Differential Impacts of Alternative Splicing Networks on Apoptosis

Abstract

Apoptosis functions as a common mechanism to eliminate unnecessary or damaged cells during cell renewal and tissue development in multicellular organisms. More than 200 proteins constitute complex networks involved in apoptotic regulation. Imbalanced expressions of apoptosis-related factors frequently lead to malignant diseases. The biological functions of several apoptotic factors are manipulated through alternative splicing mechanisms which expand gene diversity by generating discrete variants from one messenger RNA precursor. It is widely observed that alternatively-spliced variants encoded from apoptosis-related genes exhibit differential effects on apoptotic regulation. Alternative splicing events are meticulously regulated by the interplay between trans-splicing factors and cis-responsive elements surrounding the regulated exons. The major focus of this review is to highlight recent studies that illustrate the influences of alternative splicing networks on apoptotic regulation which participates in diverse cellular processes and diseases.

RNA splicing alteration in the response to platinum chemotherapy in ovarian cancer: A possible biomarker and therapeutic target

“…The fact that AS strongly regulates apoptosis is well established and has been recently reviewed. 93,94 It is known that DNA damage, including the ones induced by PT, mainly activates the intrinsic apoptotic pathway, initiated by mitochondrial permeabilization and leading to caspase activation, principally through the activity of caspase-8 and -9. (also known as p47 and DeltaNp53) is an N-terminal truncation of full-length p53 that lacks the first transcriptional activation domain (TAD1).…”

Splicing isoform-specific functional genomic in cancer cells

“…Although there is example of splicing isoforms promoting each hallmark of cancer [13,63,64], the phenotype of a [65,66].…”

Comprehensive analysis of alternative splicing and transcriptome related to the prognosis of cervical squamous cell cancer

“…There are seven types of alternative splicing pattern, that is, mutually exclusive exons (ME), retained intron (RI), alternate donor site (AD), alternate acceptor site (AA), alternate promotor (AP), alternate terminator (AT) and exon skip (ES) [11]. Under the physiological condition, AS plays a vitally important regulating effect in the process of development, tissue identity, differentiation, cell-to-cell communication, cell senescence and apoptosis [12][13][14]. AS is accurately regulated by extensive splicing factors which participate in the precise selection of splicing sites and subsequent splicing events [15].…”