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  • Open Access

    ARTICLE

    SENEX-mediated CDK4/6 inhibition promotes senescence and confers apoptosis resistance in B-cell non-Hodgkin lymphoma

    JIYU WANG1,#, LIUYING YI2,#, KEKE HUANG1, YANGYANG WANG1, HUIPING WANG1, ZHIMIN ZHAI1,*

    BIOCELL, Vol.48, No.3, pp. 453-462, 2024, DOI:10.32604/biocell.2024.047871

    Abstract Background: The primary cause of treatment failure in patients with refractory or relapsed B-cell non-Hodgkin lymphoma (r/r B-NHL) is resistance to current therapies, and therapy-induced senescence (TIS) stands out as a crucial mechanism contributing to tumor drug resistance. Here, we analyzed SENEX/Rho GTPase Activating Protein 18 (ARHGAP18) expression and prognostic significance in doxorubicin-induced B-NHL-TIS model and r/r B-NHL patients, investigating its target in B-NHL cell senescence and the effect of combining specific inhibitors on apoptosis resistance in B-NHL-TIS cells. Methods: Raji cells were transfected with the human SENEX shRNA recombinant lentiviral vector (Sh-SENEX) and the empty vector negative (NC) to… More >

  • Open Access

    ARTICLE

    Inhibition of proliferation, migration, and invasiveness of bladder cancer cells through SAPCD2 knockdown

    CHONG SHEN, JIAJUN YAN*, YU REN, ZHIRONG ZHU, XIAOLONG ZHANG, SHUIXIANG TAO

    BIOCELL, Vol.48, No.1, pp. 97-109, 2024, DOI:10.32604/biocell.2023.045303

    Abstract Introduction: Bladder cancer (BC) has a high incidence and mortality rate worldwide. Suppressor anaphase-promoting complex domain containing 2 (SAPCDC2) is over-expressed in a variety of tumors. Objectives: This study investigated the effects of SAPCD2 knockdown on BC cells. Methods: T24 and UMUC3 cell models and the xenografted BC tumor model with SAPCD2 knockdown were established to observe the malignant phenotype of BC cells by cell counting kit-8 assay, colony formation test, wound healing, and Transwell assay, mRNA and proteins expressions were measured with quantitative real-time polymerase chain reaction, western blotting, and tissue immunohistochemistry. Lithium chloride agonist on the Wnt/β-catenin pathway… More > Graphic Abstract

    Inhibition of proliferation, migration, and invasiveness of bladder cancer cells through SAPCD2 knockdown

  • Open Access

    ARTICLE

    Long noncoding RNA TFAP2A-AS1 exerts promotive effects in non-small cell lung cancer progression via controlling the microRNA-548a-3p/CDK4 axis as a competitive endogenous RNA

    YANG ZHANG, LIXIA MA, TINGTING ZHANG, PEIDONG LI, JIABIN XU, ZHUO WANG*

    Oncology Research, Vol.29, No.2, pp. 129-139, 2021, DOI:10.32604/or.2022.03563

    Abstract In this study, we mainly focus on probing expression profile and detailed functions of long non-coding RNA TFAP2A antisense RNA 1 (TFAP2A-AS1) in non-small cell lung cancer (NSCLC). Moreover, the mechanisms played by TFAP2A-AS1 were unraveled comprehensively. Herein, a notable overexpressed TFAP2A-AS1 in NSCLC was observed by TCGA and our own cohort. An increased TFAP2A-AS1 level displayed a negative correlation with the overall survival of patients with NSCLC. Loss-of-function approaches illustrated that the absence of TFAP2A-AS1 weakened NSCLC cell proliferation, colony formation, migration and invasion in vitro. Also, interference of TFAP2A-AS1 caused in vivo tumor growth suppression. Mechanistically, TFAP2A-AS1 could… More >

  • Open Access

    ARTICLE

    MicroRNA-338-3p Inhibits Proliferation and Promotes Apoptosis of Multiple Myeloma Cells Through Targeting Cyclin-Dependent Kinase 4

    Yang Cao*, Xu Shi, Yingmin Liu, Ren Xu§, Qing Ai*

    Oncology Research, Vol.27, No.1, pp. 117-124, 2019, DOI:10.3727/096504018X15213031799835

    Abstract MicroRNA-338-3p (miR-338-3p) has been reported to be a tumor suppressor in multiple cancer types. However, the biological role of miR-338-3p and its underlying mechanism in multiple myeloma (MM) remain unclear. In the present study, we investigated the biological role and potential of miR-338-3p in MM. We found that miR-338-3p was significantly decreased in newly diagnosed and relapsed MM tissues and cell lines. Overexpression of miR-338-3p in MM cells significantly inhibited proliferation and promoted apoptosis, caspase 3, and caspase 8 activity. Bioinformatics algorithm analysis predicted that cyclin-dependent kinase 4 (CDK4) was a direct target of miR-338-3p, and this was experimentally verified… More >

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