Department of Medicine and Surgery, University of Parma, Plesso Biotecnologico Integrato, Via Volturno 39, 43126 Parma, Italy.
Department of Clinical and Experimental Medicine, University of Foggia, Via Pinto 1, 71122 Foggia, Italy.
Int J Mol Sci. 2024 May 20;25(10):5569. doi: 10.3390/ijms25105569.
Due to its propensity to metastasize, cancer remains one of the leading causes of death worldwide. Thanks in part to their intrinsic low cytotoxicity, the effects of the flavonoid family in the prevention and treatment of various human cancers, both in vitro and in vivo, have received increasing attention in recent years. It is well documented that Apigenin (4',5,7-trihydroxyflavone), among other flavonoids, is able to modulate key signaling molecules involved in the initiation of cancer cell proliferation, invasion, and metastasis, including JAK/STAT, PI3K/Akt/mTOR, MAPK/ERK, NF-κB, and Wnt/β-catenin pathways, as well as the oncogenic non-coding RNA network. Based on these premises, the aim of this review is to emphasize some of the key events through which Apigenin suppresses cancer proliferation, focusing specifically on its ability to target key molecular pathways involved in angiogenesis, epithelial-to-mesenchymal transition (EMT), maintenance of cancer stem cells (CSCs), cell cycle arrest, and cancer cell death.
由于其易于转移的特性，癌症仍然是全球主要的死亡原因之一。近年来，由于黄酮类化合物家族内在的低细胞毒性，其在预防和治疗各种人类癌症中的作用，无论是在体外还是体内，都受到了越来越多的关注。有充分的文献记载表明，包括芹菜素（4',5,7-三羟基黄酮）在内的黄酮类化合物能够调节参与癌细胞增殖、侵袭和转移启动的关键信号分子，包括 JAK/STAT、PI3K/Akt/mTOR、MAPK/ERK、NF-κB 和 Wnt/β-catenin 途径，以及致癌性非编码 RNA 网络。基于这些前提，本综述的目的是强调芹菜素抑制癌症增殖的一些关键事件，特别关注其靶向参与血管生成、上皮-间充质转化（EMT）、维持癌症干细胞（CSC）、细胞周期停滞和癌细胞死亡的关键分子途径的能力。
