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. 2013 Feb 17;104(4):431–436. doi: 10.1111/cas.12104

Figure 5.

Figure 5

c‐MET has a role in the maintenance of prostate cancer stem‐like cells (CSCs)/cancer‐initiating cells (CICs). (A) Reverse transcription‐polymerase chain reaction (RT‐PCR) of MET knockdown cells. MET‐specific siRNA and control siRNA were transfected into 22Rv1 cells. Two days after transfection, total RNA was purified and analyzed by RT‐PCR. Glyceraldehyde 3‐phosphate dehydrogenase (GAPDH) was used as an internal control. (B) ALDEFLUOR assay of MET knockdown cells. MET siRNA3‐ and control siRNA‐transfected 22Rv1 cells were analyzed by ALDEFLUOR assay. Percentages indicate rates of ALDH1high cells. (C) MET gene knockdown inhibited cell growth in vitro. MET siRNA3‐ and control siRNA‐transfected 22Rv1 cells were seeded into a six‐well plate, and cell numbers were counted at 24, 48 and 72 h. An asterisk represents a statistically significant difference (P < 0.05, t‐test). (D) MET gene knockdown inhibited prostasphere formation in vitro. MET siRNA3‐ and control siRNA‐transfected 22Rv1 cells were seeded into an Ultra‐Low Attachment plate and cultured for 3 days. (E) MET gene knockdown inhibited tumor initiation in vivo. MET siRNA3‐ and control siRNA‐transfected 22Rv1 cells were transplanted into male NOD/SCID mice subcutaneously. Tumor growth was measured every week. Tumor growth curve and a representative picture are shown. An asterisk represents a statistically significant difference (P < 0.05, t‐test). (F) ALDH1 expression in MET knockdown tumor. ALDH1 expression was investigated by immunohistochemical staining. Representative pictures are shown. Magnification, ×100.