12-O-tetradecanoyl phorbol-13-acetate (TPA) is an activator of ERK/MAPK with the concentration of 50μm [1].
ERK is an extracellular signal-regulated kinase and transfers signals from a receptor on the cell surface to DNA cooperated with MAPK. It is reported that ERK deficiency leads to the cell uncontrolled growth and is regarded as a target to cure cancers.
TPA is a potent ERK activator. When tested with A549 cells (human lung cancer cell line), TPA treatment led to an early, strong, and relatively transient ERK phosphorylation [2]. In mouse embryo fibroblasts from DUSP5 (+/+) mice, administration of TPA increased levels of ERK expression [3].
In transgenic (Eisuke) mice expressing a F?rster resonance energy transfer (FRET) biosensor for ERK, ERK activity was gradually stimulated upon topical TPA treatment and reached the peak approximately 6 hr later [1].
It is also reported that TPA treatment increased the accumulation of immature myeloid cells and the formation of papillomas during epidermal carcinogenesis (important in the tumor formation) when tested with S100A9 transgenic mice [4].
12-O-十四烷基芦丁酸-13-乙酰化物（TPA）是一种ERK/MAPK激活剂，浓度为50μm [1]。
ERK是一种细胞外信号调节激酶，它将来自细胞表面受体的信号传递到与MAPK合作的DNA上。据报道，ERK缺乏会导致细胞无法控制地增长，并被视为治疗癌症的目标。
TPA是一种强效的ERK激活剂。在使用人类肺癌细胞系A549进行测试时，TPA处理导致早期、强烈且相对短暂的ERK磷酸化[2]。在来自DUSP5（+/+）小鼠的胚胎成纤维细胞中，给予TPA会增加ERK表达水平[3]。
在表达ERK FRET生物传感器的转基因（Eisuke）小鼠中，经过局部TPA处理后，ERK活性逐渐被刺激，并在大约6小时后达到峰值[1]。
据报道，当与S100A9转基因小鼠一起测试时，TPA治疗增加了未成熟髓样细胞的积累和乳头状瘤的形成（在肿瘤形成中很重要）。
References:
[1]. Hiratsuka, T., et al., Intercellular propagation of extracellular signal-regulated kinase activation revealed by in vivo imaging of mouse skin. Elife, 2014. 4.
[2]. Refsnes, M., et al., Differential NF-kappaB and MAPK activation underlies fluoride- and TPA-mediated CXCL8 (IL-8) induction in lung epithelial cells. J Inflamm Res, 2014. 7: p. 169-85.
[3]. Rushworth, L.K., et al., Dual-specificity phosphatase 5 regulates nuclear ERK activity and suppresses skin cancer by inhibiting mutant Harvey-Ras (HRasQ61L)-driven SerpinB2 expression. Proc Natl Acad Sci U S A, 2014. 111(51): p. 18267-72.
[4]. Ortiz, M.L., et al., Immature myeloid cells directly contribute to skin tumor development by recruiting IL-17-producing CD4+ T cells. J Exp Med, 2015.