ArticleCell death & disease2020
Splicing factor SF3B1 promotes endometrial cancer progression via regulating KSR2 RNA maturation.
Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
42 citing papers in PubMed, 84 citations in OpenAlex.
- NCBP2 Regulates PGAM5-Mediated Mitophagy Via KIF23 Alternative Splicing To Promote Cervical Cancer ProgressionRun Title: NCBP2 Promotes Cervical Cancer Via Mitophagy.Applied biochemistry and biotechnology · 2026Article
- Integrative CRISPR Screening and RNA Analyses Discover an Essential Role for PUF60 Interactions with 3' Splice Sites in Cancer Progression.Cancer research · 2026Article
- Unveiling Alternative Splicing in HPV-Negative HNSCC: Links to Tumorigenesis and Immune Landscape.International dental journal · 2026Article
- Novel transcriptomic alterations in poorly differentiated endometrial carcinomas: evidence from South African women.Frontiers in oncology · 2026Article
- A Bioinformatics Analysis on the Subtypes of Hepatocellular Carcinoma Related to RNA Processing Genes to Reveal Prognosis and Immune Microenvironment Features.Digestive diseases and sciences · 2025Article
- An SpC editor targeting pre-mRNA splicing for precise CRISPR control and enhanced antitumor efficacy.Nucleic acids research · 2025Article
- CK1α in Sertoli cells is essential for testicular development and spermatogenesis in mice.Zoological research · 2025Article
- TTK promotes mitophagy by regulating ULK1 phosphorylation and pre-mRNA splicing to inhibit mitochondrial apoptosis in bladder cancer.Cell death and differentiation · 2025Article
- DDX42 Enhances Hepatocellular Carcinoma Cell Proliferation, Radiation and Sorafenib Resistance via Regulating GRB2 RNA Maturation and Activating PI3K/AKT Pathway.Journal of cellular and molecular medicine · 2025Article
- The potential impact of RNA splicing abnormalities on immune regulation in endometrial cancer.Cell death & disease · 2025Review
- Targeting the splicing factor SNRPB inhibits endometrial cancer progression by retaining the POLD1 intron.Experimental & molecular medicine · 2025Article
- Insulin-like Growth Factor 1 (IGF1) and Its Isoforms: Insights into the Mechanisms of Endometrial Cancer.Cancers · 2025Review
- YY1 drives PARP1 expression essential for PARylation of NONO in mRNA maturation during neuroblastoma progression.Journal of translational medicine · 2024Article
- A Contrastive-Learning-Based Deep Neural Network for Cancer Subtyping by Integrating Multi-Omics Data.Interdisciplinary sciences, computational life sciences · 2024Article
- Alternative splicing in ovarian cancer.Cell communication and signaling : CCS · 2024Review
- The splicing factor SF3B1 confers ferroptosis resistance and promotes lung adenocarcinoma progression via upregulation of SLC7A11.Cancer gene therapy · 2024Article
- Genome-Wide Methylation Profiling of Peripheral T-Cell Lymphomas Identifies TRIP13 as a Critical Driver of Tumor Proliferation and Survival.Epigenomes · 2024Article
- Assessing the Methylation Status of Two Potential Key Factors Involved in Cervical Oncogenesis.Reports (MDPI) · 2024Article
- Article
- LINC00460-FUS-MYC feedback loop drives breast cancer metastasis and doxorubicin resistance.Oncogene · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Although endometrial cancer is the most common cancer of the female reproductive tract, we have little understanding of what controls endometrial cancer beyond the transcriptional effects of steroid hormones such as estrogen. As a result, we have limited therapeutic options for the ~62,000 women diagnosed with endometrial cancer each year in the United States. Here, in an attempt to identify new prognostic and therapeutic targets, we focused on a new area for this cancer-alternative mRNA splicing-and investigated whether splicing factor, SF3B1, plays an important role in endometrial cancer pathogenesis. Using a tissue microarray, we found that human endometrial tumors expressed more SF3B1 protein than non-cancerous tissues. Furthermore, SF3B1 knockdown reduced in vitro proliferation, migration, and invasion of the endometrial cancer cell lines Ishikawa and AN3CA. Similarly, the SF3B1 inhibitor, Pladienolide-B (PLAD-B), reduced the Ishikawa and AN3CA cell proliferation and invasion in vitro. Moreover, PLAD-B reduced tumor growth in an orthotopic endometrial cancer mouse model. Using RNA-Seq approach, we identified ~2000 differentially expressed genes (DEGs) with SF3B1 knockdown in endometrial cancer cells. Additionally, alternative splicing (AS) events analysis revealed that SF3B1 depletion led to alteration in multiple categories of AS events including alternative exon skipping (ES), transcript start site usage (TSS), and transcript termination site (TTS) usage. Subsequently, bioinformatics analysis showed KSR2 as a potential candidate for SF3B1-mediated functions in endometrial cancer. Specifically, loss of SF3B1 led to decrease in KSR2 expression, owing to reduced maturation of KSR2 pre-mRNA to a mature RNA. Importantly, we found rescuing the KSR2 expression with SF3B1 knockdown partially restored the cell growth of endometrial cancer cells. Taken together, our data suggest that SF3B1 plays a crucial oncogenic role in the tumorigenesis of endometrial cancer and hence may support the development of SF3B1 inhibitors to treat this disease.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.