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 Plus annual

Presents the access of premium content as premium feature

Premium Content

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 annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Purpose  The aim of this study was to explore the functions and associated mechanisms of long noncoding RNA  LINC02487  in oral squamous cell carcinoma (OSCC).    Methods  The relative expression levels of  LINC02487  in OSCC cell lines and tissue samples were examined by RT-qPCR. Intracellular localization was determined using RNA fluorescence  in situ  hybridization.  LINC02487  was cloned into the pCMV-puro vector and then introduced into OSCC cells using lentiviral transfection. Cell processes, such as proliferation, apoptosis, migration, and invasion, were subsequently examined.  LINC02487 -binding proteins were identified by ChIRP–MS and confirmed by RNA immunoprecipitation. Protein expression was determined by western blotting assay.    Results    LINC02487  has been reported to be downregulated in OSCC. Here, we confirmed that the expression of  LINC02487  was reduced in 6 OSCC cell lines compared with that in immortalized normal oral epithelial cells and in 50 OSCC samples compared with paired adjacent normal tissue in a Chinese population and that  LINC02487  expression levels were associated with cancer metastasis. We further identified that  LINC02487  was localized to the cytoplasm, aggregated around the nuclear membrane. Functional studies demonstrate that overexpression of  LINC02487  significantly suppresses cell migration and invasion and also inhibits cell proliferation. For the mechanism, we reveal that  LINC02487  directly binds to USP17, a deubiquitinating enzyme, and regulates cell migration and invasion through the USP17–SNAI1 axis in a process that involves epithelial–mesenchymal transition (EMT).    Conclusion  Our results confirm that long noncoding RNA  LINC02487  is downregulated in OSCC tissue samples and cell lines. We also find that  LINC02487  acts as a tumor suppressor through the USP17–SNAI1 axis.

Tumor Suppressor LINC02487 Inhibits Oral Squamous Cell Carcinoma Cell Migration and Invasion Through the USP17–SNAI1 Axis