ArticleOncotarget2017
MicroRNA-1908-5p contributes to the oncogenic function of the splicing factor SRSF3.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 36 citations in OpenAlex.
- The role of splicing factor SRSF3 in cancer progression: Mechanisms, biomarkers, and therapeutic implications.Translational oncology · 2026Review
- c-Ski is a novel repressor of NF-κB through interaction with p65 and HDAC1 in U937 cells.Cell communication and signaling : CCS · 2025Article
- Analysis of different expression RNA binding protein genes in mouse microglia cell from the brains of mice 72 h after subarachnoid hemorrhage or sham operation.BMC medical genomics · 2024Article
- Oncogenic SRSF3 in health and diseases.International journal of biological sciences · 2023Review
- Splicing factor SRSF3 represses translation of p21Cell death & disease · 2022Article
- miR-1908: a microRNA with diverse functions in cancers and non-malignant conditions.Cancer cell international · 2022Review
- Biological function and molecular mechanism of SRSF3 in cancer and beyond.Oncology letters · 2022Review
- miR-1908 Dysregulation in Human Cancers.Frontiers in oncology · 2022Review
- Therapeutic Targeting of Alternative Splicing: A New Frontier in Cancer Treatment.Frontiers in oncology · 2022Review
- miR1908-5p regulates energy homeostasis in hepatocyte models.Scientific reports · 2021Article
- Extracellular microRNA profiling for prognostic prediction in patients with high-grade serous ovarian carcinoma.Cancer science · 2021Article
- Pan-Cancer Analysis Reveals Common and Specific Relationships between Intragenic miRNAs and Their Host Genes.Biomedicines · 2021Article
- Article
- Emerging Roles of SRSF3 as a Therapeutic Target for Cancer.Frontiers in oncology · 2020Review
- miRNA signatures in childhood sarcomas and their clinical implications.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2019Review
- Degradation of splicing factor SRSF3 contributes to progressive liver disease.The Journal of clinical investigation · 2019Article
- Improved survival prognostication of node-positive malignant melanoma patients utilizing shotgun proteomics guided by histopathological characterization and genomic data.Scientific reports · 2019Article
- Let-7b acts as a tumor suppressor in osteosarcoma via targeting IGF1R.Oncology letters · 2019Article
- Interplay between miRNAs and host genes and their role in cancer.Briefings in functional genomics · 2018Review
- Inhibition of the expression of oncogene SRSF3 by blocking an exonic splicing suppressor with antisense oligonucleotides.RSC advances · 2018Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Serine/arginine (SR)-rich proteins that contain RS domains and SR repeats have diverse cellular functions including transcription, polyadenylation, translation, and RNA export. The splicing factor SRSF3, also termed SRp20, is the smallest member of the SR protein family and is a known proto-oncogene. Although it is implicated in the malignant phenotypes of various cancer cells, the molecular mechanism underlying SRSF3-mediated cancer progression is still obscure. We investigated here the oncogenic functions of SRSF3 in osteosarcoma U2OS cells. Knockdown of SRSF3 inhibited proliferation, clonogenicity, and metastatic potential including migration and invasion. It also decreased the level of miR-1908 independent of its host gene FADS1. Although FADS1 was not associated with SRSF3-mediated malignant properties, overexpression of miR-1908-5p increased cell proliferation, migration, and invasion, suggesting that miR-1908-5p is responsible for the oncogenic functions of SRSF3. Knockdown of SRSF3 decreased the expression of miR-1908-5p by inhibiting transactivation of NF-κB. We observed that miR-1908-5p downregulated NF-κB inhibitor interacting Ras-like 2 (NKIRAS2), a negative regulator of the NF-κB pathway by directly binding to the 3'UTR of NKIRAS2 mRNA. Consistent with overexpression of miR-1908-5p, knockdown of NKIRAS2 diminished the expression level of IκB-β and provoked translocation of NF-κB into the nucleus where it transcriptionally activates its target genes including miR-1908-5p expression, thus elevating the proliferation and metastatic potential. Taken together, our results demonstrate that SRSF3 confers the malignant characteristics on cancer cells via the SRSF3/miR-1908-5p/NKIRAS2 axis.
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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.