Department of Biochemical Science "A. Rossi Fanelli", Faculty of Pharmacy and Medicine, Sapienza University of Rome, P.le Aldo Moro 5, 00185 Rome, Italy.
Institute of Molecular Biology and Pathology, CNR National Research Council, Via degli Apuli, 4, 00185 Rome, Italy.
Int J Mol Sci. 2024 Jun 4;25(11):6181. doi: 10.3390/ijms25116181.
Organochlorine pesticides (OCPs) are a class of environmentally persistent and bioaccumulative pollutants. Among these, β-hexachlorocyclohexane (β-HCH) is a byproduct of lindane synthesis, one of the most worldwide widespread pesticides. β-HCH cellular mechanisms inducing chemical carcinogenesis correspond to many of those inducing chemoresistance, in particular, by the activation of signal transducer and activator of transcription 3 (STAT3) signaling pathways. For this purpose, four cell lines, representative of breast, lung, prostate, and hepatocellular cancers, were treated with β-HCH, specific tyrosine kinase inhibitors (TKIs), and a STAT3 inhibitor. All cell samples were analyzed by a viability assay, immunoblotting analysis, a wound-healing assay, and a colony formation assay. The results show that β-HCH reduces the efficacy of TKIs. The STAT3 protein, in this context, plays a central role. In fact, by inhibiting its activity, the efficacy of the anticancer drug is restored. Furthermore, this manuscript aimed to draw the attention of the scientific and socio-healthcare community to the issue of prolonged exposure to contaminants and their impact on drug efficacy.
有机氯农药(OCPs)是一类在环境中持久存在且具有生物累积性的污染物。其中,β-六氯环己烷(β-HCH)是林丹合成的副产物,林丹是世界范围内广泛使用的农药之一。β-HCH 诱导化学致癌的细胞机制与诱导化学耐药性的机制很多是相同的,特别是通过激活信号转导和转录激活因子 3(STAT3)信号通路。为此,我们用β-HCH、特定的酪氨酸激酶抑制剂(TKIs)和 STAT3 抑制剂处理了代表乳腺癌、肺癌、前列腺癌和肝癌的四种细胞系。对所有细胞样本进行了活力测定、免疫印迹分析、划痕愈合试验和集落形成试验。结果表明,β-HCH 降低了 TKIs 的疗效。在这种情况下,STAT3 蛋白起着核心作用。事实上,通过抑制其活性,恢复了抗癌药物的疗效。此外,本文旨在引起科学界和社会医疗保健界对长期接触污染物及其对药物疗效影响问题的关注。