Evidence map›Paper›PMID 40542768›Full record

ArticleAsian Pacific journal of cancer prevention : APJCP2025

Thiosemicarbazide Derivative of Captopril (8) imposes Cellular-Dependent Death Modalities on Breast Cancer Cell Lines.

Baan M Al-Jasani, Hayder B Sahib, Hiba N Al-Saad

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Article in Asian Pacific journal of cancer prevention : APJCP, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

3 authors.

Baan M Al-Jasani1Department of Pharmacology & Toxicology, College of Pharmacy, University of Basrah, Basrah, Iraq.
Hayder B SahibDepartment of Pharmacology, College of Pharmacy, Al-Nahrain University, Baghdad, Iraq.ORCID 0000-0002-0939-5622
Hiba N Al-SaadDepartment of Pharmaceutical Chemistry, College of Pharmacy, University of Basrah, Basrah, Iraq.ORCID 0000-0001-6691-919X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveBreast cancer prevalence is continuing to rise worldwide. Despite the diversity of the current approaches and protocols to treat this heterogeneous disease, most of these face the challenges of side effects and resistance. Hence, novel and innovative approaches to the treatment of breast cancer are almost constantly needed. This study aimed to investigate the antiproliferative and death modalities induced by three thiosemicarbazide derivatives of captopril in two subtypes of breast cancer cell lines, the Estrogen- receptor positive MCF-7, and the Estrogen/progesterone- receptor-negative AMJ13.

methodsMTT assay was used to determine the cytotoxicity of the derivatives and their parent compound Captopril, Hematoxylin and Eosin (H&E) staining, Acridine Orange/ Ethidium Bromide (AO/EtBr) staining, Caspase immunocytochemistry analysis and ROS generation by Human ROMO1 ELISA assays were conducted to explore the type of cellular death induced by these derivatives.

resultsOne of the derivatives denoted as (8) demonstrated the best antiproliferative profile recording the highest cytotoxic effect with IC50 of (88.06 µM) and (66.82 µM) compared to that of captopril (849.8 µM),(1075µM) in MCF-7 and AMJ13 breast cancer cells respectively. In MCF-7 cells, derivative (8) imposed an apoptotic cellular death with the involvement of caspase-3, and caspase-9 and displayed a time-dependent ROS generation. In AMJ13 breast cancer cells, results revealed an extensive vacuole forming, non-apoptotic cellular death, without ROS generation, but with a significant implication of caspase-9.   Conclusion: This study demonstrated the thiosemicarbazide derivative of captopril (8) as a promising antiproliferative agent against breast cancer cells displaying different cellular death modalities, signifying the versatility of the derivative and suggesting multitarget pathways. This study strongly recommends derivative (8) as a future leading molecule.

Indexed as

ApoptosisBreast NeoplasmsCaptoprilSemicarbazidesCell ProliferationFemaleHumansMCF-7 CellsReactive Oxygen SpeciesTumor Cells, CulturedCaptoprilReactive Oxygen SpeciesSemicarbazidesthiosemicarbazideBreast Cancer Cell Lines AntiproliferativeDeath modalitiesThiosemicarbazide Derivative of Captopril

Identifiers

PMID40542768
PMCPMC12374511

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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.