Affiliated Hospital of Chengde Medical University, Chengde, Hebei, China.
Adv Exp Med Biol. 2019;1182:79-118. doi: 10.1007/978-981-32-9421-9_3.
The anticancer potential of Ganoderma (Lingzhi) and its extracts has been widely demonstrated, including antiproliferative and apoptosis inductive, antimetastatic, antiangiogenic, and multidrug resistance reversional activities, involving a variety of cellular and molecular mechanisms besides antitumor immunology. Intrinsic- and extrinsic-initiated apoptotic pathway in association with cell cycle arresting, telomerase inhibiting, autophagy, and oxidative stress is involved in the antiproliferative and apoptosis inductive activities of Ganoderma and its extracts. The inhibition of tumor cell adhesion, invasion, and migration by Ganoderma and its extracts involves molecular mechanisms such as AP-1, NF-κB, MMP, cadherin, β-integrin, c-Met, FAK, EMT, and so on. Targeting the major pro-angiogenic stimulus, VEGF, and its receptor contributes to the inhibition of tumor angiogenesis by Ganoderma and its extracts. Inhibition against the ATP-dependent transmembrane drug transporter such as P-glycoprotein (P-gp) on the surface of resistant tumor cells to prevent reduction of the intracellular accumulation of anticancer drugs by pumping out the drugs plays an important role in the activities of Ganoderma and its extracts to reverse tumor cell multidrug resistance.
灵芝（Ganoderma）及其提取物具有广泛的抗癌潜力，包括抗增殖和诱导细胞凋亡、抗转移、抗血管生成和多药耐药逆转活性，除了肿瘤免疫学外，还涉及多种细胞和分子机制。灵芝及其提取物的抗增殖和诱导细胞凋亡活性涉及内在和外在引发的凋亡途径，与细胞周期停滞、端粒酶抑制、自噬和氧化应激有关。灵芝及其提取物通过抑制肿瘤细胞黏附、侵袭和迁移，涉及 AP-1、NF-κB、MMP、钙黏蛋白、β-整联蛋白、c-Met、FAK、EMT 等分子机制。针对主要的促血管生成刺激因子 VEGF 及其受体，有助于灵芝及其提取物抑制肿瘤血管生成。抑制位于耐药肿瘤细胞表面的 ATP 依赖性跨膜药物转运体，如 P 糖蛋白（P-gp），以防止药物泵出减少抗癌药物在细胞内的积累，在灵芝及其提取物逆转肿瘤细胞多药耐药的活性中发挥重要作用。
