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Search Results (14)
  • Open Access


    Overexpression of lnc-ERP44-3:6 Causes Cell Death and Sensitivity to Cisplatin in Breast Cancer Cell Lines

    Elda A. Flores-Contreras1, Everardo González-González2,3, Ana I. Zarazúa-Niño1, Elsa N. Garza-Treviño1, Natalia Martínez-Acuña1, Viviana C. Zomosa-Signoret4, Román Vidaltamayo4, Gerardo E. Muñoz-Maldonado5, Raquel Garza-Guajardo6, Manuel de J. García-Solís7, Alejandro Abarca-Blanco3, Ana M. G. Rivas-Estilla1, Carlos Córdova-Fletes1,*

    Oncologie, Vol.23, No.3, pp. 373-392, 2021, DOI:10.32604/oncologie.2021.017786

    Abstract Breast cancer (BC) is one of the leading causes of death in women worldwide. A major challenge in BC is chemoresistance, which is often modulated by epigenetic regulators such as long non-coding RNAs (lncRNAs). Because these regulator lncRNAs may play diverse roles, determining their specific pathways and/or functions is crucial to identify possible biomarkers and/or therapeutic targets for BC. In this study, we used gene expression microarrays in order to identify lncRNAs related to the BC biology. We found, among six differentially expressed (DE) lncRNAs, that the expression of lnc-ERP44-3:6 was consistently down-regulated in all breast tumor tissues compared to… More >

  • Open Access


    Integrated Network Pharmacology and Molecular Docking to Reveal the Mechanism of Tetrandrine in Tumor Chemoresistance

    Xuehua Luo1,#, Huijun Xie2,#, Li Han1, Qiaoming Zhong3, Meng Xu4,*, Ling Jin1,*

    Oncologie, Vol.23, No.3, pp. 425-438, 2021, DOI:10.32604/Oncologie.2021.017267

    Abstract Tetrandrine has a variety of anti-tumor effects including against or reversal of tumor chemoresistance, but its mechanism of against tumor chemoresistance is still unclear. Therefore, the analytical method of network pharmacology and molecular docking was used to investigate the mechanism by which tetrandrine acts in tumor chemoresistance. We used public databases (PubChem, SwissADEM, SwissTargetPrediction) to obtain the physicochemical information and targets of tetrandrine, and used gene databases (GeneCards and OMIM) to collected disease targets, respectively. The intersection targets of disease and drug were analyzed by RStudio. We built protein-protein interaction network through the STRING database, and used Cystoscope to screen… More >

  • Open Access


    MicroRNA-708 inhibits the proliferation and chemoresistance of pancreatic cancer cells

    Wensong LIU1, Yunjie LU1, Dong ZHANG1, Longqing SHI1, Guangchen ZU1, Haijiao YAN2,*, Donglin SUN1,*

    BIOCELL, Vol.44, No.1, pp. 73-80, 2020, DOI:10.32604/biocell.2020.08613

    Abstract Pancreatic cancer is one of the most aggressive malignancies with poor prognosis and high mortality. Recent studies showed that microRNAs are dysregulated and involved in the initiation and progression of pancreatic cancer. In this study, we found that miR-708 was significantly downregulated in pancreatic cancer tissues and cell lines. Lentivirus-mediated overexpression of miR-708 could significantly inhibit the proliferation and invasion, while enhanced chemosensitivity to gemcitabine in both Panc-1 and SW1990 cells. Luciferase reporter assay showed that miR-708 bound the 3’-untranslated region of survivin and suppressed the expression of survivin in pancreatic cancer cells. In pancreatic cancer tissues, survivin protein was… More >

  • Open Access


    XRCC1 Arg399Gln and Arg194Trp polymorphisms regulate XRCC1 expression and chemoresistance of non-small cell lung cancer cells

    Dairong LI1, Xianlu ZHUO1,2, Lumi HUANG1, Xiaohui JI1, Donglin WANG1

    BIOCELL, Vol.43, No.3, pp. 139-144, 2019, DOI:10.32604/biocell.2019.06460

    Abstract X-ray repair cross-complementing protein 1 (XRCC1) could repair cisplatin-induced DNA damage. XRCC1 Arg399Gln and Arg194Trp variants alter XRCC1 expression and function, leading to changes in cancer sensitivity to cisplatin treatment. This study aimed to investigate the effects of XRCC1 Arg399Gln and Arg194Trp polymorphisms on cell viability, apoptosis and XRCC1 expression in cisplatin-sensitive A549 and cisplatin-resistant A549/DDP nonsmall cell lung cancer (NSCLC) cells. Plasmids carrying XRCC1 Arg399Gln and Arg194Trp were constructed and transfected into A549 and A549/DDP cells. RT–PCR, Western blot, MTT assay, and flow cytometry analysis were performed to assess cell viability, apoptosis, and XRCC1 expression. Compared to control cells,… More >

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