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 cellular location and knockdown impairs cell proliferation. (A–C) qRT-PCR showing the nuclear and cytoplasmic fractions of LOC389641 in H1299, H838 and PC-9 cells. GAPDH is used as cytoplasmic control and U1 snRNA as nuclear control. LOC389641 is primarily in cytoplasm (61% - 77%). (D) LOC389641 siRNA knockdown efficiency (48 h) in H1299, H838 and PC-9 cell lines measured by qRT-PCR. GAPDH is used as loading control. (E) Cell proliferation is decreased after LOC389641 siRNAs treatment in H1299, H838 and PC-9 cell lines. ** p F, G) Flow cytometry analysis to evaluate the effects of LOC389641 on cell cycle distribution in H1299 and H838 cell lines.

Figure 3. LOC389641 cellular location and knockdown impairs cell proliferation. (AC) qRT-PCR showing the nuclear and cytoplasmic fractions of LOC389641 in H1299, H838 and PC-9 cells. GAPDH is used as cytoplasmic control and U1 snRNA as nuclear control. LOC389641 is primarily in cytoplasm (61% - 77%). (D) LOC389641 siRNA knockdown efficiency (48 h) in H1299, H838 and PC-9 cell lines measured by qRT-PCR. GAPDH is used as loading control. (E) Cell proliferation is decreased after LOC389641 siRNAs treatment in H1299, H838 and PC-9 cell lines. ** p < 0.01 by t test. (F, G) Flow cytometry analysis to evaluate the effects of LOC389641 on cell cycle distribution in H1299 and H838 cell lines.