Most
genes are processed by
alternative splicing for
gene expression, resulting in the complexity of the
transcriptome in
eukaryotes. It allows a limited number of
genes to encode various
proteins with intricate functions.
Alternative splicing is regulated by genetic
mutations in cis-regulatory factors and
epigenetic events. Furthermore, splicing events occur differently according to
cell type, developmental stage, and various
diseases, including
cancer.
Genome instability and flexible
proteomes by
alternative splicing could
affect cancer cells to grow and survive, leading to
metastasis.
Cancer cells that are transformed by aberrant and uncontrolled mechanisms could produce
alternative splicing to maintain and spread them continuously. Splicing variants in various
cancers represent crucial
roles for
tumorigenesis. Taken together, the identification of alternative spliced variants as
biomarkers to distinguish between normal and
cancer cells could cast
light on
tumorigenesis.