Evidence map›Paper›PMID 39791585›Full record

ArticleInvestigative and clinical urology2025

DRG2 levels in prostate cancer cell lines predict response to PARP inhibitor during docetaxel treatment.

Jeong Min Lee, Won Hyeok Lee, Seung Hyeon Cho, Jeong Woo Park, Hyuk Nam Kwon, Ji Hye Kim, Sang Hun Lee, Ji Hyung Yoon, Sungchan Park, Seong Cheol Kim

Abstract read
In one paragraph

Article in Investigative and clinical urology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Article
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

10 authors.

Jeong Min Lee *School of Biological Sciences, University of Ulsan, Ulsan, Korea.ORCID 0000-0001-7563-3089
Won Hyeok Lee *School of Biological Sciences, University of Ulsan, Ulsan, Korea.ORCID 0000-0002-3845-9314
Seung Hyeon ChoSchool of Biological Sciences, University of Ulsan, Ulsan, Korea.ORCID 0009-0009-2701-5281
Jeong Woo ParkSchool of Biological Sciences, University of Ulsan, Ulsan, Korea.ORCID 0000-0002-3355-6908
Hyuk Nam KwonSchool of Biological Sciences, University of Ulsan, Ulsan, Korea.ORCID 0000-0003-4096-4712
Ji Hye KimDepartment of Pathology, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan, Korea.ORCID 0000-0001-7160-8601
Sang Hun LeeBasic-Clinic Convergence Research Institute, University of Ulsan, Ulsan, Korea.ORCID 0000-0002-6907-8143
Ji Hyung YoonBasic-Clinic Convergence Research Institute, University of Ulsan, Ulsan, Korea.ORCID 0000-0001-7307-4359
Sungchan ParkBasic-Clinic Convergence Research Institute, University of Ulsan, Ulsan, Korea.ORCID 0000-0002-2337-983X
Seong Cheol KimBasic-Clinic Convergence Research Institute, University of Ulsan, Ulsan, Korea.ORCID 0000-0003-0228-0037

Funding

NRF NRF-2021R1G1A1093761UUH UUH-2021-03
6 · The paper itself

Abstract

purposeDevelopmentally regulated GTP-binding protein 2 (DRG2) regulates microtubule dynamics and G2/M arrest during docetaxel treatment. Poly ADP-ribose polymerase (PARP) acts as an important repair system for DNA damage caused by docetaxel treatment. This study investigated whether DRG2 expression affects response to PARP inhibitors (olaparib) using prostate cancer cell lines PC3, DU145, LNCaP-FGC, and LNCaP-LN3. MATERIALS AND

methodsThe cell viability and DRG2 expression levels were assessed using colorimetric-based cell viability assay and western blot. Cells were transfected with DRG2 siRNA, and pcDNA6/V5-DRG2 was used to overexpress DRG2. Flow cytometry was applied for cell cycle assay and apoptosis analysis using the Annexing V cell death assay.

resultsThe expression of DRG2 was highest in LNCaP-LN3 and lowest in DU145 cells. Expressions of p53 in PC3, DU145, and the two LNCaP cell lines were null-type, high-expression, and medium-expression, respectively. In PC3 (DRG2 high, p53 null) cells, docetaxel increased G2/M arrest without apoptosis; however, subsequent treatment with olaparib promoted apoptosis. In DU145 and LNCaP-FGC (DRG2 low), docetaxel increased sub-G1 but not G2/M arrest and induced apoptosis, whereas olaparib had no additional effect. In LNCaP-LN3 (DRG2 high, p53 wild-type), docetaxel increased sub-G1 and G2/M arrest, furthermore olaparib enhanced cell death. Docetaxel and olaparib combination treatment had a slight effect on DRG2 knockdown PC3, but increased apoptosis in DRG2-overexpressed DU145 cells.

conclusionsDRG2 and p53 expressions play an important role in prostate cancer cell lines treated with docetaxel, and DRG2 levels can predict the response to PARP inhibitors.

Indexed as

Antineoplastic AgentsDocetaxelPoly(ADP-ribose) Polymerase InhibitorsProstatic NeoplasmsApoptosisCell Line, TumorCell SurvivalGTP-Binding ProteinsHumansMalePhthalazinesPiperazinesAntineoplastic AgentsDocetaxelDRG2 protein, humanGTP-Binding ProteinsolaparibPhthalazinesPiperazinesPoly(ADP-ribose) Polymerase InhibitorsDocetaxelPARP inhibitorProstate cancer

Identifiers

PMID39791585
PMCPMC11729229

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Registered trials

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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.