[Corrigendum] Netrin‑1 induces the proliferation of gastric cancer cells via the ERK/MAPK signaling pathway and FAK activation

Figure 5.

In vivo analysis of NTN1 in the regulation of gastric cancer cell growth. (A) Following transfection with NTN1 knockdown or overexpression lentivirus, MGC803 cells were injected into the right flank of nude mice. Mice were sacrificed after 4 weeks and tumors were obtained from nude mice. Representative images of isolated tumors in the NTN1 knockdown group (first row), control group (second row) and NTN1 overexpression group (third row). Tumor (B) volume and (C) weight were examined at 5 different time points following injection with MGC803 cells with NTN1 knockdown or overexpression. (D) SGC7901 cells were injected into the right flank of nude mice. Representative images of isolated tumors in the NTN1 knockdown group (first row), control group (second row) and NTN1 overexpression group (third row). Tumor (E) volume and (F) weight were examined at 5 different time points following injection with SGC7901 cells with NTN1 knockdown or overexpression. The expression of NTN1 in tissues collected from nude mice that were injected with (G) MGC803 and (H) SGC7901 cells was examined by reverse transcription-quantitative polymerase chain reaction. Ki-67 IHC staining was used to determine the effects of NTN1 expression on the cell proliferation abilities in the samples collected from nude mice injected with (I) MGC803 and (J) SGC7901 cells. Original magnification, ×100; Scale bar, 100 µm. *P<0.05, **P<0.01 and ***P<0.001. NTN1, Netrin-1; sh, shRNA; CTL, control.