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Published on: August 23, 2019
miR-26a-5p Inhibit Gastric Cancer Cell Proliferation and Invasion Through Mediated Wnt5a
Yu Li1, Peng Wang1, Lei-Lei Wu2
1Department of Oncology, First Affiliated Hospital, Heilongjiang University of Chinese Medicine, Harbin 150040, Heilongjiang Province, People's Republic of China.
Purpose:
Gastric cancer (GC) is a malignant disease of digestive tract. Clinically, radiation therapy is widely applied in treating GC, while with undesirable outcome due to tumor re-proliferation and recurrence and metastasis after radiation. Therefore, it is crucial to explore potential molecular mechanisms to develop therapeutic strategies. The present study found that miR-26a-5p has low expression in GC patients and could regulate Wnt5a to inhibit tumor growth, which was a potential therapeutic target for GC. To explore the expression and related mechanism of miR-26a-5p and Wnt5a in GC.
Patients And Methods:
MiR-26a-5p and Wnt5a were extracted from the transcriptome data of GC downloaded from TCGA database for analysis. The expression levels of miR-26a-5p and Wnt5a in patients' tissues and serum were detected by qRT-PCR, and their correlation with patients' pathological data and survival was analyzed. In addition, miR-26a-5p and Wnt5a overexpression and inhibition vectors were transfected into cells to observe the effects on the proliferation, invasion and apoptosis of GC cells. The relationship between miR-26a-5p and Wnt5a was analyzed by dual luciferase report.
Results:
The database and clinical samples showed that miR-26a-5p level was low while Wnt5a was high in GC. MiR-26a-5p level decreased in patients with stage III+IV, lymphatic metastasis and tumor ≥3cm, and Wnt5a was contrary to that of the miR-26a-5p, with diagnostic value. Overexpressed miR-26a-5p and inhibited Wnt5a enhanced apoptosis, decreased proliferation and invasion, reduced Bcl-2 and β-catenin proteins, and elevated Caspase 3, E-cadherin and Bax proteins, while inhibited miR-26a-5p and over-expressed Wnt5a showed the opposite results. Dual luciferase report confirmed that miR-26a-5p targeted to regulate Wnt5a, and rescue experiments found that these effects could be counteracted by reducing miR-26a-5p level.
Conclusion:
Overexpressed miR-26a-5p can inhibit Wnt5a expression, promote cell apoptosis, and suppress cell proliferation and invasion in GC.
Insights
Low miR-26a-5p expression in gastric cancer (GC) correlates with high Wnt5a. Restoring miR-26a-5p inhibits GC progression and Wnt5a, offering a potential therapeutic strategy.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Gastric cancer (GC) remains a significant global health challenge, often exhibiting poor outcomes due to post-radiation recurrence and metastasis.
- Identifying molecular targets is crucial for developing effective therapeutic strategies against GC.
- The dysregulation of microRNAs (miRNAs) plays a critical role in cancer development and progression.
Purpose of the Study:
- To investigate the expression levels of miR-26a-5p and Wnt5a in gastric cancer (GC) patients.
- To elucidate the underlying molecular mechanism of miR-26a-5p and Wnt5a in GC progression.
- To evaluate the therapeutic potential of targeting the miR-26a-5p/Wnt5a axis in GC.
Main Methods:
- Analysis of transcriptome data from The Cancer Genome Atlas (TCGA) database for miR-26a-5p and Wnt5a expression.
- Quantitative real-time PCR (qRT-PCR) to measure miR-26a-5p and Wnt5a levels in GC tissues and serum.
- In vitro experiments involving transfection of miR-26a-5p and Wnt5a vectors to assess effects on GC cell proliferation, invasion, and apoptosis.
- Dual-luciferase reporter assays to confirm the direct regulatory relationship between miR-26a-5p and Wnt5a.
Main Results:
- Significantly lower miR-26a-5p and higher Wnt5a expression were observed in GC samples compared to normal controls.
- Decreased miR-26a-5p levels correlated with advanced tumor stage, lymphatic metastasis, and larger tumor size, while Wnt5a showed an inverse correlation.
- Overexpression of miR-26a-5p suppressed GC cell proliferation and invasion while promoting apoptosis, accompanied by altered expression of key proteins (Bcl-2, β-catenin, Caspase 3, E-cadherin, Bax).
- Dual-luciferase assays confirmed Wnt5a as a direct target of miR-26a-5p.
Conclusions:
- MiR-26a-5p acts as a tumor suppressor in gastric cancer by inhibiting Wnt5a expression.
- Restoring miR-26a-5p levels can effectively suppress GC cell proliferation and invasion while enhancing apoptosis.
- The miR-26a-5p/Wnt5a axis represents a promising therapeutic target for gastric cancer treatment.
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