Inhibition of Acetylcholine Expression in the Tumor Microenvironment by Mustard Oil: A Potential Strategy to Retard Colon Cancer Progression.

Objective: This study aims to investigate the potential of mustard oil-induced reduction in acetylcholine expression as a means to delay the progression of colon cancer within the internal environment. Methods: The study design in this research involved both in vitro cellular experiments and in vivo animal experiments to employ mustard oil to modulate acetylcholine expression levels and evaluate its impact on colon cancer. Cellular experiments involved the introduction of six concentrations of acetylcholine (10-2, 10-3, 10-4, 10-5, 10-6, and 10-7 mol/L) into colon cancer cell cultures to monitor cell proliferation. Animal experiments encompassed the subcutaneous CT26 colon cancer cells implantation into 28 Balb/c mice, divided into experimental and control groups. After tumor establishment, both groups were fed standard diets for two weeks. Serum acetylcholine concentrations were measured from eye blood samples. Additionally, Balb/c mice were inoculated with CT26-derived colon cancer cells and further categorized into experimental and control groups. A total of 14 mice comprised each group, with experimental mice fed mustard oil and control mice fed soybean oil. Post two weeks, serum acetylcholine expression in both groups was assessed. After sacrifice, subcutaneous tumors were excised, and tumor dimensions were measured using a Vernier scale. Results: Acetylcholine concentration augmentation in the culture medium corresponded to gradual cell proliferation escalation, peaking at 10-5 mol/L, exhibiting statistical significance. Comparative analysis revealed significantly elevated relative acetylcholine expression levels in Balb/c mice with tumor-bearing colon cancers compared to normal Balb/c mice. Experimental group mice exhibited substantially lower serum acetylcholine concentrations than control group mice. Mustard oil administration effectively curtailed acetylcholine expression in normal Balb/c mice, consequently retarding tumor growth. These findings underscore mustard oil's potential to diminish serum acetylcholine expression, thereby delaying colon cancer progression. Conclusions: This study suggests that mustard oil's modulation of acetylcholine expression within the internal environment holds the potential for impeding colon cancer growth.

Qigesan reduces the motility of esophageal cancer cells via inhibiting Gas6/Axl and NF-κB expression.

The present study is mainly to explore the mechanism that how Qigesan (QGS) affects the movement capacity of esophageal cancer (EC) cell. QGS incubates ECA109 and TE1 cell lines and detecting the motility of tumor cells by different experiments. Growth arrest-specific 6 (Gas6) and Anexelekto (Axl) were co-localized, and then detecting Gas6, Axl signaling pathway, and protein expression after QGS intervention. Similarly, Observing the signal localization and protein expression of P-phosphoinositide3-kinases (PI3K), P-AKT protein kinase B (AKT), P-nuclear factor-kappa B (NF-κB), matrix metalloproteinase-2 (MMP2), and matrix metalloproteinase-9 (MMP9). The results showed that the concentration of QGS was less than 200 ug/ml, and the cultured cells did not exceed 24 h, that no obvious cytotoxicity was observed. QGS significantly inhibited the mobility of ECA109 and TE1 cell lines in the concentration-dependent manner. In addition, QGS can regulate the Gas6/Axl pathway, inhibit the formation and localization of the Gas6/Axl complex, and reduce the protein activation of PI3K/AKT, NF-κB, MMP2, and MMP9. Experimental innovation shows that QGS can significantly slow down the mobility of EC cells by regulating the Gas6/Axl complex and downstream signaling pathways, and provides a theoretical basis for the pharmacological effects of QGS in the therapy of EC.