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

Bladder cancer is one of the most common malignant tumors of the urinary system, and its incidence is increasing worldwide. However, the underlying mechanisms that trigger migration, invasion and chemotherapy resistance are unclear. Bioinformatics analysis of bladder cancer cohort indicated that  LINC00839  is deregulated in bladder cancer.  LINC00839  was validated and highly expressed in bladder cancer patients and cell lines. In addition,  LINC00839  induced the migration, invasion and Gemcitabine resistance of bladder cancer cells. We identified that the transcription factor EGR1 directly repressed  LINC00839  and thereby suppressed the migration and invasion of bladder cancer cells. Furthermore,  LINC00839  interacted with miR-142, which subsequently regulated the expression of SOX5, a well-studied oncogene and targeted by miR-142. In addition, EGR1 served as a suppressive transcription factor of  SOX5 . Therefore, EGR1 directly or indirectly regulates SOX5 via  LINC00839 /miR-142 axis.  LINC00839  induced Gemcitabine resistance by promoting autophagy. EGR1,  LINC00839 /miR-142 and SOX5 form a coherent feed-forward loop that modulates the migration, invasion and Gemcitabine resistance of bladder cancer.

EGR1/ LINC00839 /SOX5 axis modulates migration, invasion and Gemcitabine resistance of bladder cancer cells