ABSTRACT
Despite significant advances in our understanding of the molecular basis of pain, the precise contributions of individual genes to our perception of this primal sensation remains incomplete. However, transcriptomic studies - providing a snapshot of the mRNA expression of a given cell or tissue - have considerably increased insight into the gene expression fingerprint of specific sensory neuronal subtypes, as well as gene expression changes that occur in diverse pathologies associated with pain. Moreover, transcriptomic studies have accelerated the identification of venom-derived peptides that may provide novel leads for the development of analgesics. This review discusses some of the key techniques, insights and limitations of transcriptomic studies that have contributed to pain research and highlights how the application of transcriptomics can be used to accelerate analgesic venom peptide drug discovery.
Subject(s)
Gene Expression Profiling , Pain/etiology , Research , Transcriptome , Animals , Biotechnology/methods , Computational Biology/methods , Drug Discovery , Gene Expression Profiling/methods , Humans , Organ Specificity/genetics , Pain/metabolism , Peptides/chemistry , Peptides/pharmacology , Proteomics/methodsABSTRACT
Abstract Breast cancer is the most prominent cause of cancer-related deaths among women worldwide. It has been found that genetic mutations play distinct roles in the onset and progression of breast cancer. Androgenic, beta, receptor kinase 1 (ADRBK1) has been reported to possess oncogenic characteristics vital for cancer cell viability. This study was designed to investigate the effects of small interference RNA (si-RNA)-mediated ADRBK1 knockdown on breast cancer cell growth in vitro. High-expression levels of ADRBK1 were observed in all tested breast cancer cell lines (MDA-MB-231, MCF-7, T-47D, and BT-474). ADRBK1 si-RNA was delivered to breast cancer cells using lentivirus delivery system. Depletion of ADRBK1 significantly attenuated the cell viability and colony-formation ability. Flow cytometry analysis further demonstrated that ADRBK1 silencing led to MDA-MB-231 cell arrest in the G0/G1 phase. Collectively, these results indicate that knockdown of ADRBK1 gene has detrimental effects on breast cancer cell growth, which may be a potential therapeutic approach for the treatment of breast cancer.
