Transcriptional Plasticity - Enhancing Molecular Diversity in a Cell Through Chimeric Transcripts

Spontaneous and inheritable genetic changes have a steadfast association with cancer. It is realized that flexibility within the regulatory mechanisms of transcription and translation can also create diverse landscapes of expression from a limited number of genes.  Within this scope, perturbed cellular functions through epigenetically altered chromatin structure affects transcription - translation kinetics leading to consequent generation of non-canonical and non-coding RNA through alternative/back splicing, RNA recombination, read-through mechanisms result in altered transcripts and proteins. Differential splicing within same gene or between different genes leads to formation of novel variants or chimeric transcripts respectively, which can generate either a complex proteome or non-coding RNAs that further influences cellular transformation. Formation of chimeric/novel transcripts is increasingly found to associated with tumorigenesis, and will provide us a new facet of cellular regulatory processes. In general transcriptome variation which is commonly been found in different cancers contribute to tumor progression. Such transcriptome alterations are also evident at the protein level which ultimately defines functional capacity of cells. Our studies on chimeric transcripts in ovarian cancer thus will provide a novel approach to understanding such transcriptional plasticity.