Changes in the apoptosis rate of transplantation tumors in nude mice injected with virus and 5-FU (x±s, n = 5).

<p>*: PBS+5-FU vs. V-BCRPi+5-FU, p<0.01.</p

Knockdown of BCRP/ABCG2 expression by V-BCRPi in JAR cells, shown by Western blot analysis.

<p>The results for experimental groups 1 to 7 are shown: 1: mock cells or cells infected with 2: V-BCRP1i, 3: V-BCRP1i-c, 4: V-BCRP2i, 5: V-BCRP2i-c, 6: V-BCRP3i, or 7: V-BCRP3i-c. The BCRP/ABCG2 protein expression of the V-BCRP3i treatment group was the lowest (group 6).</p

Knockdown of BCRP/ABCG2 expression by V-BCRPi in JAR cells using immunofluorescence analysis (×100).

<p>The results for experimental groups 1 to 8 are shown: 1: mock cells with MoAb or 2: PBS or cells infected with 3: V-BCRP1i, 4: V-BCRP1i-c, 5: V-BCRP2i, 6: V-BCRP2i-c, 7: V-BCRP3i, or 8: V-BCRP3i-c. The fluorescence intensity of cells subjected to V-BCRP3i treatment was the lowest.</p

TUNEL staining of the tumor bodies of hairless mice bearing JAR cancer cells injected with V-BCRPi and 5-FU (×200).

<p>The number of apoptotic cells in tumors injected with V-BCRPi and 5-FU was greater than that of the tumors injected with 5-FU alone. The red arrows indicate the apoptotic cells.</p

Relative BCRP/ABCG2 transcript levels of the transplantation tumors in nude mice injected with virus and drugs (x±s, n = 5).

<p>*: PBS+5-FU vs. V-BCRPi+5-FU, p<0.01.</p

Tumor bodies of hairless mice after injection of JAR cancer cells infected with V-BCRPi and treatment with 5-FU.

<p>A1: Tumor body injected with PBS alone; A2: Tumor body injected with PBS and 5-FU; B1: Tumor body injected with V-BCRPi alone; and B2: Tumor body injected with V-BCRPi and 5-FU. After injecting 5-FU, the tumors in the hairless mice injected with V-BCRPi were smaller than those in the un-injected hairless mice. The anti-tumor rate was approximately a factor of 10 (<i>P</i><0.01). It was concluded that V-BCRPi increases the inhibition effects of 5-FU on tumor growth.</p

Immunohistochemical staining of tumor bodies in hairless mice bearing JAR cancer cells after injection with V-BCRPi and 5-FU (×100).

<p>The results indicate that V-BCRPi inhibits <i>BCRP/ABCG2</i> expression and improves drug sensitivity to 5-FU in tumors. The red arrows indicate the dead cells.</p

Inhibition ratio of 5-FU against JAR cells infected with V-BCRPi using cell survival analysis.

<p>Experimental groups 1 to 9, which were submitted to the following treatments, are shown: 1: 5-FU, 2: Ko143+5-FU, 3: pLenti6/vector+5-FU, 4: V-BCRP1i+5-FU, 5: V-BCRP1ic+5-FU, 6: V-BCRP2i+5-FU, 7: V-BCRP2ic+5-FU, 8: V-BCRP3i+5-FU, and 9: V-BCRP3ic+5-FU. The inhibition ratio of the V-BCRP3i treatment group was significantly higher than those of the other virus-free treatment groups. Each inhibition ratio represents the mean value of three independent experiments. *<i>P</i><0.01.</p

Residual drug volumes after infection of JAR cells with V-BCRPi according to flow cytometry analysis.

<p>The results of experimental groups 1 to 9 are shown: 1: mock cells, 2: cells with Mit, 3: cells with Mit and Ko143, or cells with Mit and infected with 4: V-BCRP1i, 5: V-BCRP2i, 6: V-BCRP3i, 7: V-BCRP1i-c, 8: V-BCRP2i-c, or 9: V-BCRP3i-c. Each residual drug volume represents the mean value of three independent experiments. *<i>P</i><0.01.</p

Changes in tumor weight and volume and the anti-tumor rate in transplantation tumors in nude mice after virus infection and drug treatment (x±s, n = 15).

<p>*: PBS+5-FU vs. V-BCRPi+5-FU, p<0.01.</p