Related Experiment Video
Updated: May 23, 2026

Exploring the Pharmacological Action and Molecular Mechanism of Salidroside in Inhibiting MCF-7 Cell Proliferation and Migration
Published on: June 9, 2023
Sesamin Mitigates Gastric Carcinogenesis via Modulation of the PI3K/AKT/mTOR Signaling Pathway in AGS Cells and
Manju Parthiban1, Ponnulakshmi Rajagopal1, Heera Maheswari Jayaveeran1
1Central Research Laboratory, Meenakshi Ammal Dental College, Meenakshi Academy of Higher Education and Research, deemed to be University, Chennai, India.
Background:
Gastric cancer (GC) is a leading cause of cancer-related death worldwide, frequently associated with dysregulated PI3K/AKT/mTOR signaling and defective apoptosis. Sesamin, a lignan from sesame seeds, is rich in antioxidant and anticancer activities, yet it has not been well investigated for its therapeutic potential in GC.
Objective:
This study aims to investigate the anticancer potential of sesamin against gastric cancer by targeting the PI3K/AKT/mTOR signaling pathway in AGS cells and MNNG-induced rats, evaluating its effects on apoptosis, oxidative stress, and tumor biomarkers to elucidate its molecular mechanism of action.
Methods:
In vitro, molecular changes in AGS gastric cancer (GC) cells were determined by RT-PCR (p53, caspase-3, MDM2, PTEN, AKT, mTOR, NF-κB). In vivo, N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) was used to induce gastric cancer in Wistar rats. The intervention of sesamin was studied by histopathological analysis, and ELISA was used for the measurement of tumor markers (CEA and CA 19-9) and oxidative stress markers. Gene expression was analyzed by RT-PCR (p53, caspase-3, AKT, NF-κB, mTOR).
Results:
Sesamin treatment in AGS cells upregulated PTEN, p53, and caspase-3, while downregulating MDM2, AKT, mTOR, and NF-κB at the mRNA level in the in vitro study. In the in vivo mRNA expression analysis, sesamin treatment confirmed enhanced p53 and caspase-3 with reduced AKT expression and slightly increased mTOR expression. In MNNG-induced rats, sesamin improved gastric histology, decreased tumor markers (CEA, CA 19-9), suppressed IL-1β, and elevated GSH. RT-PCR analysis further validated the induction of pro-apoptotic genes and suppression of oncogenic PI3K/AKT/mTOR/NF-κB signaling, consistent with in vitro findings.
Conclusion:
Sesamin has demonstrated effective anti-gastric cancer activity by inducing p53/caspase-3-mediated apoptosis and inhibiting the PI3K/AKT/mTOR/NF-κB signaling pathway. These findings illustrate the therapeutic potential of sesamin against gastric cancer and reveal molecular clues for its use as a natural chemopreventive agent.
Insights
Sesamin shows promise as a natural gastric cancer treatment by inducing apoptosis and inhibiting the PI3K/AKT/mTOR/NF-κB pathway. This study highlights sesamin
Area of Science:
- Oncology
- Molecular Biology
- Natural Product Chemistry
Background:
- Gastric cancer (GC) is a major global health concern, often linked to aberrant PI3K/AKT/mTOR signaling and impaired apoptosis.
- Sesamin, a sesame lignan, possesses known antioxidant and anticancer properties but its therapeutic role in GC remains underexplored.
Purpose of the Study:
- To investigate sesamin's anticancer effects on gastric cancer (AGS cells and MNNG-induced rats).
- To evaluate sesamin's impact on apoptosis, oxidative stress, and tumor biomarkers.
- To elucidate the molecular mechanism involving the PI3K/AKT/mTOR pathway.
Main Methods:
- In vitro: RT-PCR analysis of key genes (p53, caspase-3, MDM2, PTEN, AKT, mTOR, NF-κB) in AGS cells.
- In vivo: MNNG-induced gastric cancer in Wistar rats, followed by histopathology, ELISA for tumor/oxidative stress markers, and RT-PCR for gene expression.
Main Results:
- Sesamin upregulated pro-apoptotic genes (PTEN, p53, caspase-3) and downregulated pro-survival genes (MDM2, AKT, mTOR, NF-κB) in AGS cells.
- In vivo, sesamin improved gastric histology, reduced tumor markers (CEA, CA 19-9), and modulated oxidative stress markers (elevated GSH, suppressed IL-1β).
- Gene expression analysis confirmed sesamin's induction of apoptosis and inhibition of the PI3K/AKT/mTOR/NF-κB pathway.
Conclusions:
- Sesamin exhibits significant anti-gastric cancer activity through p53/caspase-3-mediated apoptosis induction.
- Sesamin effectively inhibits the PI3K/AKT/mTOR/NF-κB signaling pathway in gastric cancer models.
- Sesamin demonstrates potential as a natural chemopreventive agent for gastric cancer.
Related Concept Videos
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
PI3K/mTOR/AKT Signaling Pathway
Mitogens and the Cell Cycle
