Evidence map›Paper›PMID 42755301›Full record

ArticleCurrent molecular medicine2026

Tamoxifen and Colchicine Alter Mitochondrial Respiration to Induce Cell Death in Low-metastatic Breast Cancer Cells.

Tashvinder Singh, Amitha Thankachan, Anjana Munshi, Sandeep Singh

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Article in Current molecular medicine, 2026. 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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5 · Who and what money

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4 authors.

Tashvinder SinghDepartment of Human Genetics and Molecular Medicine, Central University of Punjab, Bathinda, 151401, India.
Amitha ThankachanDepartment of Human Genetics and Molecular Medicine, Central University of Punjab, Bathinda, 151401, India.
Anjana MunshiDepartment of Human Genetics and Molecular Medicine, Central University of Punjab, Bathinda, 151401, India.ORCID 0000-0002-7657-8592
Sandeep SinghDepartment of Human Genetics and Molecular Medicine, Central University of Punjab, Bathinda, 151401, India.

Funding

CSIR/UGC 09/1051(0042)/2019-EMR-IDST-FIST SR/FST/LS-I/2017/49DST-SERB EMR grant SR/SO/AS-31/2014
6 · The paper itself

Abstract

backgroundBreast cancer cells exhibit mitochondrial respiration-mediated metabolic heterogeneity and tumour aggressiveness. Tamoxifen and Colchicine are known to interfere with oxidative stress in breast cancer cells. However, their role in regulating mitochondrial respiration remains poorly understood.

methodsMCF7 and MDA-MB-231 cells were used to analyse the metabolic modulatory effects of Tamoxifen and Colchicine. The roles of Tamoxifen and Colchicine in regulating ROS production, mitochondrial membrane potential, mitochondrial membrane integrity, and oxidative phosphorylation were assessed using ROS assay, JC-1 assay, and high-resolution respirometry, respectively. Their effects on mitochondrial biogenesis and mitochondria-dependent cytotoxicity were analysed using flow cytometry and confocal microscopy.

resultsTamoxifen and Colchicine exhibited cytotoxic effects by reducing ROS production, depolarising mitochondrial membrane potential, decreasing oxygen consumption, and inhibiting mitochondrial respiration. They specifically downregulated pyruvate-mediated mitochondrial respiration, preventing N-linked state mitochondrial respiration and reducing complex I activity. Colchicine demonstrated mitochondrialindependent cytotoxic effects, whereas Tamoxifen did not. Neither drug impacted mitochondrial membrane integrity. Tamoxifen and Colchicine decreased leak respiration, inhibited proton and electron transfer, and prevented non-phosphorylating electron transfer, potentially due to reduced complex I activity. Tamoxifen significantly inhibits mitochondrial biogenesis and induces a mitochondrial-dependent cell death pathway. In contrast, Colchicine had a low impact on mitochondrial biogenesis and induced a mitochondrial-independent cell death pathway. DISCUSSION: Tamoxifen and colchicine suppress complex I-driven mitochondrial respiration in breast cancer cells, reducing oxidative phosphorylation-associated aggressiveness. Notably, only tamoxifen links this metabolic inhibition to impaired mitochondrial biogenesis and mitochondria-dependent cytotoxicity.

conclusionTamoxifen and colchicine downregulate mitochondrial respiration and biogenesis, while only tamoxifen induces mitochondrial-dependent cytotoxicity.

Indexed as

Breast NeoplasmsColchicineMitochondriaTamoxifenCell DeathCell Line, TumorCell RespirationFemaleHumansMCF-7 CellsMDA-MB-231 CellsMembrane Potential, MitochondrialOxidative PhosphorylationOxygen ConsumptionReactive Oxygen SpeciesColchicineReactive Oxygen SpeciesTamoxifenBreast CancerElectron Transport Chain (ETC)MCF7MDA-MB-231MitochondriaOxidative Phosphorylation (OxPhos)

Identifiers

PMID42755301

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