Zhang Xiangchao, Li Zhengjun, Wang Tao
Department of Anesthesiology, Shenyang Chest Hospital, No. 11 Beihai Street, Dadong District, Shenyang City, 110044 Liaoning China.
Department of Thoracic Surgery, Shenyang Chest Hospital, No. 11 Beihai Street, Dadong District, Shenyang City, 110044 Liaoning China.
Cytotechnology. 2025 Feb;77(1):4. doi: 10.1007/s10616-024-00661-y. Epub 2024 Nov 20.
Esophageal cancer remains a formidable challenge in oncology, characterized by its poor prognosis and limited therapeutic options. Recent investigations have unveiled the potential of repurposing existing drugs for cancer treatment. Notably, etomidate, an anesthetic agent traditionally used for inducing general anesthesia, has emerged as a promising candidate demonstrating significant anticancer properties across various tumor types. The present study aims to investigate the effects of etomidate on esophageal carcinoma cells, with a specific focus on its ability to modulate the PI3K/AKT signaling pathway and inhibit tumor proliferation. This study employed both in vitro and in vivo methodologies to assess the effects of etomidate on esophageal cancer cells. In vitro experiments evaluated the effects of etomidate on cell proliferation, migration, invasion, and glycolytic processes. An in vivo xenograft mouse model was established to investigate the therapeutic potential of etomidate on tumor growth and assess its impact on the PI3K/AKT signaling pathway in a physiologically relevant context. Etomidate demonstrated a significant inhibitory effect on the proliferation, migration, invasion, and glycolytic capacity of esophageal cancer cells. This multifaceted suppression of tumorigenic properties was closely associated with the inhibition of the PI3K/AKT pathway, as evidenced by reduced phosphorylation levels of PI3K and AKT. In vivo studies using a murine model of esophageal cancer corroborated these findings. Etomidate administration resulted in a substantial reduction in tumor volume and mass, accompanied by increased apoptotic activity and the inhibition of the PI3K/AKT pathway within the tumor tissue. This study demonstrates etomidate's potent inhibition of esophageal cancer progression through suppression of the PI3K/AKT pathway. These promising results warrant further clinical investigation of etomidate as a potential therapeutic strategy for esophageal cancer.
The online version contains supplementary material available at 10.1007/s10616-024-00661-y.
食管癌仍然是肿瘤学领域一项艰巨的挑战，其特点是预后不良且治疗选择有限。最近的研究揭示了将现有药物重新用于癌症治疗的潜力。值得注意的是，依托咪酯，一种传统上用于诱导全身麻醉的麻醉剂，已成为一种有前景的候选药物，在各种肿瘤类型中均表现出显著的抗癌特性。本研究旨在探讨依托咪酯对食管癌细胞的影响，特别关注其调节PI3K/AKT信号通路和抑制肿瘤增殖的能力。本研究采用体外和体内方法来评估依托咪酯对食管癌细胞的影响。体外实验评估了依托咪酯对细胞增殖、迁移、侵袭和糖酵解过程的影响。建立了体内异种移植小鼠模型，以研究依托咪酯对肿瘤生长的治疗潜力，并在生理相关背景下评估其对PI3K/AKT信号通路的影响。依托咪酯对食管癌细胞的增殖、迁移、侵袭和糖酵解能力表现出显著的抑制作用。这种对肿瘤发生特性的多方面抑制与PI3K/AKT通路的抑制密切相关，PI3K和AKT的磷酸化水平降低证明了这一点。使用食管癌小鼠模型的体内研究证实了这些发现。给予依托咪酯导致肿瘤体积和质量大幅减少，同时肿瘤组织内凋亡活性增加且PI3K/AKT通路受到抑制。本研究表明依托咪酯通过抑制PI3K/AKT通路对食管癌进展具有强大的抑制作用。这些有前景的结果值得对依托咪酯作为食管癌潜在治疗策略进行进一步的临床研究。
在线版本包含可在10.1007/s10616 - 024 - 00661 - y获取的补充材料。
