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  • Open Access

    ARTICLE

    Overexpression of inhibin α (1-32) fusion protein promotes apoptosis and cell cycle arrest in a cervical cancer cell model (Hela cells)

    Yanhong ZHEN1, Li HAN2, Kailai CAI1, Lijun HUO1, Hasan RIAZ1, Canjie WU1, Aixin LIANG1 , Lei SANG1, Liguo YANG1 *

    BIOCELL, Vol.38, No.1, pp. 17-24, 2014, DOI:10.32604/biocell.2014.38.017

    Abstract Inhibins play important roles in the reproductive system. To evaluate whether inhibin α (1-32) fusion protein plays a role in cervical cancer growth, the plasmid pVAX-inhα was constructed and its effect on proliferation and apoptosis of the human cervical cancer cell line (Hela) was checked by flow cytometry and real-time PCR. The expression and localization of inhibin α protein were detected by RT-PCR and confocal microscopy which showed that inhibin α protein was expressed and localized in the nucleus of Hela cells. Over expression of inhibin α gene significantly induced cell apoptosis and ceased S phase of cell cycle. Furthermore,… More >

  • Open Access

    ARTICLE

    Kaempferol and docetaxel diminish side population and down-regulate some cancer stem cell markers in breast cancer cell line MCF-7

    SARA SOLTANIAN1, HELIA RIAHIRAD1, ATHAREH PABARJA1, MOHAMMAD REZA KARIMZADEH2, KOLSOUM SAEIDI3,4

    BIOCELL, Vol.41, No.2-3, pp. 33-40, 2017, DOI:10.32604/biocell.2017.41.033

    Abstract Cancer stem cells (CSCs) are a small subpopulation of cancer cells whose resistance to chemotherapy and radiotherapy plays a pivotal role in treatment failure, tumor recurrence and metastasis. Today, the ability of many phytochemicals in targeting of CSCs has been identified. Kaempferol is a plant phytoestrogen that was recognized as a useful agent for targeting cancer cells by apoptosis induction, cell cycle arrest and inhibition of angiogenesis, migration, and invasion of cancer cells. In this study, we compared the effect of docetaxel as a common breast cancer chemotherapy drug and kaempferol on MCF-7 breast CSCs. Results showed that both docetaxel… More >

  • Open Access

    ARTICLE

    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 >

  • Open Access

    ARTICLE

    Experimental Characterization of MCF-10A Normal Cells Using AFM: Comparison with MCF-7 Cancer Cells

    Moharam Habibnejad Korayem1,*, Zahra Rastegar2

    Molecular & Cellular Biomechanics, Vol.16, No.2, pp. 109-122, 2019, DOI:10.32604/mcb.2019.04706

    Abstract The mechanical properties of single cells have been recently identified as the basis of an emerging approach in medical applications since they are closely related to the biological processes of cells and human health conditions. The problem in hand is how to measure mechanical properties in order to obtain them more accurately and applicably. Some of the cell’s properties such as elasticity module and adhesion have been measured before using various methods; nevertheless, comprehensive tests for two healthy and cancerous cells have not been performed simultaneously. As a Nanoscale device, AFM has been used for some biological cells, however for… More >

  • Open Access

    ARTICLE

    Epigenetic Modulations Induction Using DSCR1 Ectopic Expression in Breast Cancer Cells

    Zahra Niki Boroujeni1, Atefeh Shirkav1, Seyed Ahmad Aleyasin1,*

    Molecular & Cellular Biomechanics, Vol.16, No.1, pp. 41-58, 2019, DOI:10.32604/mcb.2019.04366

    Abstract Today, prognosis, diagnosis and treatment of cancers are progressing with non-invasive methods, including investigation and modification of the DNA methylation profile in cancer cells. One of the effective factors in regulating gene expression in mammals is DNA methylation. Methylation alterations of genes by external factors can change the expression of genes and inhibit the cancer. In the present study, we investigated the effect of Down syndrome critical region 1 gene (DSCR1) ectopic expression on the methylation status of the BCL-XL, ITGA6, TCF3, RASSF1A, DOK7, VIM and CXCR4 genes in breast cancer cell lines. The effect of DSCR1 ectopic expression on… More >

  • Open Access

    ARTICLE

    Induction of Apoptosis and Autophagy Using Ectopic DSCR1 Expression in Breast Cancer Cells

    Zahra Niki Boroujeni1, Atefeh Shirkav1, Seyed Ahmad Aleyasin1,*

    Molecular & Cellular Biomechanics, Vol.15, No.4, pp. 215-227, 2018, DOI:10.32604/mcb.2018.01813

    Abstract Down syndrome critical region 1 gene (DSCR1) is an anti-angiogenesis gene that inhibits the growth of tumor cells. In this study, the role of autophagy and apoptosis in DSCR1-induced cytotoxicity were investigated in MDA-MB-468 breast cancer cells. Lentivirus vector harboring DSCR1 (LV-DSCR1+) was constructed in HEK 293 cells and the optimal dosage of lentivirus vector for infection was determined by the MTT assay. After infection of cells using LV-DSCR1+, acridine orange and ethidium bromide staining was performed to investigation of apoptosis and autophagy. Expression of DSCR1 and marker genes for angiogenesis (VEGF), apoptosis (Bax and Bcl2) and autophagy (LC3 and… More >

  • Open Access

    ARTICLE

    Cancer Cell(s) Cycle Sequencing Reveals Universal Mechanisms of Apoptosis

    R. M. Ardito Marretta*, F. Ales

    Molecular & Cellular Biomechanics, Vol.7, No.4, pp. 225-266, 2010, DOI:10.3970/mcb.2010.007.225

    Abstract In this paper, cell cycle in higher eukaryotes and their molecular networks signals both inG1/SandG2/Mtransitions are replicatedin silico. Biochemical kinetics, converted into a set of differential equations, and system control theory are employed to design multi-nested digital layers to simulate protein-to-protein activation and inhibition for cell cycle dynamics in the presence of damaged genomes. Sequencing and controlling the digital process of four micro-scale species networks (p53/Mdm2/DNA damage, p21mRNA/cyclin-CDK complex, CDK/CDC25/wee1/ SKP2/APC/CKI and apoptosis target genes system) not only allows the comprehension of the mechanisms of these molecule interactions but paves the way for unraveling the participants and their by-products, until… More >

  • Open Access

    ARTICLE

    On p21 Tracking Property in Cancer Cell Unravelled Bio-Digitally in silico. Are Apoptosis Principles Universal?

    R. M. Ardito Marretta∗,†, G. Barbaraci

    Molecular & Cellular Biomechanics, Vol.7, No.3, pp. 135-164, 2010, DOI:10.3970/mcb.2010.007.135

    Abstract Upon severe DNA damage, p21 acts in a dual mode; on the one hand, it inhibits the cyclin-CDK complex for arresting the G2/M transition and on the other hand, it indirectly becomes an apoptotic factor by activating - in sequence - the retinoblastoma protein, E2F1 and APAF1 expressions. But, in a cancer cells proliferation, the mechanisms of, and participants in, the apoptosis failure remain unclear. Since the p21/p53/Mdm2 proteins network normally involves a digital response in a cancer cell, through an original design of a cell signalling-protein simulator, we demonstrate,in silico, that apoptosis phase instability is fully reciprocated by p21mRNA… More >

  • Open Access

    ARTICLE

    Digital control circuitry of cancer cell and its apoptosis

    R. M. Ardito Marretta*, G. Barbaraci

    Molecular & Cellular Biomechanics, Vol.6, No.3, pp. 175-190, 2009, DOI:10.3970/mcb.2009.006.175

    Abstract This study, through a typical aerospace systems architecture, suggests an engineering design of a human cancer cell circuitry in which a digital optimal control matrix is assigned to repair the DNA damage level and/or to trigger its apoptosis.
    Here, the conceived machinery is proposed taking into account the state of the art in cancer investigation. However, it could be further generalized. The most recent studies on cancer pathologies give a predominant role to the oncosuppressor protein p53 and its antagonist, the oncogene Mdm2.
    Experimental and theoretical approaches are in agreement in deducing a “digital” response of the p53 when genomic… More >

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