English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Zendy Open

Presents the pdf analysis as premium feature

PDF Analysis

Insights

Presents the summarisation as premium feature

Summarisation

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the zaia usage as premium feature

ZAIA

Zendy Tools

Zendy Plus

Presents the access of premium content as premium feature

Premium Content

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.

MiR‐520b restrains cell growth by targeting HDAC4 in lung cancer