Evidence map›Paper›PMID 41644649›Full record

ArticleScientific reports2026

miR-340 improves the efficiency of p53 gene therapy in metastatic prostate cancer cells through downregulation of MDM2.

Roham Deyhimfar, Mousa Kehtari, Fatemeh Saadatpour, Alireza Nikoofar, Ramin Heshmat, Hamid Arshadi, Hossein Dialameh, Ehsan Arefian, Seyed Mohammad Kazem Aghamir

Abstract read
In one paragraph

Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Roham DeyhimfarDepartment of Stem Cells Technology and Tissue Regeneration, School of Biology, College of Science, University of Tehran, Tehran, Iran.
Mousa KehtariDepartment of Stem Cells Technology and Tissue Regeneration, School of Biology, College of Science, University of Tehran, Tehran, Iran.
Fatemeh SaadatpourDepartment of Microbiology, School of Biology, College of Science, University of Tehran, Tehran, Iran.
Alireza NikoofarDepartment of Radiation Oncology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Ramin HeshmatChronic Diseases Research Center, Endocrinology and Metabolism Population Sciences Institute, Tehran University of Medical Sciences, Tehran, Iran.
Hamid ArshadiPediatric Urology and Regenerative Medicine Research Center, Gene, Cell & Tissue Research Institute, Tehran University of Medical Sciences (TUMS), Tehran, Iran.
Hossein DialamehUrology Research Center, Tehran University of Medical Sciences, Tehran, Iran.
Ehsan ArefianDepartment of Stem Cells Technology and Tissue Regeneration, School of Biology, College of Science, University of Tehran, Tehran, Iran. arefian@ut.ac.ir.
Seyed Mohammad Kazem AghamirUrology Research Center, Tehran University of Medical Sciences, Tehran, Iran. mkaghamir@tums.ac.ir.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite current standard treatments such as chemotherapy, radiotherapy, and hormone therapy, the five-year survival rate for patients with metastatic castration-resistant prostate cancer (mCRPC) remains about 50%. While p53 gene therapy has been widely investigated in cancer research, its clinical efficacy is limited by tumor evasion mechanisms, including the upregulation of p53 negative regulators, such as MDM2. This study aims to evaluate the impact of miR-340-mediated downregulation of MDM2 on the therapeutic efficacy of p53 gene therapy in p53 non-expressing PC3 cells. Lentiviral vectors, produced using HEK293T cells, were employed to generate scramble, miR-340-overexpressing, p53-overexpressing, and co-overexpressing PC3 cells. Quantitative polymerase chain reaction (qPCR) was used to determine the expression of p53, MDM2, p21, VEGF, and miR-340. Cell viability, apoptosis, necrosis, cell cycle alterations, cellular migration, proliferation in 2D/3D culture, and HUVECs’ angiogenic potential were assessed in vitro. Additionally, the efficacy of radiotherapy and docetaxel chemotherapy was evaluated through MTT, flow cytometry, and colony formation assay. miR-340 reduced MDM2 mRNA expression by 66% compared to the scramble control and by 45% compared to p53-overexpressing PC3 cells. miR-340 also decreased MDM2 protein expression by 30% compared to both the scramble control and p53-overexpressing PC3 cells. In PC3 cells co-expressing miR-340 and p53, miR-340 induced a 21-fold increase in p21 mRNA levels and a 58.8% increase in p53 protein expression relative to p53-overexpressing cells. Moreover, miR-340/p53 gene therapy effectively inhibited cell proliferation, migration, and angiogenic potential of PC3 cells, without markedly affecting apoptosis rates. Interestingly, this combined gene therapy substantially enhanced the therapeutic response to radiotherapy and low-dose docetaxel chemotherapy. In conclusion, miR-340 can enhance the efficacy of p53 gene therapy and holds promise for the management of mCRPC.

Indexed as

Genetic TherapyMicroRNAsProstatic NeoplasmsProto-Oncogene Proteins c-mdm2Tumor Suppressor Protein p53ApoptosisCell Line, TumorCell MovementCell ProliferationCell SurvivalDocetaxelDown-RegulationGene Expression Regulation, NeoplasticHEK293 CellsHumansMaleDocetaxelMDM2 protein, humanMicroRNAsMIRN340 microRNA, humanProto-Oncogene Proteins c-mdm2TP53 protein, humanTumor Suppressor Protein p53ApoptosisGene therapyMDM2MiR-340p53Prostate cancer

Identifiers

PMID41644649
PMCPMC12932766

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.