Serine and arginine-rich splicing factor 1 mRNA (SRSF1 mRNA)

Serine and arginine-rich splicing factor 1 (SRSF1) mRNA is the transcript encoding the archetype member of the SR protein family, which serves as a master regulator of RNA metabolism. The SRSF1 protein is essential for both constitutive and alternative splicing, and it also plays critical roles in mRNA nuclear export, stability, and translation [1][5][6]. As a potent proto-oncogene, SRSF1 is frequently overexpressed in various malignancies—including breast, lung, and colon cancers—where it promotes the production of pro-survival and pro-proliferative splice variants [3][13]. Beyond oncology, targeting SRSF1 mRNA is being explored in neurodegenerative diseases like ALS and FTD, where reducing SRSF1 levels can inhibit the export of toxic repeat-containing RNAs [7]. Therapeutic strategies targeting the SRSF1 mRNA include antisense oligonucleotides (ASOs) and siRNAs designed to trigger transcript degradation or modulate autoregulatory splicing events [10][12]. Small molecules like SRSF1-IN-1 (STP2) have demonstrated the ability to reduce SRSF1 expression and inhibit tumor growth in preclinical models [4]. However, because SRSF1 is vital for cellular homeostasis and genome integrity, systemic depletion presents significant safety challenges; for instance, its deficiency in the liver has been shown to cause DNA damage and NASH-like pathology [9]. Consequently, therapeutic development often focuses on tissue-specific delivery or moderate modulation to achieve a therapeutic window [2][7].

Other names

ASF mRNASF2 mRNASF2/ASF mRNASFRS1 mRNASplicing factor 2 mRNAAlternative-splicing factor 1 mRNA

Drugs targeting SRSF1 mRNA primarily act through RNase H-mediated degradation (antisense oligonucleotides), RNA interference (siRNA), or by modulating the autoregulation of SRSF1's own alternative splicing to reduce productive transcript levels [7][10]. Small molecules like SRSF1-IN-1 (STP2) are reported to inhibit the expression of the SRSF1 transcript and protein, leading to the restoration of normal splicing patterns for downstream oncogenic targets like Bcl-x [4][11].