell proliferation was determined by cell viability assays, bromodeoxyuridine incorporation, and flow cytometry. The relationships among BAALC‐AS1, RasGAPSH3 domain‐binding protein 2 (G3BP2), and c‐Myc were determined using RNA immunoprecipitation, RNA pull‐down assays, and luciferase assays. Results The expression of BAALC‐AS1 was highly up‐regulated and associated with malignant phenotypes in ESCC tissues and cell lines. In vivo and in vitro assays showed that BAALC‐AS1 promoted ESCC cell proliferation, migration, and invasion. BAALC‐AS1 directly interacted with G3BP2, and thereby inhibited the degradation of c‐Myc RNA 3'‐UTR by G3BP2, thus leading to the accumulation of c‐Myc expression. Additionally, c‐Myc acted as a transcription factor that can induce the expression of BAALC‐AS1 by directly binding to its promoter region. Conclusions BAALC‐AS1/G3BP2/c‐Myc feedback loop plays a critical role in the development of ESCC, which might provide a novel therapeutic target and facilitate the development of new therapeutic strategies for the treatment of ESCC.
    Type of Medium: Online Resource
    ISSN: 2523-3548 , 2523-3548
    URL: Issue
    URL: Article
    DOI: 10.1002/cac2.v41.3
    DOI: 10.1002/cac2.12127
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 2922913-3
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  • 3
    Online Resource
    Online Resource
    MAGE‐C3 promotes cancer metastasis by inducing epithelial‐mesenchymal transition and immunosuppression in esophageal squamous cell carcinoma
    Wiley ; 2021
    In:  Cancer Communications Vol. 41, No. 12 ( 2021-12), p. 1354-1372
    Details
    In: Cancer Communications, Wiley, Vol. 41, No. 12 ( 2021-12), p. 1354-1372
    Abstract: Evading immune surveillance is necessary for tumor metastasis. Thus, there is an urgent need to better understand the interaction between metastasis and mechanisms of tumor immune evasion. In this study, we aimed to clarify a novel mechanism that link tumor metastasis and immunosuppression in the development of esophageal squamous cell carcinoma (ESCC). Methods The expression of melanoma‐associated antigen C3 (MAGE‐C3) was detected using immunohistochemistry. Transwell assays were used to evaluate the migration and invasion ability of esophageal squamous cell carcinoma (ESCC) cells. Metastasis assays in mice were used to evaluate metastatic ability in vivo . Lymphocyte‐mediated cytotoxicity assays were performed to visualize the immune suppression function on tumor cells. RNA sequencing was performed to identify differentially expressed genes between MAGE‐C3 overexpressing ESCC cells and control cells. Gene ontology (GO) enrichment analyses was performed to identify the most altered pathways influenced by MAGE‐C3. The activation of the interferon‐γ (IFN‐γ) pathway was analyzed using Western blotting, GAS luciferase reporter assays, immunofluorescence, and flow cytometry. The role of MAGE‐C3 in the IFN‐γ pathway was determined by Western blotting and immunoprecipitation. Furthermore, immunohistochemistry and flow cytometry analysis monitored the changes of infiltrated T cell populations in murine lung metastases. Results MAGE‐C3 was overexpressed in ESCC tissues. High expression of MAGE‐C3 had a significant association with the risk of lymphatic metastasis and poor survival in patients with ESCC. Functional experiments revealed that MAGE‐C3 promoted tumor metastasis by activating the epithelial‐mesenchymal transition (EMT). MAGE‐C3 repressed antitumor immunity and regulated cytokine secretion of T cells, implying an immunosuppressive function. Mechanistically, MAGE‐C3 facilitated IFN‐γ signaling and upregulated programmed cell death ligand 1 (PD­L1) by binding with IFN‐γ receptor 1 (IFNGR1) and strengthening the interaction between IFNGR1 and signal transducer and activator of transcription 1 (STAT1). Interestingly, MAGE‐C3 displayed higher tumorigenesis in immune‐competent mice than in immune‐deficient nude mice, confirming the immunosuppressive role of MAGE‐C3. Furthermore, mice bearing MAGE‐C3‐overexpressing tumors showed worse survival and more lung metastases with decreased CD8 + infiltrated T cells and increased programmed cell death 1 (PD‐1) + CD8 + infiltrated T cells. Conclusion MAGE‐C3 enhances tumor metastasis through promoting EMT and protecting tumors from immune surveillance, and could be a potential prognostic marker and therapeutic target.
    Type of Medium: Online Resource
    ISSN: 2523-3548 , 2523-3548
    URL: Issue
    URL: Article
    DOI: 10.1002/cac2.v41.12
    DOI: 10.1002/cac2.12203
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 2922913-3
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