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B7-H3 overexpression in pancreatic cancer promotes tumor progression.

Zhao X, Li DC, Zhu XG, Gan WJ, Li Z, Xiong F, Zhang ZX, Zhang GB, Zhang XG, Zhao H - Int. J. Mol. Med. (2012)

Bottom Line: In the present study, we compared B7-H3 expression in normal pancreas and pancreatic cancer tissue specimens, and determined the effects of low B7-H3 expression on the human pancreatic cancer cell line Patu8988 using lentivirus-mediated RNA interference.This demonstrated that inhibition of B7-H3 expression reduced pancreatic cancer metastasis in vivo.In conclusion, B7-H3 is aberrantly expressed in pancreatic cancer.

View Article: PubMed Central - PubMed

Affiliation: Department of General Surgery, The First Affiliated Hospital of Soochow University, Suzhou, P.R. China.

ABSTRACT
B7-H3, a member of the B7-family molecules, plays an important role in adaptive immune responses. In addition, B7-H3 is also expressed in several types of human cancers and is correlated with the poor outcome of cancer patients. However, its exact role in cancer is not known. In the present study, we compared B7-H3 expression in normal pancreas and pancreatic cancer tissue specimens, and determined the effects of low B7-H3 expression on the human pancreatic cancer cell line Patu8988 using lentivirus-mediated RNA interference. B7-H3 expression in pancreatic specimens was determined by enzyme-linked immunosorbent assay (ELISA). A Patu8988 cell line with low B7-H3 expression was established by lentivirus-mediated RNA interference to investigate the effect of B7-H3 on cell proliferation, migration and invasion in vitro. By establishing subcutaneous transplantation tumor and orthotopic transplantation pancreatic cancer mouse models, the effect of B7-H3 on cell proliferation, migration and invasion was studied in vivo. B7-H3 in tissue samples was significantly higher in the pancreatic cancer group than in the normal pancreas group (mean ± SD, 193.6±9.352 vs. 87.74±7.433 ng/g; P<0.0001). B7-H3 knockdown by RNA interference decreased cell migration and Transwell invasion up to 50% in vitro. No apparent impact was observed on cell proliferation in vitro. In the subcutaneous transplantation tumor mouse model, the tumor growth rate was reduced by the knockdown of B7-H3. In the orthotopic transplantation pancreatic cancer mouse model, the effect of inhibiting metastasis by knocking down B7-H3 was assessed in terms of the average postmortem abdominal visceral metastatic tumor weight. This demonstrated that inhibition of B7-H3 expression reduced pancreatic cancer metastasis in vivo. In conclusion, B7-H3 is aberrantly expressed in pancreatic cancer. In addition to modulating tumor immunity, B7-H3 may have a novel role in regulating pancreatic tumor progression.

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Tumor growth in the subcutaneous transplantation mouse model. (A) A subcutaneoustransplantation mouse model was established, and subcutaneous transplantation xenograftswere excised after 6 weeks. (B) Growth curves of pancreatic cancer subcutaneousxenografts in nude mice are shown. Each group consisted of 6 mice, and the data areexpressed as means ± SD. The tumor volume of the LV-B7-H3 group was obviouslysmaller (*P<0.01, vs. the control group).
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f8-ijmm-31-02-0283: Tumor growth in the subcutaneous transplantation mouse model. (A) A subcutaneoustransplantation mouse model was established, and subcutaneous transplantation xenograftswere excised after 6 weeks. (B) Growth curves of pancreatic cancer subcutaneousxenografts in nude mice are shown. Each group consisted of 6 mice, and the data areexpressed as means ± SD. The tumor volume of the LV-B7-H3 group was obviouslysmaller (*P<0.01, vs. the control group).

Mentions: The in vitro experiments with the Patu8988 cells showed the effects ofB7-H3 on tumor progression. Hence, we examined whether this could be observed invivo. LV-B7-H3, LV-NC and control cells were injected subcutaneously into nudemice. All of the 18 mice developed detectable tumors at the beginning of this experiment.The growth rate was reduced by the knockdown of B7-H3 (Fig. 8). Inhibition of tumor growth was observed in the LV-B7-H3group at 6 weeks, when compared to the LV-NC group (211±47 mm3) or thecontrol group (235±57 mm3). The average tumor volume (22±5mm3) in the LV-B7-H3 group was significantly lower than that in the LV-NC andcontrol groups (P<0.01). There was no statistical significance in tumor volumebetween the LV-NC and the control group (P>0.05).


B7-H3 overexpression in pancreatic cancer promotes tumor progression.

Zhao X, Li DC, Zhu XG, Gan WJ, Li Z, Xiong F, Zhang ZX, Zhang GB, Zhang XG, Zhao H - Int. J. Mol. Med. (2012)

Tumor growth in the subcutaneous transplantation mouse model. (A) A subcutaneoustransplantation mouse model was established, and subcutaneous transplantation xenograftswere excised after 6 weeks. (B) Growth curves of pancreatic cancer subcutaneousxenografts in nude mice are shown. Each group consisted of 6 mice, and the data areexpressed as means ± SD. The tumor volume of the LV-B7-H3 group was obviouslysmaller (*P<0.01, vs. the control group).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4042878&req=5

f8-ijmm-31-02-0283: Tumor growth in the subcutaneous transplantation mouse model. (A) A subcutaneoustransplantation mouse model was established, and subcutaneous transplantation xenograftswere excised after 6 weeks. (B) Growth curves of pancreatic cancer subcutaneousxenografts in nude mice are shown. Each group consisted of 6 mice, and the data areexpressed as means ± SD. The tumor volume of the LV-B7-H3 group was obviouslysmaller (*P<0.01, vs. the control group).
Mentions: The in vitro experiments with the Patu8988 cells showed the effects ofB7-H3 on tumor progression. Hence, we examined whether this could be observed invivo. LV-B7-H3, LV-NC and control cells were injected subcutaneously into nudemice. All of the 18 mice developed detectable tumors at the beginning of this experiment.The growth rate was reduced by the knockdown of B7-H3 (Fig. 8). Inhibition of tumor growth was observed in the LV-B7-H3group at 6 weeks, when compared to the LV-NC group (211±47 mm3) or thecontrol group (235±57 mm3). The average tumor volume (22±5mm3) in the LV-B7-H3 group was significantly lower than that in the LV-NC andcontrol groups (P<0.01). There was no statistical significance in tumor volumebetween the LV-NC and the control group (P>0.05).

Bottom Line: In the present study, we compared B7-H3 expression in normal pancreas and pancreatic cancer tissue specimens, and determined the effects of low B7-H3 expression on the human pancreatic cancer cell line Patu8988 using lentivirus-mediated RNA interference.This demonstrated that inhibition of B7-H3 expression reduced pancreatic cancer metastasis in vivo.In conclusion, B7-H3 is aberrantly expressed in pancreatic cancer.

View Article: PubMed Central - PubMed

Affiliation: Department of General Surgery, The First Affiliated Hospital of Soochow University, Suzhou, P.R. China.

ABSTRACT
B7-H3, a member of the B7-family molecules, plays an important role in adaptive immune responses. In addition, B7-H3 is also expressed in several types of human cancers and is correlated with the poor outcome of cancer patients. However, its exact role in cancer is not known. In the present study, we compared B7-H3 expression in normal pancreas and pancreatic cancer tissue specimens, and determined the effects of low B7-H3 expression on the human pancreatic cancer cell line Patu8988 using lentivirus-mediated RNA interference. B7-H3 expression in pancreatic specimens was determined by enzyme-linked immunosorbent assay (ELISA). A Patu8988 cell line with low B7-H3 expression was established by lentivirus-mediated RNA interference to investigate the effect of B7-H3 on cell proliferation, migration and invasion in vitro. By establishing subcutaneous transplantation tumor and orthotopic transplantation pancreatic cancer mouse models, the effect of B7-H3 on cell proliferation, migration and invasion was studied in vivo. B7-H3 in tissue samples was significantly higher in the pancreatic cancer group than in the normal pancreas group (mean ± SD, 193.6±9.352 vs. 87.74±7.433 ng/g; P<0.0001). B7-H3 knockdown by RNA interference decreased cell migration and Transwell invasion up to 50% in vitro. No apparent impact was observed on cell proliferation in vitro. In the subcutaneous transplantation tumor mouse model, the tumor growth rate was reduced by the knockdown of B7-H3. In the orthotopic transplantation pancreatic cancer mouse model, the effect of inhibiting metastasis by knocking down B7-H3 was assessed in terms of the average postmortem abdominal visceral metastatic tumor weight. This demonstrated that inhibition of B7-H3 expression reduced pancreatic cancer metastasis in vivo. In conclusion, B7-H3 is aberrantly expressed in pancreatic cancer. In addition to modulating tumor immunity, B7-H3 may have a novel role in regulating pancreatic tumor progression.

Show MeSH
Related in: MedlinePlus