7,12-Dimethylbenz[a]anthracene is an immunosuppressor as well as a potent organ-specific carcinogen.Co-treatment of 7,12‑dimethylbenz[a]anthracene with 12-O-tetradecanoylphorbol-13-acetate (TPA) promotes tumor growth in certain two-stage carcinogenesis models[1].
7,12-Dimethylbenz[a]anthracene (1μM; 4h) increased the expression of CCL20, IL-36γ, and p19 in NHKCs[2]. 7,12-Dimethylbenz[a]anthracene (20μM; 24 and 44h) inhibited the expansion of cumulus cells at 24 hours and promoted the separation of cumulus cells from oocytes at 44 hours,induces sharp ROS rise[3].
7,12-Dimethylbenz[a]anthracene (1mg/kg; po; 6weeks) exposure enhanced the activation of EGFR, ErbB2, Akt, and Erk in the premalignant mammary tissues [4]. After treatment with 7,12-Dimethylbenz[a]anthracene (20μg/ml; 24h), the expression of E-CAD was decreased and the expression of α-SMA was increased in MCF10A cells[5].7,12-Dimethylbenz[a]anthracene (50mg/kg; po; 4weeks) induced elevation in PGE2 levels of tumors [6].
References:
[1].Sung YM, He G, Fischer SM. Lack of expression of the EP2 but not EP3 receptor for prostaglandin E2 results in suppression of skin tumor development. Cancer Res. 2005 Oct 15;65(20):9304-11.
[2].Sato Y, Fujimura T, Hidaka T, Lyu C, Tanita K, Matsushita S, Yamamoto M, Aiba S. Possible Roles of Proinflammatory Signaling in Keratinocytes Through Aryl Hydrocarbon Receptor Ligands for the Development of Squamous Cell Carcinoma. Front Immunol. 2020 Oct 16;11:534323
[3].Song ZQ, Li X, Wang YK, Du ZQ, Yang CX. 7,12-DIMETHYLBENZ[Α]ANTHRACENE acts on cumulus cells to desynchronize nuclear and cytoplasmic maturation of pig oocytes. Sci Rep. 2017 May 10;7(1):1687.
[4].Ma Z, Kim YM, Howard EW, Feng X, Kosanke SD, Yang S, Jiang Y, Parris AB, Cao X, Li S, Yang X. 7,12-DIMETHYLBENZ[Α]ANTHRACENE promotes ErbB2 mediated carcinogenesis via ErbB2 and estrogen receptor pathway activation and genomic instability. Oncol Rep. 2018 Sep;40(3):1632-1640.
[5].Liu G, Lim D, Cai Z, Ding W, Tian Z, Dong C, Zhang F, Guo G, Wang X, Zhou P, Feng Z. The Valproate Mediates Radio-Bidirectional Regulation Through RFWD3-Dependent Ubiquitination on Rad51. Front Oncol. 2021 Mar 25;11:646256.
[6].Karimi B, Ashrafi M, Shomali T, Yektaseresht A. Therapeutic effect of simvastatin on 7,12-DIMETHYLBENZ[Α]ANTHRACENE-induced breast cancer in mice. Fundam Clin Pharmacol. 2019 Feb;33(1):84-93.
7,12-Dimethylbenz[a]anthracene是一种免疫抑制剂，也是一种强效的器官特异性致癌物。在某些两阶段致癌模型中，7,12‑dimethylbenz[a]anthracene与 12-O-十四烷酰佛波醇-13-乙酸酯 (TPA)共同处理可促进肿瘤生长[1]。
7,12-Dimethylbenz[a]anthracene （1μM；4h）可增加 NHKCs 中 CCL20、IL-36γ 和 p19 的表达[2]。7,12-Dimethylbenz[a]anthracene (20μM；24 和 44h) 可在 24 小时时抑制卵丘细胞的扩张，在 44 小时时促进卵丘细胞与卵母细胞的分离，并诱导 ROS 急剧增加[3]。用 7,12-Dimethylbenz[a]anthracene （20μg/ml；24h）处理 MCF10A 细胞可降低 E-CAD 表达并增加 α-SMA 表达[4]。
7,12-Dimethylbenz[a]anthracene（1mg/kg；po；6weeks）暴露可增强癌前乳腺组织中 EGFR、ErbB2、Akt 和 Erk 的活化[5]。7,12-Dimethylbenz[a]anthracene（50mg/kg；po；4weeks）可诱导肿瘤中 PGE2 水平升高 [6]。