Notch2 regulates matrix metallopeptidase 9 via PI3K/AKT signaling in human gastric carcinoma cell MKN-45

Figure 1 Verification of successful transfection and knockdown of Notch2. ^aP < 0.05, ^bP < 0.01 vs the Mock or Scra groups. Scra: Scrambled small interfering RNA (siRNA); qPCR: Quantitative reverse transcription polymerase chain reaction.

Figure 2 Knockdown of Notch2 led to an increased migration and invasion of MKN-45 cells. Cells were transfected with scrambled small interfering RNA (siRNA) (Scra, A, C) or Notch2 siRNA (B, D) for 48 h, and the effect of the migration (A, B, E) and invasion (C, D, F) were assayed as described in “Materials and Methods”. The number of migrated cells or invaded cells were quantitated (E, F). ^aP < 0.05 vs the Scra groups. A, B, ×200; C, D, ×400.

Figure 3 Knockdown of Notch2 enhanced the expression and activity of matrix metallopeptidase 9. The small interfering RNA (siRNA) mediated knockdown of Notch2 (A) and Notch2 intracellular domain (N2ICD) (B, C) was associated with a marked increase in the expression (A, B, C) and activity (D) of matrix metallopeptidase 9 (MMP9). ^aP < 0.05, ^bP < 0.01 vs the blank control groups. qPCR: Quantitative reverse transcription polymerase chain reaction.

Figure 4 Knockdown of Notch2 enhanced the expression of matrix metallopeptidase 9 via increased phosphorylation of p-Akt in MKN-45 cells. A, B: Knockdown of Notch2 led to an increased phosphorylation of Akt (p-Akt); C, D: Blockade of PI3K/Akt pathway by LY294002 (20 μmol/L) abolished the effect of Notch small interfering RNA (siRNA) in Akt phosphorylation and matrix metallopeptidase 9 (MMP9). ^aP < 0.05 vs the all control groups. DMSO: Dimethyl sulfoxide.