Transcriptome profiling of cervical cancer cells acquired resistance to cisplatin by deep sequencing

التفاصيل البيبلوغرافية
العنوان: Transcriptome profiling of cervical cancer cells acquired resistance to cisplatin by deep sequencing
المؤلفون: Zhong Chen, Yamin Wang, Linna Liu
المصدر: Artificial Cells, Nanomedicine, and Biotechnology. 47:2820-2829
بيانات النشر: Informa UK Limited, 2019.
سنة النشر: 2019
مصطلحات موضوعية: Biomedical Engineering, Uterine Cervical Neoplasms, Pharmaceutical Science, Medicine (miscellaneous), 02 engineering and technology, Deep sequencing, HeLa, Phosphatidylinositol 3-Kinases, 03 medical and health sciences, 0302 clinical medicine, medicine, Humans, Gene silencing, KEGG, PI3K/AKT/mTOR pathway, Cisplatin, biology, Gene Expression Profiling, High-Throughput Nucleotide Sequencing, General Medicine, 021001 nanoscience & nanotechnology, biology.organism_classification, Gene Expression Regulation, Neoplastic, Reverse transcription polymerase chain reaction, Drug Resistance, Neoplasm, Apoptosis, 030220 oncology & carcinogenesis, Cancer research, Female, 0210 nano-technology, Proto-Oncogene Proteins c-akt, HeLa Cells, Signal Transduction, Biotechnology, medicine.drug
الوصف: Cervical cancer is one of the most fatal malignancies in females. Acquired resistance to chemotherapeutic agent is one reason behind this lethality. In this study, we developed cisplatin resistance cell line, subsequently examined the molecular mechanisms linked. Transcriptome sequencing technology was utilized to compare the various expression models between the cisplatin-resistant cell line (Hela/DDP) and its parental cell line human cervical adenocarcinoma Hela. The present study has identified 2,312 differentially expressed genes (DEGs). Results showed there were 1,437 up-regulated genes and 875 down-regulated ones. Databases analysis including Gene ontology (GO), Cluster of Orthologous Groups of proteins (COG) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway were performed to reveal potential molecular mechanisms. We studied AKT3, a crucial gene in the PI3K/AKT pathway which clustered the most DEGs. Silencing AKT3 in Hela/DDP could enhance its sensibility to cisplatin. Quantitative real-time reverse transcription PCR (qRT-PCR) and western blot experiments were showed that expression of AKT3 was decreased after siRNA interference and inhibitor treatment. CCK-8 experiments showed that low expression of Akt3/pAkt enhanced the sensitivity of drug-resistant cells to cisplatin. Apoptotic analysis demonstrated that inhibition of AKT3 increased the rate of Hela/DDP apoptosis. Our results suggest a novel mechanism by which upregulated expression of AKT3 in cervical cancer may lead to resistance to cisplatin.
تدمد: 2169-141X
2169-1401
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::3bfd3eb7b15419b704c253f44aec61e6Test
https://doi.org/10.1080/21691401.2019.1637882Test
حقوق: OPEN
رقم الانضمام: edsair.doi.dedup.....3bfd3eb7b15419b704c253f44aec61e6
قاعدة البيانات: OpenAIRE