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/

Global: Zendy Tools annual

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Presents the access of premium content as premium feature

Premium Content

Global: Zendy Plus annual

Global: Zendy Free Plan

Objective  Understanding the characteristics of tumor suppressor genes (TSGs) is of great significance for the development of new targeted treatment strategies for non-small cell lung cancer (NSCLC). Therefore, this present article is to explore the underlying molecular mechanism of ZFN24 inhibiting the development of NSCLC.    Methods  We performed RT-PCR and Western blotting for evaluating associated RNA and protein expression. CCK8, colony forming and sphere-forming assays were used to evaluate the proliferation and stemness of NSCLC cells. NSCLC cell senescence was examined by  β -galactosidase staining assay. Luciferase assay was performed to evaluate  β -catenin transcriptional activity. The effect of ZNF24 on NSCLC cells  in vivo  was evaluated by the xenograft tumor experiment.    Results  Ectopic expression of ZNF24 significantly inhibited cell viability, colony forming ability, and stemness of NSCLC cells. WNT signaling pathway was inhibited by ZNF24 resulting in NSCLC cell senescence.  β -catenin transcriptional activity was significantly inhibited by ZNF24 (P < 0.05). Ectopic expression of ZNF24 significantly inhibited xenotransplant tumors growth  in vivo  (P < 0.05).    Conclusion  ZNF24 could notably inhibit the development of NSCLC by inhibiting the WNT signaling pathway.

A Novel Tumor Suppressor Gene, ZNF24, Inhibits the Development of NSCLC by Inhibiting the WNT Signaling Pathway to Induce Cell Senescence