Table 1.
Clinico-pathological features of patients with bladder cancer and normal controls.
Fig 1.
Loss of c-MET reduced anchorage-independent proliferation (A) and invasion (B) of T24 bladder cancer cells with an increased cisplatin-induced cell apoptosis (C).
All experiments were performed using three c-MET knockdown cell lines (sic-MET-1, sic-MET-2, and sic-MET-3) transfected with different METsiRNAs, and two controls cell lines (Ctrl and NT). Ctrl, control; NT, non-transfected.*p<0.05.
Fig 2.
MMP2 and MMP9 may be downstream effectors of c-MET knockdown, leading to suppression of migration in T24 bladder cancer cells.
(A) Wound-healing assay showing that knockdown of c-MET inhibitsthe migration of T24 cells. (B) Loss of c-MET downregulated the expression of matrix metalloproteinases (MMP)-2 and MMP-9. All experiments were performed using two c-MET knockdown cell lines (sic-MET-1 and sic-MET-2) transfected with different MET siRNAs, and two control cell lines (Ctrl and NT). Ctrl, control; NT, non-transfected.
Fig 3.
Kaplan–Meier curves showing that high expression of c-MET genes correlates with poor overall survival of MIBC patients.
Table 2.
c-MET gene expression correlates to OS of MIBC patients.
Table 3.
AXL mRNA expression in bladder cancer (NMIBC and MIBC) patients and normal controls.
Table 4.
Expression of PDGFR isoforms in bladder cancer (NMIBC and MIBC) patients.
Fig 4.
Kaplan–Meier curves showing that high expression of PDGFRL (one of the PDGFR isoforms) correlates with disease progression in NMIBC patients.
Table 5.
Expression of PDGFR isoforms and clinicopathological features of bladder cancer.
Fig 5.
Kaplan–Meier curves showing that high expression of c-MET network genes correlates with (A) poor progression-free survival in NMIBC patientsand (B) poor overall survival in MIBC patients.
Table 6.
c-MET network gene expression correlates with NMIBC progression and with OS of MIBC patients.