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L-Selenomethylselenocysteine Exerts Inhibitory Effects on the Progression of Esophageal Cancer by Targeting the
Keyi Ji1,2, Suhui Wu1,3, Jiayao Yuan1
1Henan University of Traditional Chinese Medicine, Zhengzhou, 450046, China.
Background:
Esophageal cancer is a common malignant tumor, making the search for effective treatments a critical research focus. L-methylselenocysteine (L-SeMC) has been reported to exert anticancer effects in various cancers; however, its role and underlying mechanisms in esophageal cancer remain unclear. This study aimed to investigate the anticancer effects of L-SeMC on esophageal cancer both in vitro and in vivo, and to explore its potential mechanisms of action.
Methods:
For cellular studies, flow cytometry, colony formation assay, MTT assay, wound healing assay, and ROS measurement were employed. Western blotting was used to assess the expression levels of apoptotic proteins. A subcutaneous tumor xenograft model was established. The analysis included the evaluation of proteins related to the PI3K/AKT signaling pathway, TUNEL, and Ki-67 staining, as well as HE staining.
Results:
L-SeMC caused cell death and, in a concentration-dependent manner, reduced the migration, invasion, and proliferation of esophageal cancer cells. Western blot analysis showed that L-SeMC was associated with a decrease in the anti-apoptotic protein Bcl-2 and an increase in the pro-apoptotic protein Bax. It also triggered the mitochondrial apoptosis pathway, promoting the activation of caspase-3 and subsequent cancer cell death induced by L-SeMC. In a dosedependent manner, L-SeMC decreased the phosphorylation of phosphatidylinositol 3-kinase (PI3K) downstream effector molecules. This suggests that L-SeMC inhibits the PI3K/AKT signaling pathway in esophageal cancer cells, contributing to its anticancer effects.
Discussion:
Our results suggest that L-Selenomethylselenocysteine acts as a potential therapeutic pathway in esophageal cancer through the PI3K/AKT signaling pathway. Although the current evidence is limited, we are actively increasing the sample size to conduct further verification.
Conclusion:
L-SeMC has a strong anticancer effect on human esophageal cancer cells and promotes apoptosis by inhibiting the PI3K/AKT signaling pathway, suggesting that L-SeMC may represent a novel strategy for the treatment of esophageal cancer.
Insights
L-methylselenocysteine (L-SeMC) demonstrates significant anticancer effects against esophageal cancer by promoting apoptosis and inhibiting the PI3K/AKT pathway. This compound shows promise as a novel therapeutic strategy for esophageal cancer treatment.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Esophageal cancer presents a significant global health challenge, necessitating the development of effective therapeutic interventions.
- L-methylselenocysteine (L-SeMC), a selenium compound, has shown potential anticancer properties in various cancer types, but its efficacy and mechanisms in esophageal cancer require elucidation.
Purpose of the Study:
- To investigate the anticancer effects of L-methylselenocysteine (L-SeMC) on esophageal cancer cells both in vitro and in vivo.
- To explore the underlying molecular mechanisms responsible for L-SeMC's anti-esophageal cancer activity.
Main Methods:
- Cellular assays including MTT, colony formation, wound healing, and flow cytometry were utilized to assess L-SeMC's impact on cell viability, proliferation, migration, and apoptosis.
- Western blotting was employed to analyze the expression of apoptosis-related proteins (Bcl-2, Bax, caspase-3) and key components of the PI3K/AKT signaling pathway.
- In vivo efficacy was evaluated using a subcutaneous tumor xenograft model in mice, with analyses including TUNEL, Ki-67, and HE staining.
Main Results:
- L-SeMC significantly inhibited esophageal cancer cell proliferation, migration, and invasion in a dose-dependent manner.
- L-SeMC treatment induced apoptosis by modulating Bcl-2 and Bax expression and activating caspase-3, thereby triggering the mitochondrial apoptosis pathway.
- In vivo studies confirmed L-SeMC's antitumor activity and demonstrated its ability to inhibit the PI3K/AKT signaling pathway by reducing the phosphorylation of downstream effectors.
Conclusions:
- L-methylselenocysteine (L-SeMC) exhibits potent anticancer effects against human esophageal cancer.
- L-SeMC promotes cancer cell apoptosis and inhibits tumor growth primarily through the downregulation of the PI3K/AKT signaling pathway.
- L-SeMC represents a promising novel therapeutic candidate for the treatment of esophageal cancer.
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