First Affiliated Hospital of Guizhou, University of Traditional Chinese Medicine, Guiyang, 550001, China.
Department of Endoscopy, Guizhou Provincial People's Hospital, Guiyang, 550002, China.
Hum Cell. 2024 Oct 28;38(1):11. doi: 10.1007/s13577-024-01140-4.
Lung cancer is one of the most common malignant tumors in the world, with high incidence rate and mortality. Monocarboxylate transporter (MCT) 1 has been found to be widely expressed in various tumors and plays a crucial role in regulating energy metabolism. Emodin, as an important traditional Chinese medicine in China, has been reported to inhibit the progression of lung cancer. However, its potential mechanism has not been fully elucidated. The effects of emodin and MCT1 inhibitor AZD3965 on the proliferation, migration, and invasion of lung cancer cells were detected using cell counting kit-8 (CCK-8) assay, wound-healing assay, and transwell small chamber assay. The content of glucose, lactate, and pyruvate in the cell culture medium was detected using a glucose, lactate, and pyruvate detection kit, and also detected protein expression using western blotting. In addition, to investigate the effects of emodin and AZD3965 on lung cancer in vivo, we constructed nude mice subcutaneous transplant tumor model by subcutaneous injection of lung cancer cells. The results showed that emodin and AZD3965 could inhibit the proliferation, migration, and invasion of lung cancer cells. At the same time, they could inhibit the expression of MCT1 in lung cancer cells and promote the release of lactate, but did not affect the content of glucose and pyruvate. In vivo experiments had shown that emodin and AZD3965 could effectively inhibit the growth of lung cancer and inhibit the expression of MCT1. All in all, our data suggested that emodin inhibited the proliferation, migration, and invasion of lung cancer cells, possibly by inhibiting MCT1, providing important theoretical basis for elucidating the mechanism of emodin in treating lung cancer.
肺癌是世界上最常见的恶性肿瘤之一，发病率和死亡率都很高。单羧酸转运蛋白（MCT）1 已被发现广泛表达于各种肿瘤中，在调节能量代谢中发挥着关键作用。大黄素作为中国的一种重要中药，已被报道能抑制肺癌的进展。然而，其潜在的机制尚未完全阐明。本研究采用细胞计数试剂盒-8（CCK-8）检测、划痕愈合实验和 Transwell 小室实验检测大黄素和 MCT1 抑制剂 AZD3965 对肺癌细胞增殖、迁移和侵袭的影响。采用葡萄糖、乳酸和丙酮酸检测试剂盒检测细胞培养上清液中葡萄糖、乳酸和丙酮酸的含量，并采用 Western blot 检测蛋白表达。此外，为了研究大黄素和 AZD3965 对体内肺癌的影响，我们通过肺癌细胞皮下注射构建了裸鼠皮下移植瘤模型。结果表明，大黄素和 AZD3965 能抑制肺癌细胞的增殖、迁移和侵袭。同时，它们能抑制肺癌细胞中 MCT1 的表达，促进乳酸的释放，但不影响葡萄糖和丙酮酸的含量。体内实验表明，大黄素和 AZD3965 能有效抑制肺癌的生长，抑制 MCT1 的表达。总之，我们的数据表明，大黄素抑制肺癌细胞的增殖、迁移和侵袭，可能是通过抑制 MCT1 实现的，为阐明大黄素治疗肺癌的机制提供了重要的理论依据。
