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Study on Autophagy Death of Alpha TC1 Clone 6 (αTC1-6) Cells Induced by Trametenolic Acid Through PI3K/AKT Pathway
Wangyang Ye1, Shangling Pan1, Hongqi Zhang2
1School of Basic Medical Sciences, Guangxi Medical University, Nanning 530021, China.
Abstract:
Glucagonoma, a rare neuroendocrine tumor, lacks targeted treatment drugs. Excessive secretion of glucagon is the main cause of its clinical syndrome. To explore targeted therapeutic drugs that can inhibit glucagon secretion and tumor proliferation, we investigated the effect of Trametenolic Acid (TA) on mouse pancreatic alpha TC1 clone 6 (αTC1-6) cells and its regulatory role in the PI3K/AKT signaling pathway. Cell viability of αTC1-6 cells was assessed via the MTT assay. Glucagon content in cell culture supernatants was measured using an Enzyme-Linked Immunosorbent Assay (ELISA). Autophagic vacuoles were visualized through Monodansylcadaverine (MDC) staining. The expression of autophagy-related proteins including Atg7, LC3 Ⅱ and PI3K/AKT signaling pathway-related proteins mTOR and FoxO1 were determined by Western blot. The results showed that the proliferation of αTC1-6 cells was significantly inhibited by TA in a dose- and time-dependent manner, and the IC50 was 140.71, 26.77 and 1.99 μM after treatment of 12, 24, and 48 h, respectively. The secretion of glucagon was significantly inhibited by TA. The MDC staining results showed that the fluorescent labeled autophagic vesicles in the TA group were increased. The Western blot results showed that the expression of Atg7 and LC3 Ⅱ was promoted by TA in a dose-dependent manner, the phosphorylation of PI3K, AKT, mTOR and FoxO1 was significantly inhibited, and the expression of FoxO1 protein was increased. These results demonstrated that TA can inhibit glucagon secretion, induce autophagy, and suppress cell proliferation in αTC1-6 cells. The mechanism may be associated with the PI3K/AKT signaling pathway.
Insights
Trametenolic Acid (TA) inhibits glucagonoma cell proliferation and glucagon secretion by inducing autophagy and suppressing the PI3K/AKT pathway. This offers a potential targeted therapy for glucagonoma.
Area of Science:
- Biochemistry
- Cell Biology
- Pharmacology
Background:
- Glucagonoma, a rare neuroendocrine tumor, currently lacks targeted therapies.
- Excessive glucagon secretion drives the clinical syndrome associated with glucagonoma.
Purpose of the Study:
- To investigate Trametenolic Acid (TA) as a potential therapeutic agent for glucagonoma.
- To elucidate TA's effects on glucagon secretion, cell proliferation, and autophagy in αTC1-6 cells.
- To explore TA's regulatory role in the PI3K/AKT signaling pathway.
Main Methods:
- Cell viability assessed using MTT assay.
- Glucagon secretion measured by ELISA.
- Autophagic vacuoles visualized via Monodansylcadaverine (MDC) staining.
- Protein expression (Atg7, LC3 II, mTOR, FoxO1) analyzed by Western blot.
Main Results:
- TA significantly inhibited αTC1-6 cell proliferation and glucagon secretion in a dose- and time-dependent manner.
- TA treatment increased autophagic vacuoles and the expression of autophagy-related proteins Atg7 and LC3 II.
- TA suppressed PI3K/AKT/mTOR signaling pathway phosphorylation and increased FoxO1 protein expression.
Conclusions:
- Trametenolic Acid demonstrates potential as a targeted therapy for glucagonoma by inhibiting cell proliferation and glucagon secretion.
- TA induces autophagy and modulates the PI3K/AKT signaling pathway in αTC1-6 cells.
- TA's mechanism of action involves autophagy induction and PI3K/AKT pathway inhibition, offering a novel therapeutic strategy.
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