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 induces autophagy and apoptosis in lung cancer cell lines. (A, B) H1299, A549 and H838 were treated with LOC389641 siRNAs for 48h and transfected with Premo Autophagy Tandem Sensor RFP-GFP-LC3B for 24h. Cells were visualized live using a fluorescence microscope. Autophagosomes and autolysosomes in each 200X field were counted, at least 100 cells were counted for each siRNA treatment per cell line. Autophagic flow was increased upon LOC389641 silencing in A549 and H1299 cells but were decreased in H838 cells. Scale bar: 5 μm. (C) Western blot showing the changes of autophagy, apoptosis and cell cycle related proteins upon LOC389641 silencing in H1299 and H838 cells (LOC389641 siRNAs treated for 72 h). Apoptosis marker (cleaved-PARP) was induced upon LOC389641 knockdown in H838 cell line.

Figure 5. LOC389641 knockdown induces autophagy and apoptosis in lung cancer cell lines. (A, B) H1299, A549 and H838 were treated with LOC389641 siRNAs for 48h and transfected with Premo Autophagy Tandem Sensor RFP-GFP-LC3B for 24h. Cells were visualized live using a fluorescence microscope. Autophagosomes and autolysosomes in each 200X field were counted, at least 100 cells were counted for each siRNA treatment per cell line. Autophagic flow was increased upon LOC389641 silencing in A549 and H1299 cells but were decreased in H838 cells. Scale bar: 5 μm. (C) Western blot showing the changes of autophagy, apoptosis and cell cycle related proteins upon LOC389641 silencing in H1299 and H838 cells (LOC389641 siRNAs treated for 72 h). Apoptosis marker (cleaved-PARP) was induced upon LOC389641 knockdown in H838 cell line.