Research Paper Volume 13, Issue 2 pp 2539—2552

Silencing of LOC389641 impairs cell proliferation and induces autophagy via EGFR/MET signaling in lung adenocarcinoma

LOC389641 knockdown decreases EGFR, MET and STAT3 proteins expression. (A) Western blot showing total EGFR, total MET and phosphor-STAT3 proteins were decreased upon LOC389641 silencing (si389641) in H1299 and H838 cells. LOC389641 siRNA treatment was for 72 h. GAPDH was uses as protein loading control. (B) Western blot showing the changes of EGFR, MET and STAT3 proteins after EGFR or MET siRNAs treatment in PC-9 and H1975 cells. siRNAs treated for 72 h, α-Tubulin used as protein loading control. (C) Gene Ontology (GO) analysis of LOC389641 positively-correlated genes. Cell cycle related biology processes were on the top of the list. (D) The schematic model of the cell proliferation, autophagy, apoptosis signaling regulated by MET, EGFR and STAT3 triggered by LOC389641 knockdown in lung cancer.

Figure 6. LOC389641 knockdown decreases EGFR, MET and STAT3 proteins expression. (A) Western blot showing total EGFR, total MET and phosphor-STAT3 proteins were decreased upon LOC389641 silencing (si389641) in H1299 and H838 cells. LOC389641 siRNA treatment was for 72 h. GAPDH was uses as protein loading control. (B) Western blot showing the changes of EGFR, MET and STAT3 proteins after EGFR or MET siRNAs treatment in PC-9 and H1975 cells. siRNAs treated for 72 h, α-Tubulin used as protein loading control. (C) Gene Ontology (GO) analysis of LOC389641 positively-correlated genes. Cell cycle related biology processes were on the top of the list. (D) The schematic model of the cell proliferation, autophagy, apoptosis signaling regulated by MET, EGFR and STAT3 triggered by LOC389641 knockdown in lung cancer.