Arjama Roy, Amity University Kolkata
Endometrial cancer is the foremost common type of cancer that affects the feminine reproductive tract. It grows rapidly and tends to spread to other parts of the body. Earlier, the causative agent of endometrial carcinoma wasn’t known aside from the transcriptional effects of steroid hormones. As a result of which limited therapeutic options were provided to the diagnosed women. Recent work reveals that dysregulation of splicing factors can cause the generation of abnormal mature transcripts which drive tumorigenesis.
The study published within the Nature journal researchers stated that splicing factor- SF3B1, plays a vital role in carcinoma pathological progression. SF3B1 is one amongst the frequently mutated splicing factors in endometrium cancer. it’s a core component of the U2 nuclear ribonucleoprotein, which distinguishes the 3′ splice site at intron-exon junctions. SF3B1 appears to act as an oncogene in endometrial carcinoma as most of the mutation occurs in the hotspot. employing a tissue microarray, it’s found that endometrial tumours express more SF3B1 protein than non-cancerous tissues. Furthermore, SF3B1 is required for carcinoma cell proliferation, cell cycle progression. it’s also required for tumour cell migration and invasion. Furthermore, SF3B1 inhibitor Pladienolide-B reduces endometrial carcinoma cell proliferation, migration, and invasion in vitro. It also inhibits tumour growth in vivo.
Alternative splicing events analysis revealed that SF3B1 depletion led to an alteration in many different splicing events. The analysis showed that KSR2 can likely candidate for SF3B1 facilitated functions in carcinoma. Researchers discovered that releasing of the KSR2 expression with SF3B1 knockdown partially restored the cell growth of carcinoma cells.
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Source: Popli, P., Richters, M.M., Chadchan, S.B. et al. Splicing factor SF3B1 promotes endometrial cancer progression via regulating KSR2 RNA maturation. Cell Death Dis 11, 842 (2020). https://doi.org/10.1038/s41419-020-03055-y. D.O.I-http://10.1038/s41419-020-03055-y.
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