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. 2019 Jan 9;11(1):63. doi: 10.3390/cancers11010063

Figure 3.

Figure 3

LDOC1 mediates the in vitro malignancy progression in lung cancer cell lines. (A) Expression of LDOC1mRNA and protein were stably suppressed in the A549-derived cell lines. The A549 cell line was transducing lentivirus carrying either scramble control vector (A549-shCtrl) or siRNA targeting LDOC1 (A549-shLDOC1). (B) Restoration of LDOC1 expression in A549-shLDOC1-derived cells. A549-shLDOC1 was only transducing GFP-tagged lentivirus vectors (A549-sh-rCtrl) or those fused with an LDOC1 open reading frame (A549-sh-rLDOC1). Expression of LDOC1mRNA (left) and protein (right) was measured using qPCR and Western blotting analysis, respectively. (C–F) Cell proliferation (C, by MTT), cell cycle progression (D, by BrdU incorporation assay), and cell invasion (E,F by Matrigel coated trans-well invasiveness assay) were assessed in the parental A549 cells and the generated A549-derived cell lines (C–E) or H1299 ectopic-expressing LDOC1 (F). H1299 cells were transduced with lentivirus carrying either open reading frame (ORF) of LDOC1 or empty vector (V, controls). Expression of LDOC1 and GAPDH proteins were measured using Western blotting analysis (F, upper panels). The number of invading cells was the average of four independent experiments; data were analyzed using a Student’s t-test., where * p < 0.05 and ** p < 0.01. Representative photographs of the invading cells are presented. Scale Bar, 1 mm.