Evidence map›Paper›PMID 39062784›Full record

ArticleInternational journal of molecular sciences2024

The Induction of G2/M Phase Cell Cycle Arrest and Apoptosis by the Chalcone Derivative 1C in Sensitive and Resistant Ovarian Cancer Cells Is Associated with ROS Generation.

Šimon Salanci, Mária Vilková, Lola Martinez, Ladislav Mirossay, Radka Michalková, Ján Mojžiš

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Acridine-Based Chalcone 1C and ABC Transporters.International journal of molecular sciences · 2025
    Article
  9. Article
  10. Review
  11. Drug Repurposing for Cancer Treatment: A Comprehensive Review.International journal of molecular sciences · 2024
    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

6 authors.

Šimon SalanciDepartment of Pharmacology, Faculty of Medicine, Pavol Jozef Šafárik University, 040 01 Košice, Slovakia.
Mária VilkováInstitute of Chemistry, Faculty of Science, Pavol Jozef Šafárik University, 040 01 Košice, Slovakia.ORCID 0000-0003-2833-7361
Lola MartinezFlow Cytometry Unit, Biotechnology Programme, Spanish National Cancer Research Center (CNIO), 28029 Madrid, Spain.
Ladislav MirossayDepartment of Pharmacology, Faculty of Medicine, Pavol Jozef Šafárik University, 040 01 Košice, Slovakia.
Radka MichalkováDepartment of Pharmacology, Faculty of Medicine, Pavol Jozef Šafárik University, 040 01 Košice, Slovakia.ORCID 0000-0002-9987-1556
Ján MojžišDepartment of Pharmacology, Faculty of Medicine, Pavol Jozef Šafárik University, 040 01 Košice, Slovakia.ORCID 0000-0002-7974-4525

Funding

EDRF ITMS2014 + 313011D103EDRF ITMS2014+: 313011V455Grant Agency of the Ministry of the Education, Science, Research and Sport of the Slovak Repub-lic VEGA 1/0498/23Grant Agency of the Ministry of the Education, Science, Research and Sport of the Slovak Repub-lic VEGA 1/0539/21Slovak Research and Development Agency APVV-16-0446
6 · The paper itself

Abstract

Ovarian cancer ranks among the most severe forms of cancer affecting the female reproductive organs, posing a significant clinical challenge primarily due to the development of resistance to conventional therapies. This study investigated the effects of the chalcone derivative 1C on sensitive (A2780) and cisplatin-resistant (A2780cis) ovarian cancer cell lines. Our findings revealed that 1C suppressed cell viability, induced cell cycle arrest at the G2/M phase, and triggered apoptosis in both cell lines. These effects are closely associated with generating reactive oxygen species (ROS). Mechanistically, 1C induced DNA damage, modulated the activity of p21, PCNA, and phosphorylation of Rb and Bad proteins, as well as cleaved PARP. Moreover, it modulated Akt, Erk1/2, and NF-κB signaling pathways. Interestingly, we observed differential effects of 1C on Nrf2 levels between sensitive and resistant cells. While 1C increased Nrf2 levels in sensitive cells after 12 h and decreased them after 48 h, the opposite effect was observed in resistant cells. Notably, most of these effects were suppressed by the potent antioxidant N-acetylcysteine (NAC), underscoring the crucial role of ROS in 1C-induced antiproliferative activity. Moreover, we suggest that modulation of Nrf2 levels can, at least partially, contribute to the antiproliferative effect of chalcone 1C.

Indexed as

ApoptosisChalconesDrug Resistance, NeoplasmG2 Phase Cell Cycle CheckpointsOvarian NeoplasmsReactive Oxygen SpeciesAntineoplastic AgentsCell Line, TumorCell ProliferationCell SurvivalChalconeDNA DamageFemaleHumansSignal TransductionAntineoplastic AgentsChalconeChalconesReactive Oxygen SpeciesantiproliferativeapoptosischalconesG2/M arrestN-acetylcysteineNrf2ovarian canceroxidative stress

Identifiers

PMID39062784
PMCPMC11277160

What Socratic 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 Socratic graph.