ArticleInternational journal of immunopathology and pharmacology
Triptolide inhibits benign prostatic epithelium viability and migration and induces apoptosis via upregulation of microRNA-218.
Article in International journal of immunopathology and pharmacology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 1 paper.
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
1 citing paper in PubMed, 5 citations in OpenAlex.
- MicroRNAs as crucial mediators in the pharmacological activities of triptolide (Review).Experimental and therapeutic medicine · 2021Review
Corrections and comments
- Retraction · 2021-09-02Duplication of Data · Duplication of/in Image · Investigation by Journal/Publisher · Investigation by Third Party · Manipulation of Images · Paper Mill · Unreliable Results and/or Conclusions · Upgrade/Update of Prior Notice(s) ·
- Expression of concern · 2021-02-24Concerns/Issues about Data · Concerns/Issues about Image · Concerns/Issues about Results and/or Conclusions · Investigation by Journal/Publisher · Investigation by Third Party · Paper Mill · Updated to Retraction ·
- Expression of concern
- Retracted
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Benign prostatic hypertrophy (BPH) has become a troublesome disease for elder men. Triptolide (TPL) has been reported to be a potential anticancer agent. However, the potential effects of TPL on BPH have not been shown out. BPH-1 cells were treated with different concentrations of TPL and/or transfected with microRNA-218 (miR-218) inhibitor, pc-survivin, sh-survivin, or their corresponding controls (NC). Thereafter, cell viability was determined by CCK-8 assay. Cell migration was accessed by modified two-chamber migration assay. Cell apoptosis was checked by propidium iodide (PI) and fluorescein isothiocyanate (FITC)-conjugated Annexin V staining. In addition, messenger RNA (mRNA) and protein levels were detected using quantitative real-time polymerase chain reaction (qRT-PCR) and western blot analysis, respectively. BPH-1 cell viability and migration were significantly decreased, while cell apoptosis and expression of miR-218 were statistically enhanced by TPL ( P < 0.05 or P < 0.01). However, downregulation of miR-218 increased cell viability and migration, while decreased cell apoptosis compared with the negative control group ( P < 0.05 or P < 0.01). Furthermore, the expression of cell cycle-related proteins and cell apoptosis-related proteins were also led to the opposite results with NC. In addition, we found that miR-218 negatively regulated the expression of survivin ( P < 0.01) and suppression of survivin significantly enhanced cell apoptosis ( P < 0.01). Moreover, the results demonstrated that TPL could inactivate mammalian target of rapamycin (mTOR) pathway, while inhibition of miR-218 alleviated the effects. TPL inhibits viability and migration of BPH-1 cells and induces cell apoptosis and also inactivates mTOR signal pathway via upregulation of miR-218. This study provides evidence for the further studies representing triptolide as a potential agent in the treatment of human BPH.
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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 Socratic graph.