Evidence map›Paper›PMID 34649150›Full record

ArticleTranslational oncology2022

Mechanisms of abemaciclib, a CDK4/6 inhibitor, induced apoptotic cell death in prostate cancer cells in vitro.

Gamze Guney Eskiler, Asuman Deveci Ozkan, Ayten Haciefendi, Cemil Bilir

Open access · goldAbstract read
In one paragraph

Article in Translational oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

16 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Abemaciclib Inhibits Retinoblastoma Tumor Growth by Targeting CDK1/2.Investigative ophthalmology & visual science · 2026
    Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Targeting mitochondria and programmed cell death as potential interventions for metastatic castration-resistant prostate cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Review
  10. Article
  11. Review
  12. [Molecular tumor boards in uro-oncology-prostate cancer].Urologie (Heidelberg, Germany) · 2024
    Article
  13. Article
  14. Apoptosis and eryptosis: similarities and differences.Apoptosis : an international journal on programmed cell death · 2024
    Review
  15. Article
  16. 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

4 authors at 2 institutions in 1 country.

Gamze Guney EskilerDepartment of Medical Biology, Faculty of Medicine, Sakarya University, Korucuk Campus, Sakarya 54290, Turkey. Electronic address: gamzeguney@sakarya.edu.tr.
Asuman Deveci OzkanDepartment of Medical Biology, Faculty of Medicine, Sakarya University, Korucuk Campus, Sakarya 54290, Turkey.
Ayten HaciefendiDepartment of Medical Biology, Institute of Health Sciences, Sakarya University, Sakarya, Turkey.
Cemil BilirDepartment of Medical Oncology, Faculty of Medicine, Istinye University VMMedical Park Pendik Hospital, Istanbul, Turkey.
Sakarya University · TRIstinye University · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The therapeutic effects of abemaciclib (ABE), an inhibitor of cyclin- dependent kinases (CDK) 4/6, on the proliferation of two types of prostate cancer (PC) cells were revealed. In this study, in vitro cytotoxic and apoptotic effects of ABE on metastatic castration-resistant prostate cancer (mCRPC) androgen receptor (AR) negative PC-3 and AR mutant LNCaP PC cells were analyzed with WST-1, Annexin V, cell cycle, reactive oxygen species (ROS), mitochondrial membrane potential, RT-PCR, western blot, and apoptosis protein array. ABE considerably inhibited the growth of PC cells in a dose-dependent manner (p<0.01) and caused significant apoptotic cell death through the suppression of CDK4/6-Cyclin D complex, ROS generation and depolarization of mitochondria membrane potential. However, PC-3 cells were more sensitive to ABE than LNCaP cells. Furthermore, the expression levels of several pro-apoptotic and cell cycle regulatory proteins were upregulated by ABE in especially PC-3 cells with the downregulation of apoptotic inhibitor proteins. Our results suggest that ABE inhibits PC cell growth and promotes apoptosis and thus ABE treatment may be a promising treatment strategy in especially mCRPC. Further preclinical and clinical studies should be performed to clarify the clinical use of ABE for the treatment of PC.

Indexed as

AbemaciclibApoptosisCDK4/6Prostate cancer

Identifiers

PMID34649150
PMCPMC8517924
OpenAlexW3207550390

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.