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  • Open Access


    miR-34b Targets HSF1 to Suppress Cell Survival in Acute Myeloid Leukemia

    Gangcan Li, Yanping Song, Yunjie Zhang, Hao Wang, Jia Xie

    Oncology Research, Vol.24, No.2, pp. 109-116, 2016, DOI:10.3727/096504016X14611963142254

    Abstract Acute myeloid leukemia (AML) is the most lethal hematological malignancy, and the occurrence of chemoresistance prevents the achievement of complete remission following the standard therapy. MicroRNAs have been extensively investigated as critical regulators of hematopoiesis and leukemogenesis, and they represent a promising strategy for AML therapy. In this study, we identified miR-34b as a novel regulator in myeloid proliferation and apoptosis of leukemic cells. We found that miR-34b was developmentally upregulated in plasma and myeloid cells of healthy subjects, while it was significantly reduced in blood samples of patients with AML and AML cell lines.… More >

  • Open Access


    MicroRNA-21 Inhibits the Apoptosis of Osteosarcoma Cell Line SAOS-2 via Targeting Caspase 8

    Bin Xu, Hehuan Xia, Junming Cao, Zhihong Wang, Yipeng Yang, Yongsheng Lin

    Oncology Research, Vol.25, No.7, pp. 1161-1168, 2017, DOI:10.3727/096504017X14841698396829

    Abstract Currently, multiple microRNAs (miRNAs) have been found to play vital roles in the pathogenesis of osteosarcoma. This study aimed to investigate the role of miR-21 in osteosarcoma. The level of miR-21 in 20 pairs of osteosarcoma and corresponding adjacent tissues was monitored by qPCR. Human osteosarcoma cell line SAOS-2 was transfected with either miR-21 mimic or miR-21 inhibitor, and then cell viability, survival, and apoptosis were measured by MTT, colony formation assay, and flow cytometry. A target of miR-21 was predicted by the microRNA.org database and verified in vitro by using luciferase reporter, qPCR, and More >

  • Open Access


    KIFC1 overexpression promotes prostate cancer cell survival and proliferation in vitro by clustering of amplified centrosomes via interaction with Centrin 2


    BIOCELL, Vol.45, No.5, pp. 1369-1391, 2021, DOI:10.32604/biocell.2021.016654

    Abstract Mitotic kinesin KIFC1 plays critical roles in mitosis by regulating the spindle length, pole formation, and known for clustering extra centrosomes in cancer cells. Centrosome clustering is associated with the survival of cancer cells, but this phenomenon remains obscure in prostate cancer (PCa). The present study demonstrated that PCa cells showed centrosome amplification and clustering during interphase and mitosis, respectively. KIFC1 is highly expressed in PCa cells and tumor tissues of prostatic adenocarcinoma (PAC) patients. Up-regulation of KIFC1 facilitated the PCa cell survival in vitro by ensuring bipolar mitosis through clustering the multiple centrosomes, suggesting centrosome… More >

  • Open Access


    Metabolizing SHED Cell Survival in Dental Pulp Tissue Engineered Constructs

    P. E. Murray1, F. Garcia-Godoy1

    Molecular & Cellular Biomechanics, Vol.3, No.4, pp. 139-140, 2006, DOI:10.32604/mcb.2006.003.139

    Abstract This article has no abstract. More >

  • Open Access


    Systems Neuroprotective Mechanisms in Ischemic Stroke

    Shu Q. Liu*

    Molecular & Cellular Biomechanics, Vol.16, No.2, pp. 75-85, 2019, DOI:10.32604/mcb.2019.06920

    Abstract Ischemic stroke, although causing brain infarction and neurological deficits, can activate innate neuroprotective mechanisms, including regional mechanisms within the ischemic brain and distant mechanisms from non-ischemic organs such as the liver, spleen, and pancreas, supporting neuronal survival, confining brain infarction, and alleviating neurological deficits. Both regional and distant mechanisms are defined as systems neuroprotective mechanisms. The regional neuroprotective mechanisms involve release and activation of neuroprotective factors such as adenosine and bradykinin, inflammatory responses, expression of growth factors such as nerve growth factors and neurotrophins, and activation and differentiation of resident neural stem cells to neurons… More >

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