ArticleInternational journal of clinical and experimental pathology2017
Overexpression of miR-96 promotes cell proliferation by targeting FOXF2 in prostate cancer.
Article in International journal of clinical and experimental pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
What it found
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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
4 citing papers in PubMed, 1 synthesis or guideline pooled it, 5 citations in OpenAlex.
- Role of the Forkhead box family protein FOXF2 in the progression of solid tumor: systematic review.Journal of cancer research and clinical oncology · 2024Pooled it
- A review on the role of cyclin dependent kinases in cancers.Cancer cell international · 2022Review
- MicroRNA-96: A therapeutic and diagnostic tumor marker.Iranian journal of basic medical sciences · 2022Review
- FOXF2 Regulates PRUNE2 Transcription in the Pathogenesis of Colorectal Cancer.Technology in cancer research & treatmentArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prostate cancer (PC) is one of the most common cancers in males. MicroRNAs (miRNAs) are demonstrated to be involved in prostate cancer development and progression. Recently, miR-96 was identified to play a tumor promoting role in several tumors including PC, however, the underlying function of miR-96 in PC still need to be known. In the study, our results demonstrated that miR-96 was higher in prostate cancer tissues compared with adjacent normal tissues. Higher miR-96 was association with higher PSA level, lymph node metastasis, pathologic stage and distant metastasis in prostate cancer patients. Lose-of-function studies showed that down-regulated expression of miR-96 inhibited cell proliferation and cell cycle by regulating down-regulating CyclinA1, CDK2 and CDK4 expression in PC cells. Furthermore, we found that FOXF2 was a target of miR-96 in PC cells and miR-96 promoted cell proliferation by suppressing FOXF2 expression. Thus, these results showed that inhibition of miR-96 may be a target for prostate cancer treatment.
Indexed as
Identifiers
31966604PMC6965223W3028505692What 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.