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Radiosensitivity of Cancer Stem Cells in Lung Cancer Cell Lines
Published on: August 21, 2019
Anticancer function of α-solanine in lung adenocarcinoma cells by inducing microRNA-138 expression
Furui Zhang1, Rui Yang1, Guojun Zhang2
1Department of Respiratory Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.
Abstract:
Currently, lung cancer is still a main cause of malignancy-associated death worldwide. Even though various methods for prevention and treatment of lung cancer have been improved in recent decades, the 5-year survival rate has remained very low. Insights into the anticancer function of small-molecule anticancer compounds have opened our visual field about cancer therapy. α-Solanine has been well studied for its antitumor properties, but its effect in lung cancer and associated molecular mechanisms have not yet been evaluated. To explore the anticancer function of α-solanine, we performed an MTT assay, Transwell arrays, colony-forming survival assay, quantitative reverse transcription PCR (qRT-PCR), Western blotting, and dual luciferase reporter assays in A549 and H1299 cells. We found that α-solanine not only inhibited cell migration and invasion ability but also enhanced the chemosensitivity and radiosensitivity of A549 and H1299 cells. Moreover, we discovered that α-solanine could affect the expression of miR-138 and focal adhesion kinase (FAK), both of which were also found to affect the chemosensitivity and radiosensitivity of A549 and H1299 cells. In conclusion, α-solanine could affect miR-138 and FAK expression to restrict cell migration and invasion and enhance the chemosensitivity and radiosensitivity of A549 and H1299 cells. The α-solanine/miR-138/FAK cascade can probably be a potential therapy target against lung adenocarcinoma.
Insights
Alpha-solanine demonstrates anticancer effects in lung cancer cells by inhibiting migration and invasion. This compound enhances sensitivity to chemotherapy and radiation by modulating miR-138 and focal adhesion kinase (FAK) expression.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Lung cancer remains a leading cause of cancer death globally, with low survival rates despite treatment advances.
- Small-molecule compounds offer novel therapeutic strategies for cancer treatment.
- The antitumor properties of alpha-solanine are known, but its specific effects and mechanisms in lung cancer were unevaluated.
Purpose of the Study:
- To investigate the anticancer effects of alpha-solanine in lung cancer.
- To elucidate the molecular mechanisms underlying alpha-solanine's action in lung cancer cells.
- To explore alpha-solanine's potential to enhance chemosensitivity and radiosensitivity.
Main Methods:
- MTT assay, Transwell assays, and colony-forming survival assays were used to assess cell viability, migration, and invasion.
- Quantitative reverse transcription PCR (qRT-PCR) and Western blotting were employed to analyze gene and protein expression.
- Dual luciferase reporter assays were utilized to investigate regulatory pathways.
Main Results:
- Alpha-solanine significantly inhibited cell migration and invasion in A549 and H1299 lung cancer cell lines.
- The compound enhanced the chemosensitivity and radiosensitivity of these lung cancer cells.
- Alpha-solanine was found to modulate the expression of miR-138 and focal adhesion kinase (FAK).
Conclusions:
- Alpha-solanine exhibits anticancer properties against lung cancer by affecting cell migration and invasion.
- The alpha-solanine/miR-138/FAK pathway represents a potential therapeutic target for lung adenocarcinoma.
- Modulation of miR-138 and FAK by alpha-solanine enhances lung cancer cell sensitivity to chemotherapy and radiotherapy.
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