ArticleMolecular medicine reports2017
miR‑30c suppresses prostate cancer survival by targeting the ASF/SF2 splicing factor oncoprotein.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 27 citations in OpenAlex.
- Prognostic alternative mRNA splicing signature and immune infiltration in prostate cancer.Journal of applied genetics · 2026Article
- Alternative splicing impacts microRNA regulation within coding regions.NAR genomics and bioinformatics · 2023Article
- Deregulated microRNAs Involved in Prostate Cancer Aggressiveness and Treatment Resistance Mechanisms.Cancers · 2023Review
- The interplay between non-coding RNAs and alternative splicing: from regulatory mechanism to therapeutic implications in cancer.Theranostics · 2023Review
- Lidocaine represses proliferation and cisplatin resistance in cutaneous squamous cell carcinomaBioengineered · 2022Article
- Alternative Splicing, Epigenetic Modifications and Cancer: A Dangerous Triangle, or a Hopeful One?Cancers · 2022Review
- SRSF1 acts as an IFN-I-regulated cellular dependency factor decisively affecting HIV-1 post-integration steps.Frontiers in immunology · 2022Article
- Article
- Noncoding RNAs regulate alternative splicing in Cancer.Journal of experimental & clinical cancer research : CR · 2021Review
- E2F7, regulated by miR‑30c, inhibits apoptosis and promotes cell cycle of prostate cancer cells.Oncology reports · 2020Article
- A Novel Predictor Tool of Biochemical Recurrence after Radical Prostatectomy Based on a Five-MicroRNA Tissue Signature.Cancers · 2019Article
- miR‑505 suppresses prostate cancer progression by targeting NRCAM.Oncology reports · 2019Article
- miR-30c Impedes Glioblastoma Cell Proliferation and Migration by Targeting SOX9.Oncology research · 2019Article
- MicroRNA-30e inhibits adhesion, migration, invasion and cell cycle progression of prostate cancer cells via inhibition of the activation of the MAPK signaling pathway by downregulating CHRM3.International journal of oncology · 2019Article
- Non-Coding RNAs in Breast Cancer: Intracellular and Intercellular Communication.Non-coding RNA · 2018Review
- Disruption by SaCas9 Endonuclease of HERV-KViruses · 2018Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Our previous study revealed that microRNA (miR) ‑30c represents a potential tumor suppressor gene, the expression of which is associated with decreased oncogenic potential in prostate cancer (PCa) cell lines. However, the functional role and underlying mechanisms of miR‑30c in PCa remain to be fully elucidated. Reverse transcription‑quantitative polymerase chain reaction and immunohistochemical analysis were used to detect the expression levels of alternative splicing factor/splicing factor 2 (ASF/SF2) in PCa tissues. A luciferase reporter assay was used to investigate whether ASF/SF2 may be a direct target gene of miR‑30c. In addition, the effects of miR‑30c on the proliferation and apoptosis of PCa cell lines were examined, following transfection with miR‑30c mimics. Furthermore, correlation analysis was performed to investigate the relationship between the expression of miR‑30c and ASF/SF2 and various clinicopathological parameters of patients with PCa. The present results demonstrated that PCa tissues exhibited higher levels of alternative splicing factor/splicing factor 2 (ASF/SF2), compared with normal tissues. In addition, miR‑30c was revealed to targete the 3'‑untranslated region of the ASF/SF2 gene, causing a decrease in the mRNA and protein levels of ASF/SF2. Furthermore, miR‑30c was reported to decrease cell proliferation, increase the percentage of cells in the G1 cell cycle phase, and promote apoptosis through the inhibition of ASF/SF2. Following correlation analysis using patient samples, the expression of ASF/SF2 was revealed to be tightly correlated with the pathological stage of PCa and biochemical recurrence (BCR). In addition, patients with PCa exhibiting low expression levels of miR‑30c and high expression of ASF/SF2 had significantly lower rates of BCR‑free survival. In conclusion, the present study suggested that the tumor suppressor miR‑30c may be involved in PCa tumorigenesis, possibly via targeting ASF/SF2. The combined analysis of the expression of ASF/SF2 and miR‑30c may be a valuable tool for early prediction of BCR in patients with PCa following radical prostatectomy.
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