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Splicing factor SF3B1 promotes endometrial cancer progression via regulating KSR2 RNA maturation

ABSTRACT: The goal of this study is to compare transcriptome profiling of SF3B1 depleted Ishikawa endometrial cancer cells by RNA-sequencing Methods: SF3B1 depleted mRNA profiles of control siRNA treated and SF3B1 siRNA treated Ishikawa endometrial cancer cells were generated by deep sequencing, in triplicate using Illumina HiSeq 3000 sequencers with 2×150 paired-end reads. Basecalls and demultiplexing were performed with Illumina’s RTA version 1.9 and bcl2fastq2 software with a maximum of one mismatch in the indexing read. RNA-seq reads were then aligned to the Ensembl release 76 primary assembly with STAR version 2.0.4b. qRT–PCR validation was performed using TaqMan assays Results: Using a 2.5-fold cutoff and Benjamini-Hochberg false discovery rate (FDR) of <0.01 threshold for inclusion, we identified 1,992 differentially expressed genes (DEGs) between Control and SF3B1 depleted Ishikawa cells Conclusions: Our study represents the first detailed analysis of SF3B1 depleted Ishikawa endometrial cancer cells transcriptomes, with biologic replicates, generated by RNA-seq technology.

ORGANISM(S): Homo sapiens

PROVIDER: GSE156775 | GEO | 2020/12/30

REPOSITORIES: GEO

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Project description:Endometrial cancer is the most commonly diagnosed gynecologic malignancy in women after breast, lung and colorectal cancer. Despite numerous scientific advances, the incidence and mortality rate of endometrial cancer is on the rise. Considerable research effort has therefore been placed on understanding the pathogenesis of this disease to combat this growing issue. There is now emerging evidence to suggest a putative role for dysregulation of the renin angiotensin system (RAS) and in particular the (pro)renin receptor ((P)RR), in the ontogenesis of endometrial cancer. Support for this notion arises from previous literature implicating (P)RR in cancer pathophysiology (e.g., breast cancer and pancreatic carcinoma) by virtue of its role in proliferation, angiogenesis, fibrosis, migration and invasion. In view of these data, we aimed to investigate the functional role of (P)RR in human endometrial cancer progression and development. To this end, we employed an siRNA-mediated knock down approach to abrogate (P)RR expression in the immortalized endometrial epithelial cell lines; Ishikawa, AN3CA and HEC-1A to explore the role of (P)RR in cellular proliferation and cellular viability. To further extend these analyses we also carried out a sophisticated proteomic screen, that investigated the potential pathways via which (P)RR is acting in endometrial cancer physiology. These data confirmed that (P)RR is critical for endometrial cell cancer development, contributing to both its proliferative capacity and in the maintenance cell viability. This is likely mediated through proteins such as MGA, SLC4A7, SLC7A11 or DHRS2, which were reduced following (P)RR knockdown. These putative protein interactions/pathways, which rely on the presence of (P)RR, are likely to contribute to endometrial cancer progression and could therefore, represent several novel therapeutic targets in the treatment of this cancer. Finally we contend that (P)RR, in its soluble form (s(P)RR) in blood, may have substantial potential as a novel biomarker for cancer diagnosis and prognosis prediction going forward.

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Splicing factor SF3B1 promotes endometrial cancer progression via regulating KSR2 RNA maturation

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