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

The epidermal growth factor (EGF) pathway plays critical roles during cancer cell epithelial-mesenchymal transition (EMT) process and metastasis. Epidermal growth factor receptor (EGFR), as one of the important receptors of EGF, undergoes autophosphorylation with the stimulation of EGF and activates MAPK/ERK, PI3K/Akt/mTOR, and other pathways. Here, we identified EGFR was a target of miR-338-5p. Upon EGF treatment, overexpression of miR-338-5p not only downregulated EGFR expression and inhibited MAPK/ERK signaling, but also inhibited EMT and metastasis process of pancreatic cancer (PC) cells. In the clinical pathological analysis, miR-338-5p was significantly down-regulated in 44 pairs PC tissues and its expression was negatively associated with lymph node metastasis and AJCC stage. Furthermore, Overexpression of EGFR partially reversed the protective effect of miR-338-5p overexpression on EGF-mediated migration and invasion in PC cells. Taken together, miR-338-5p controls EGF-mediated EMT and metastasis in PC cells by targeting EGFR/ERK pathways. Here, we hope to provide new insights into the molecular mechanisms of pancreatic cancer, and may help facilitating development of EGFR-based therapies for human cancer.

MiR-338-5p Inhibits EGF-Induced EMT in Pancreatic Cancer Cells by Targeting EGFR/ERK Signaling