Browsing by Subject "Cell cycle arrest"

Now showing 1 - 4 of 4
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    Bioactive compounds of tomato: Cancer chemopreventive effects and influence on the transcriptome in hepatocytes
    (Elsevier, 2018-01-03) Periago, María Jesús; Navarro-González, Inmaculada; García-Alonso, Javier; Tecnología de Alimentos, Nutrición y Bromatología
    The mechanisms of the effects of tomato extracts (containing lycopene and phenolic compounds) and these pure bioactive compounds on the viability, apoptosis, cell cycle, and the scavenging of ROS of HepG2 cells were investigated. Simultaneously, a transcriptomic analysis in human hepatocytes from obese patients, after the intake of tomato juice, was carried out using Human Gene Expression Array (Affymetrix). The viability of HepG2 decreased after exposure to tomato extracts and pure compounds, but none showed apoptotic activity; however, lycopene was able to inhibit cell cycle progression in phase S. Tomato extracts and pure compounds were able to decrease the ROS generation, the phenolic compounds being more effective than lycopene. Transcriptomic analysis suggested a involvement in the regulation of the cell cycle and apoptosis pathways after the intake of tomato juice, through the lycopene accumulation. These results showed that tomato juice have potential as functional foods for maintenance of liver health.
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    Downregulation of KIF15 inhibits the tumorigenesis of non-small-cell lung cancer via inactivating Raf/MEK/ERK signaling
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Luo, Yingbin; Zhang, Bo; Xu, Lili; Li, Minghua; Wu, Jianchun; Zhou, Yiyang; Li, Yan
    Background. Lung cancer is one of the most common causes of cancer-associated mortality worldwide. Upregulation of kinesin family member 15 (KIF15) expression has been observed in non-small cell lung cancer (NSCLC), and high expression levels of KIF15 are associated with a poor prognosis in patients with NSCLC. However, to the best of our knowledge, the mechanisms by which KIF15 regulates apoptosis, migration and invasion in NSCLC remain unclear. Methods. Cell Counting Kit-8, flow cytometry and Transwell assays were performed to determine the proliferation, apoptosis and invasion of NSCLC cells, respectively. In addition, western blotting was used to detect the levels of phosphorylated (p-)c-Raf, p-ERK and p-MEK in NSCLC cells. Results. Downregulation of KIF15 expression markedly inhibited the proliferation, migration and invasion of NSCLC cells through mediation of MMP2 and MMP9. In addition, downregulation of KIF15 markedly induced apoptosis and cell cycle arrest in NSCLC cells through regulation of active caspase 3, p27 Kip1 and cyclin D1. Furthermore, KIF15 knockdown notably decreased the levels of activating transcription factor 2, p-c-Raf, p-ERK and p-MEK in A549 and NCIH460 cells. Finally, KIF15 knockdown notably inhibited the tumor growth of NSCLC in vivo. Conclusion. In conclusion, the present study indicated that downregulation of KIF15 expression was able to inhibit the tumorigenesis of NSCLC by inactivating Raf/MEK/ERK signaling. These findings may help improve the diagnosis and treatment of NSCLC.
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    Knockdown of kinesin family member 2C restricts cell proliferation and induces cell cycle arrest in gastric cancer
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2023) Li, Shuai; Ma, Yulian; Wu, Chen; Hou, Xinfang
    Kinesin family member 2C (KIF2C) was reported to act as a vital player in several human cancers. However, the exact function of KIF2C in gastric cancer (GC) is poorly understood. In the present study, the potential role of KIF2C was studied in gastric cancer by bioinformatics analysis and proliferation assay. KIF2C expression was detected using reverse transcription-quantitative polymerase chain reaction and western blot. Our data showed that the expression of KIF2C was increased in different tumor tissues, including GC. KIF2C was overexpressed in GC tissues and might be used as a diagnostic and prognostic biomarker for GC. KIF2C expression was correlated with immune infiltration and the levels of cell cyclerelated genes in GC. Moreover, silencing of KIF2C can cause cell cycle arrest, and inhibit the proliferative ability of GC cells. Thus, our studies revealed that KIF2C levels might serve as a promising biomarker for diagnosis and prediction of prognosis of GC, and targeting KIF2C might be an effective therapeutic strategy for GC.
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    The regulatory role of HIF-1 in tubular epithelial cells in response to kidney injury
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2020) Qiu, Yumei; Huang, Xiaowen; He, Weichun
    The high sensitivity to changes in oxygen tension makes kidney vulnerable to hypoxia. Both acute kidney injury and chronic kidney disease are almost always accompanied by hypoxia. Tubular epithelial cells (TECs), the dominant intrinsic cells in kidney tissue, are believed to be not only a victim in the pathological process of various kidney diseases, but also a major contributor to kidney damage. Hypoxia inducible factor- 1 (HIF-1) is the main regulator of adaptive response of cells to hypoxia. Under various clinical and experimental kidney disease conditions, HIF-1 plays a pivotal role in modulating multiple cellular processes in TECs, including apoptosis, autophagy, inflammation, metabolic pattern alteration, and cell cycle arrest. A comprehensive understanding of the mechanisms by which HIF-1 regulates these cellular processes in TECs may help identify potential therapeutic targets to improve the outcome of acute kidney injury and delay the progression of chronic kidney disease.