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B7-H3 在胰腺癌中的过表达促进肿瘤进展。

B7-H3 overexpression in pancreatic cancer promotes tumor progression.

机构信息

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

出版信息

Int J Mol Med. 2013 Feb;31(2):283-91. doi: 10.3892/ijmm.2012.1212. Epub 2012 Dec 13.

DOI:10.3892/ijmm.2012.1212
PMID:23242015
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4042878/
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.

摘要

B7-H3 是 B7 家族分子的一员，在适应性免疫反应中发挥重要作用。此外，B7-H3 在几种人类癌症中也有表达，并与癌症患者的不良预后相关。然而，其在癌症中的确切作用尚不清楚。本研究比较了正常胰腺组织和胰腺癌组织标本中 B7-H3 的表达，并通过慢病毒介导的 RNA 干扰研究了低表达 B7-H3 对人胰腺癌细胞系 Patu8988 的影响。通过酶联免疫吸附试验（ELISA）检测胰腺标本中的 B7-H3 表达。通过慢病毒介导的 RNA 干扰建立低 B7-H3 表达的 Patu8988 细胞系，以研究 B7-H3 对细胞增殖、迁移和侵袭的体外影响。通过建立皮下移植瘤和原位移植胰腺癌小鼠模型，研究了 B7-H3 在体内对细胞增殖、迁移和侵袭的影响。与正常胰腺组相比，胰腺癌组织中 B7-H3 的表达明显升高（均数±标准差，193.6±9.352 比 87.74±7.433 ng/g；P<0.0001）。RNA 干扰下调 B7-H3 可使细胞迁移和 Transwell 侵袭减少 50%。体外细胞增殖未见明显影响。在皮下移植瘤小鼠模型中，下调 B7-H3 可降低肿瘤生长速度。在原位移植胰腺癌小鼠模型中，通过检测死后腹部内脏转移瘤的平均重量来评估下调 B7-H3 抑制转移的效果。这表明抑制 B7-H3 表达可减少体内胰腺癌转移。综上所述，B7-H3 在胰腺癌中异常表达。除了调节肿瘤免疫外，B7-H3 可能在调节胰腺肿瘤进展方面具有新的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6232/4042878/5b2f8da8fe73/IJMM-31-02-0283-g13.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6232/4042878/f6babf781b35/IJMM-31-02-0283-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6232/4042878/5ac8275e3a4b/IJMM-31-02-0283-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6232/4042878/ad43555f2ebb/IJMM-31-02-0283-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6232/4042878/364976803c25/IJMM-31-02-0283-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6232/4042878/d146aef83a39/IJMM-31-02-0283-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6232/4042878/769a0434251a/IJMM-31-02-0283-g07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6232/4042878/93cd4fb2dd83/IJMM-31-02-0283-g08.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6232/4042878/4a0f53d5da94/IJMM-31-02-0283-g10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6232/4042878/466364ee6880/IJMM-31-02-0283-g12.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6232/4042878/5b2f8da8fe73/IJMM-31-02-0283-g13.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6232/4042878/f6babf781b35/IJMM-31-02-0283-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6232/4042878/5ac8275e3a4b/IJMM-31-02-0283-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6232/4042878/ad43555f2ebb/IJMM-31-02-0283-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6232/4042878/364976803c25/IJMM-31-02-0283-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6232/4042878/d146aef83a39/IJMM-31-02-0283-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6232/4042878/769a0434251a/IJMM-31-02-0283-g07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6232/4042878/93cd4fb2dd83/IJMM-31-02-0283-g08.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6232/4042878/4a0f53d5da94/IJMM-31-02-0283-g10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6232/4042878/466364ee6880/IJMM-31-02-0283-g12.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6232/4042878/5b2f8da8fe73/IJMM-31-02-0283-g13.jpg

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