Evidence map›Paper›PMID 36509750›Full record

ArticleCell death & disease2022

Idarubicin combats abiraterone and enzalutamide resistance in prostate cells via targeting XPA protein.

Ying Zhang, Wei Wei, Changying Li, Siyuan Yan, Shanshan Wang, Shudong Xiao, Chenchen He, Jing Li, Zhi Qi, Benyi Li and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.9field-weighted citation impact, top 24% of its field
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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
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

12 authors at 5 institutions in 2 countries.

Ying Zhang *Institute of Precision Medicine, Jining Medical University, 272067, Jining, China.
Wei Wei *Center for Experimental Medicine, School of Public Health, Jining Medical University, 272067, Jining, China.
Changying LiTianjin Institute of Urology, The Second Hospital of Tianjin Medical University, 300211, Tianjin, China.
Siyuan YanInstitute of Precision Medicine, Jining Medical University, 272067, Jining, China.
Shanshan WangInstitute of Precision Medicine, Jining Medical University, 272067, Jining, China.
Shudong XiaoInstitute of Precision Medicine, Jining Medical University, 272067, Jining, China.
Chenchen HeDepartment of Radiation Oncology, The First Affiliated Hospital, Xi'An Jiaotong University School of Medicine, 710061, Xi'An, China.
Jing LiDepartment of Histology and Embryology, School of Medicine, Nankai University, 300071, Tianjin, China.
Zhi QiDepartment of Histology and Embryology, School of Medicine, Nankai University, 300071, Tianjin, China.
Benyi LiDepartment of Urology, The University of Kansas Medical Center, Kansas City, KS, 66160, USA.ORCID 0000-0001-6242-5117
Kuo YangTianjin Institute of Urology, The Second Hospital of Tianjin Medical University, 300211, Tianjin, China. ykuoster@126.com.ORCID 0000-0001-6192-8804
Changlin LiInstitute of Precision Medicine, Jining Medical University, 272067, Jining, China. changlinli@mail.nankai.edu.cn.
Jining Medical University · CNSecond Hospital of Tianjin Medical University · CNNankai University · CNFirst Affiliated Hospital of Xi'an Jiaotong University · CNUniversity of Kansas Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although second-generation therapies like abiraterone (ABI) and enzalutamide (ENZ) benefit patients with castration-resistant prostate cancer (CRPC), drug resistance frequently occurs, eventually resulting in therapy failure. In this study, we used two libraries, FDA-approved drug library and CRISP/Cas9 knockout (GeCKO) library to screen for drugs that overcome treatment resistance and to identify the potential drug-resistant genes involved in treatment resistance. Our screening results showed that the DNA-damaging agent idarubicin (IDA) overcame abiraterone and enzalutamide resistance in prostate cancer cells. IDA treatment inhibited the DNA repair protein XPA expression in a transcription-independent manner. Consistently, XPA knockout sensitized prostate cancer cells to abiraterone and enzalutamide treatment. In conclusion, IDA combats abiraterone and enzalutamide resistance by reducing XPA protein level in prostate cancer.

Indexed as

Prostatic Neoplasms, Castration-ResistantBenzamidesDocetaxelHumansIdarubicinMaleNitrilesPhenylthiohydantoinProstateTaxoidsXeroderma Pigmentosum Group A ProteinBenzamidesDocetaxelenzalutamideIdarubicinNitrilesPhenylthiohydantoinTaxoidsXeroderma Pigmentosum Group A ProteinXPA protein, human

Identifiers

PMID36509750
PMCPMC9744908
OpenAlexW4311580279

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.