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MiR-520b restrains cell growth by targeting HDAC4 in lung cancer
Ke Jin1, Weixin Zhao2,3, Xuan Xie1
1Department of Thoracic Surgery, Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
Background:
MicroRNAs (miRNAs) function as tumor promoting or tumor suppressing factors in many cancers. MiR-520b contributes to progression in head-neck and liver cancers, spinal osteosarcoma, and glioma; however, the association of miR-520b with lung cancer progression remains unknown. In this investigation, we explore the effect of miR-520b targeting HDAC4 on lung cancer growth.
Methods:
The regulation of miR-520b or its inhibitor on HDAC4 expression was analyzed using Western blot analysis. After treatment of miR-520b or its inhibitor, miR-520b and HDAC4 levels were examined using quantitative real time-PCR. The modulation of miR-520b on HDAC4 was investigated by luciferase reporter gene assay. Cell proliferation evaluation was performed using colony formation and methyl-thiazolyl-tetrazolium assays. The correlation between miR-520b and HDAC4 in human clinical samples was verified using Pearson's correlation coefficient.
Results:
An obvious decrease in HDAC4 expression was observed in lung cancer A549 cells treated with different doses of miR-520b. The miR-520b inhibitor enhanced HDAC4 expression in lung cancer cells. Bioinformatics predicted the targeting of miR-520b on HDAC4. MiR-520b directly targeted the 3' untranslated region of HDAC4. The introduction of miR-520b obviously inhibited cell proliferation in vitro. Anti-miR-520b was capable of accelerating lung cancer cell proliferation; however, HDAC4 knockdown destroyed anti-miR-520b-induced cell proliferation. Finally, a negative correlation between miR-520b and HDAC4 was observed in clinical human lung cancer samples.
Conclusion:
MiR-520b decreases HDAC4 expression to control cell proliferation in lung cancer.
Insights
MicroRNA-520b inhibits lung cancer growth by reducing HDAC4 expression. This microRNA (miRNA) acts as a tumor suppressor in lung cancer, with its levels negatively correlating with HDAC4 in patient samples.
Area of Science:
- Molecular Biology
- Oncology
- Gene Regulation
Background:
- MicroRNAs (miRNAs) are key regulators in cancer, with roles as either tumor promoters or suppressors.
- While miR-520b's role is known in other cancers, its involvement in lung cancer progression was previously uncharacterized.
- This study investigates the specific function of miR-520b in lung cancer.
Purpose of the Study:
- To elucidate the role of miR-520b in lung cancer progression.
- To determine if miR-520b targets Histone Deacetylase 4 (HDAC4).
- To assess the impact of the miR-520b/HDAC4 axis on lung cancer cell proliferation.
Main Methods:
- Western blot and quantitative real-time PCR (qRT-PCR) were used to analyze miR-520b and HDAC4 expression.
- Luciferase reporter assays confirmed direct targeting of HDAC4 by miR-520b.
- Cell proliferation was assessed using colony formation and MTT assays, with correlation analysis performed on clinical samples.
Main Results:
- miR-520b significantly decreased HDAC4 expression in lung cancer cells, while a miR-520b inhibitor increased it.
- Bioinformatics and luciferase assays confirmed direct binding of miR-520b to the HDAC4 3' untranslated region.
- miR-520b introduction inhibited cell proliferation, whereas HDAC4 knockdown counteracted the effects of anti-miR-520b.
Conclusions:
- MiR-520b functions as a tumor suppressor in lung cancer by directly targeting and reducing HDAC4 expression.
- This regulatory mechanism effectively controls lung cancer cell proliferation.
- A negative correlation between miR-520b and HDAC4 expression was validated in human lung cancer tissues.
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