二恶英和类二恶英化合物是在制造其他化学品过程中形成的氯化有机污染物。二恶英是芳香族羟基苯并芳香烃受体（AHR） 的配体，可以诱导 AHR介导的生物化学反应和毒性反应，并且在环境中具有持久存在性。 2,3,7,8-四氯二苯并对二恶英（TCDD）是 典型的 AHR配体，其效应代表了二恶英。TCDD会引发毒性作用、免疫抑制并被怀疑为肿瘤促进剂。然而，TCDD在癌症中的作用存在争议并且具体情境依赖。环境颗粒物、多环芳烃、全氟辛磺胺、内源 AHR配体和cAMP信号转导可以通过非 TCDD依赖途径激活 AHR。活化的 AHR 在癌症中的效应是情境依赖的。FDA批准的药物调节 AHR活性的能力引起了对它们在癌症治疗中的再利用的兴趣。通过干扰内源途径、过度刺激其他内源途径，TCDD会影响癌症的各个阶段。在这里，我们将回顾激活 AHR的信号机制，以及被活化的 AHR 调节癌症信号的机制，包括受影响的代谢途径。版权所有©2023。由Elsevier公司出版。

Dioxin and dioxin-like compounds are chlorinated organic pollutants formed during the manufacturing of other chemicals. Dioxins are ligands of the aryl hydrocarbon receptor (AHR), that induce AHR-mediated biochemical and toxic responses and are persistent in the environment. 2,3,7,8- tetrachlorodibenzo para dioxin (TCDD) is the prototypical AHR ligand and its effects represent dioxins. TCDD induces toxicity, immunosuppression and is a suspected tumor promoter. The role of TCDD in cancer however is debated and context-dependent. Environmental particulate matter, polycyclic aromatic hydrocarbons, perfluorooctane sulfonamide, endogenous AHR ligands, and cAMP signaling activate AHR through TCDD-independent pathways. The effect of activated AHR in cancer is context-dependent. The ability of FDA-approved drugs to modulate AHR activity has sparked interest in their repurposing for cancer therapy. TCDD by interfering with endogenous pathways, and overstimulating other endogenous pathways influences all stages of cancer. Herein we review signaling mechanisms that activate AHR and mechanisms by which activated AHR modulates signaling in cancer including affected metabolic pathways.Copyright © 2023. Published by Elsevier Inc.