检索结果-南通市图书馆

Regulation Effect of miR-34a Expression on Radiosensitivity of lung adenocarcinoma cells by Targeting Bcl-2 and CDK4/6 Signaling Pathways

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Journal of Cancer Therapy 2022年第4期13卷 187-198页

作者： Xue Chen Chen Yin Qingfen Liu Jianxiang Liu Institute of Radiation Medicine Chinese Academy of Medical Science Tianjin China National Institute for Radiological Protection Chinese Center for Disease Control and Prevention Beijing China

Objective: Radiotherapy has been widely used to treat lung cancer. However, non-small lung cancer cells are insensitive to radiation, diminishing their radiotherapy effects. Although the radiosensitivity of the non-small lung cancer cells was reported to be enhanced through regulating miR-34a, the regulation effects of miR-34a expression on radiosensitivity of lung adenocarcinoma cells through target genes CDK4, CDK6, CyclinD1, and Bcl-2/Bax have not been systematically investigated. Methods: In this study, we investigated the effect of miR-34a expression on the Bcl-2, CDK4, and CDK6 pathways in lung adenocarcinoma cells, to provide new insights into the sensitization treatment of lung cancer. We first studied the effect of miR-34a expression on H1299 and A549 cell activity. Then to investigate the mechanisms of radiosensitivity, we focused on apoptosis, cell cycle, and target genes. Results: We find that overexpression of miR-34a in lung adenocarcinoma cells inhibits cell activity, and improves radiosensitivity. Specifically, overexpression of miR-34a suppresses the expression of target genes CDK4, CDK6, CyclinD1, and Bcl-2/Bax, which leads to cell cycle arrest and promotes apoptosis of lung adenocarcinoma cells. Conclusions: Overall, our results demonstrate that the overexpression of miR-34a enhances the radiosensitivity of lung adenocarcinoma cells, indicating that miR-34a is a sensitizer for lung adenocarcinoma radiotherapy.

关键词： miR-34a p53 lung adenocarcinoma cells Radiosensitivity Cell Apoptosis Cell Cycle

A benzoxazine derivative specifically inhibits cell cycle progression in p53-wild type pulmonary adenocarcinoma cells

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Frontiers in Biology 2010年第2期5卷 180-186页

作者： Hua SU Ling SU Qiuxia HE Jing ZHAO Baoxiang ZHAO Shangli ZHANG Junying MIAO Institute of Developmental Biology School of Life ScienceShandong UniversityJinan 250100China The key Laboratory of Experimental Teratology Ministry of Education Jinan 250012China Institute of Organic Chemistry School of Chemistry and Chemical EngineeringShandong UniversityJinan 250100China

A fundamental aspect of cancer development is cancer cell *** for chemical agents that can interfere with cancer cell growth has been of great interest over the *** our study,we found that a benzoxazine derivative,(6-tert-butyl-3,4-dihydro-2Hbenzo[b][1,4]oxazin-3-yl)methanol(TBM),could inhibit cell growth and caused significant cell cycle arrest in pulmonary adenocarcinoma A549 and H460 cells with wild-type p53,while not affecting the cell cycle distribution in p53-deleted H1299 lung adenocarcinoma *** P53 plays an important role in regulating cell cycle progression,we analyzed the protein level of p53 by Western blot,and detected a significant elevation of p53 level after TBM treatment in A549 and H460 *** data suggested that TBM might specifically inhibit the proliferation of p53 wild-type lung adenocarcinoma cells through a p53-dependent cell cycle control *** interestingly,results indicated that TBM might serve as a useful tool for studying the molecular mechanisms of lung cancer cell growth and cell cycle control,especially for the biologic process regulated by P53.

关键词： (6-tert-butyl-3,4-dihydro-2H-benzo[b]oxazin-3-yl)methanol lung adenocarcinoma cells cell cycle arrest p53

Chemical compositions,cytotoxicity and antioxidant activity of the endophytic fungus Fusarium napiforme isolated from Psidium guajava

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Studies in Fungi 2020年第1期5卷 332-352页

作者： Chutulo EC Chalannavar RK Pramod Kumar P Department of Studies&Research in Microbiology Mangalore UniversityJnana KaveriP.G.CentreChikka AluvaraKodagu-571232KarnatakaIndia Department of Biosciences Mangalore UniversityMangalagangotri-574199KarnatakaIndia Department of Biology Wolaita Sodo UniversityWolaita SodoEthiopia Department of Applied Botany Mangalore UniversityMangalagangotri-574199KarnatakaIndia Department of Biochemistry CSIR-Central Food Technological Research InstituteMysuru-570020KarnatakaIndia

The bioactive secondary metabolites from the endophytic fungus Fusarium napiforme was evaluated for the cytotoxic effect and antioxidant *** total antioxidant capacity(TAC)of the extract was determined by 2,2-diphenyl-1-picrylhydrazyl(DPPH),phosphomolybdate,and reducing power assay *** cytotoxicity of the extract was evaluated against lung adenocarcinoma(A549)cells and mouse embryo fibroblast(NIH3T3)cells by methyl thiazolyl tetrazolium(MTT)*** major composition of the crude extract was identified by the Gas Chromatography-Mass Spectrometry(GC-MS)*** of the endophyte crude extract revealed a high amount of the total flavonoid content(TFC)and total phenolic content(TPC).The extract showed high cytotoxic activity against the A549 cell line with the mean cytotoxicity of 69.74±0.49%.The extract did not show any cytotoxic effect against the NIH3T3 cell *** extract exhibited high antioxidant activity as a function of the *** a test concentration of 1 mg ml-1,the extract showed the highest inhibition against DPPH radical at 75.4607%±0.47688,ferric ion reducing power at 0.882±0.0120,and 255.434±21.404 AAE/g of the extract by phosphomolybdenum assay(PMA).There is a significant correlation between TPC and antioxidant activity at p<*** correlation between reducing power and DPPH is significant at p<*** major types of bioactive compounds identified by the GC-MS have shown the presence of nine major *** result strongly exhibits that the endophyte *** can be a potential source for the formulation of natural anticancer drugs and protecting the body from oxidative damages.

关键词： flavonoids GC-MS analysis lung adenocarcinoma cells mouse embryo fibroblast cells MTT assay phenolics

Simvastatin Action Is Not Related to HDAC2 Expression in Non-Small Cell lung Cancer (NSCLC)

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Journal of Cancer Therapy 2016年第12期7卷 939-952页

作者： Gallelli Luca Falcone Daniela Perri Mariarita Erika Cione Pelaia Girolamo Mesuraca Maria Terracciano Rosa Spaziano Giuseppe D’Agostino Bruno Navarra Michele Savino Rocco Department of Health Science University of Catanzaro Catanzaro Italy Department of Pharmacy Health and Nutritional Science University of Calabria Cosenza Italy Department of Medical and Surgical Sciences University of Catanzaro Catanzaro Italy Department of Experimental Medicine School of Medicine Second University of Naples Naples Italy Department of Drug Sciences and Health Products University of Messina Messina Italy

In this study, we lowered the expression of HDAC2 protein, to evaluate the effects of simvastatin on the biochemical pathways involved in inflammatory and metastatic response. The model used is the non-small cell lung cancer line (GLC-82). Trypan blue staining for assessing vital cell number to be seed and MTT assay was used as cell proliferation test. Lentivus for HDAC2 was used to silence its mRNA. Western blotting analysis was used for protein extracts, and ELISA was done on culture media for cytokines (IL-6, IL-8 and TNF-alpha) release. Hydrogen peroxide (H2O2) was used to induce oxidative stress. Our results have shown that Lentivirus containing the shHDAC2 in GLC-82 cells was able to reduce protein expression of HDAC2. In the GLCshHDAC2 cell line obtained, H2O2 induced a significant increase in cytokines release and ERK1/2 phosphorylation (P 0.01);a significant decrease of RECK activation (P 0.01);a significant increased activation (P 0.01) of both MMP-2 and MMP-9 and an increased activation of NF-κB, MyD88, TRAF-6, TRADD, TRAF-2. In GLCshHDAC2 cell, the treatment with simvastatin (30 μM), significantly affected all the biochemical markers examinated (P 0.01). In conclusion, from our report emerge, that simvastatin is able per se to inhibit oxidative stress in lung cancer cells, overcoming HDAC2 expression.

关键词： lung adenocarcinoma cells HDAC2 Statins Cell Proliferation Cytokines

EXPERIMENTAL RESEARCH OF EFFECTIVENESS OF siRNA-Her-2/neu ON DRUG SENSITIVITY OF Her-2/neu-OVER-EXPRESSING lung adenocarcinoma CELL LINE

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Chinese Journal of Cancer Research 2006年第3期18卷 173-176页

作者：任淑华王井伟曲平刘义张伟张林 Department of Thoracic Surgery The First Affiliated Hospital China Medical University Shenyang 110001 Tangshan Worker Hospital Tangshan 063000 Tumor Marker Research Center Cancer Hospital & Cancer Institute Chinese Academy of Medical Sciences Beijing 100021

Objective： Her-2/neu protein overexpression has been demonstrated in lung adenocarcinoma. Its overexpression often indicates a poor prognosis and resistance to chemotherapeutic agents. The objectives of this paper is to explore the effectiveness of double-stranded short inhibitory RNAs （siRNA） targeting Her-2/neu oncogene on the drug sensitivity of Her-2/neu-overexpressing lung adenocarcinoma cells. Methods： lung adenocarcinoma cell line calu-3 was transfected with siRNAs formulated LipofectAMINE 2000, and Her-2/neu protein and P-gp were determined by flow cytometry （FCM）. The chemosensitivity of transfected cells to cisplatin （CDDP） was measured by MTT. Cell apoptosis detection kit （Annexin V method） was used to examine the drug induced apoptosis rate. Results： siRNA targeting Her-2/neu greatly reduced the cell surface expression of Her-2/neu protein and had no effect on P-gp. Consequently the inhibitory rate of CDDP in combination with siRNA targeting Her-2/neu was （67.1±2.3）%, while the inhibitory rates were （48.1±3.5）%, （46.3±5.9）% and （50.2±2.9）% in untreated control, empty vector and unrelated siRNA groups, respectively. The FCM results showed that the apoptosis rate of cells treated with CDDP combined with siRNAs-Her-2/neu was elevated when compared with unrelated siRNA group and empty vector group. Conclusion： Sequence specific siRNA targeting Her-2/neu was capable of enhancing the chemosensitivity of calu-3 cell to cisplatin.

关键词： Her-2/neu siRNA lung adenocarcinoma cells Cisplatin