Project description:Knockdown LRRK1-CAPT in NCI-H1299 lung cancer cell line by two independent siRNAs, to investigate the mechanism of LRRK1-CAPT in regulation of cell proliferation.
Project description:MiR-138 has a variety of biological functions because of its capacity to act on different target genes in various cells and tissues; however, the targets of miR-138 in human non-small cell lung cancer cell line H1299 cannot be determined by bioinformatics alone. Thus, H1299 cells overexpressing miR-138 in H1299 cells were subjected to microarray analysis to analyse the differences of gene expression.
Project description:Lung cancer is the leading cause of cancer-related mortality. The two main lung cancer types are small cell lung cancer (SCLC) and non-SCLC (NSCLC), where NSCLC comprises about 80-85% of all lung cancer. Despite the introduction of improved treatments, the overall survival rate of lung cancer patients remains low. Further elucidation of the regulatory network perturbations between cancer-related genes and proteins is one promising route to alter this mortality trend. The deregulation of the DNA replication, cell cycle, proliferation and migration are the common factors that are involved in cancer development and progression, and therefore logical targets for analysis. Minichromosome maintenance 2(MCM2) is a DNA replication licensing factor, which belongs to the heterohexameric MCM2-7 complex. MCM2 has been proposed as an excellent proliferation marker in many types of cancer. Our study will establish a global functional distribution of identified proteins in silenced-MCM2 in H1299 NSCLC by the means of iTRAQ. Understanding the molecular basis of MCM2 in lung cancer cells enables us to discover alternative target for lung cancer therapy.
Project description:Non-small cell lung cancer (NSCLC) patients are prone to drug resistance during chemotherapy. Therefore, in order to compare the changes in the gene expression profiles of NSCLC cells before and after drug resistance, we constructed cisplatin-resistant cells (NCI-H1299/CDDP), and compared the gene expression profiles with those of the parental NCI-H1299 cells. We used microarrays to study in detail the global gene expression changes before and after drug resistance in NSCLC cells and identified genes that were up- or down-regulated during this process.
Project description:The functions of EGR1, a multifunctional transcription factor, in prostate cancer are well documented. However, little is known about the functions of EGR1 in lung cancer. we observed the function of EGR1 in non-small cell lung carcinoma (NSCLC) and identified the genes that influence cell fate and tumor development. We used microarrays to detail the global programme of gene expression and identified genes differentially expressed when EGR1-overexpressed. We have demonstrated that EGR1 is able to increase cell apoptosis, and inhibit metastasis. And we sought to find genes distributed to decrease the malignancy of human non-small cell lung cancer regulated by EGR1. To that end, H1299 cells were transfected either EGR1 or pcDNA3.1. After 48h, cells were collected for RNA extraction and hybridization on Affymetrix microarrays (PEGR1 VS PCDNA3.1).
Project description:eIF3 is the largest translation initiation factor in mammalian cells, consisting of 13 subunits. This translation initiation factor is involved in multiple processes of protein translation in cells, including translation initiation, termination, and ribosome recycling. Several studies have reported that multiple subunits of eIF3 exhibit abnormal expression in tumor cells and play an important role in the occurrence and development of tumors. In this study, it was found that changes in the expression level of EIF3G significantly affected the growth of non-small cell lung cancer. Knockdown of EIF3G inhibited the intracellular protein translation process of non-small cell lung cancer cells H1299. Through the study of translatome, it was found that knockdown of EIF3G significantly affected the cell cycle processes in H1299 cells. In vitro cell experiments also showed that changes in the expression level of EIF3G influences the cell cycle distribution of H1299 cells. This study is the first to explore the impact of knockdown of EIF3G on the translatome of H1299 cells.
Project description:Analysis NCI-H1299 lung cancer cells transfected with synthetic oligo mimics for microRNAs (miRNAs) miR-34a and ghR-34a. We developed a 30-nucleotide single-strand RNA (ssRNA), termed “guide hairpin RNA (ghR),” that has a physiological function similar to that of miRNA and siRNA. The ghR caused no innate cytokine response either in vitro or in vivo. In addition, its structure does not contain a passenger strand seed sequence, reducing the potential for off-target effects relative to existing short RNA reagents. Systemic injection of ghR-form miR-34a (ghR-34a) suppressed tumor growth in a mouse model of RAS-induced lung cancer. Furthermore, ghR-34a functioned in a Dicer- and Ago2-independent manner. This novel RNAi technology may provide a novel, safe, and effective nucleic acid drug platform that will increase the clinical usefulness of nucleic acid therapy. MiR-34a–targeted mRNAs regulated by mRNA degradation rather than translational inhibition were identified using microarray data from miR-34 and ghR-34a transfectants.
Project description:Purpose: To study the effect of hyperoxia on lung cancer cells, H1299 cells were cultured in 60% O2 for 12 h and 24 h, and RNA-seq was performed.
Project description:The expression of the forkhead transcription factor CHES1, also known as FOXN3, is reduced in many types of cancers. In vitro, CHES1 expression suppresses cell proliferation in tumor cell lines but not in normal cells. Conversely shRNA-mediated depletion of CHES1 increases tumor cell proliferation. We used microarrays to characterize the gene expression changes induced by CHES1 in H1299 cancer cells H1299 cells were infected with a retroviral vector that expresses CHES1 or an empty vector. After 5 days of infection, RNA was extracted from three independent replicas of each condition. Total RNA was send to Genome Quebec service for hybridization with Affymetrix microarrays.