Genomic and proteomic studies have yielded a wealth of novel insights into molecular targets and mechanisms of cancer chemosensitivity and resistance. Donitriptan controlled by six selected miRNAs were divided into four groups according to various functions: apoptosis and proliferation (71 genes), cell cycle (68 genes), DNA damage (26 genes) and DNA repair (59 genes). The expression of a few target genes in SPC-A1/docetaxel and SPC-A1 cells were further confirmed by qRT-PCR and Western blot. Taken together, the identification of microRNA expression profiles in docetaxel-resistant NSCLC cells could provide a better understanding of mechanisms involved in drug sensitivity or resistance, which would be helpful to develop novel strategies for targeted therapies in chemorefractive NSCLC patients. Keywords:microRNA profile, non-small cell lung carcinoma, chemoresistance, docetaxel == Introduction == Non-small cell lung carcinoma (NSCLC) represents the most frequent type of lung cancer, which is one of the most common cancers in the world [1]. NSCLC is composed primarily of adenocarcinoma, squamous cell carcinoma and to a lesser extent large-cell lung cancer. Non-small cell histology accounts for 7080% of lung cancer diagnoses and the disease is generally diagnosed at an advanced stage. Although various treatment options were extensively explored in clinic, it has been Donitriptan proved that systemic chemotherapy can provide improvement in both survival and quality of life for patients with advanced NSCLC [2]. The taxanes (paclitaxel and docetaxel) are novel microtubule-stabilizing brokers, which have become an integral part of several commonly used chemotherapy regimens in NSCLC [3]. However, the development of intrinsic or acquired resistance FZD3 to taxanes remains the greatest obstacle to the successful treatment of NSCLC patients. Therefore, it is needed to identify and understand the diverse mechanisms of chemoresistance so as to develop effective strategies to overcome the docetaxel resistance of NSCLC. Genomic and proteomic studies have yielded a wealth of novel insights into molecular targets and mechanisms of cancer chemosensitivity and resistance. Up to now, a number of mechanisms of resistance to antimicrotubule brokers have been described, including the multidrug resistance gene, oncoprotein 18 (stathmin) gene, mitotic serine/threonine kinases (Aurora-A), inhibitors of apoptosis protein (survivin), alteration in tubulin dynamics and differences in -tubulin isotype expression [49]. However, the mechanism of docetaxel resistance is very complicated and still unclear, so it needs to be further elucidated. The changes of chemoresistant gene expression include DNA, mRNA and protein levels, but the levels of mRNA and the encoded proteins are often not proportional, which can have a number of causes, among them, post-transcriptional regulation by microRNAs (miRNAs). miRNAs are small non-coding RNAs of 21 to 25 nucleotides that negatively modulate protein expression [10]. miRNAs are involved in several biological Donitriptan processes, such as development, proliferation, apoptosis and differentiation [11,12]. Moreover, many studies have shown that aberrant microRNA expression is usually correlated with malignant transformation and tumour development [13,14]. Thus, we exhibited that miRNAs might play important functions in mediating chemosensitivity and resistance of human tumours. In order to identify miRNAs and determine their functions in mediating docetaxel resistance in NSCLC, we employed a microRNA array to detect a distinctive miRNA expression pattern of docetaxel-resistant NSCLC cell line (SPC-A1/docetaxel) different from that of docetaxel-sensitive NSCLC cell line (SPC-A1). Then, we employed bioinformatics methods for the analysis of miRNA expression arrays to find Donitriptan the target genes regulated by miRNAs, and further analyse their functions associated with chemoresistance of tumours. The expression of a few target genes were chosen to be confirmed by quantitative real-time RT-PCR (qRT-PCR) and Western blot assays..