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钙黏蛋白-12通过促进迁移、侵袭、黏附和血管生成，在结直肠癌的致瘤性中发挥作用。

Cadherin-12 contributes to tumorigenicity in colorectal cancer by promoting migration, invasion, adhersion and angiogenesis.

作者信息

Zhao Jingkun, Li Pu, Feng Hao, Wang Puxiongzhi, Zong Yaping, Ma Junjun, Zhang Zhuo, Chen Xuehua, Zheng Minhua, Zhu Zhenggang, Lu Aiguo

机构信息

Shanghai Minimally Invasive Surgery Center, Shanghai Key Laboratory of Gastric Neoplasms, Department of Surgery, Shanghai Institute of Digestive Surgery, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, 197 Rui Jin Er Rd, Shanghai 200025, People's Republic of China.

出版信息

J Transl Med. 2013 Nov 15;11:288. doi: 10.1186/1479-5876-11-288.

DOI:10.1186/1479-5876-11-288
PMID:24237488
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3879717/
Abstract

BACKGROUND

Cadherin 12 (CDH12), which encodes a type II classical cadherin from the cadherin superfamily, may mediate calcium-dependent cell adhesion. It has been demonstrated that CDH12 could play an important role in the invasion and metastasis of salivary adenoid cystic carcinoma. We decided to investigate the relationship between CDH12 expression level and clinicopathologic variables in colorectal carcinoma (CRC) patients and to explore the functions of CDH12 in tumorigenesis in CRC.

METHODS

The expression levels of CDH12 in colorectal carcinoma tissues were detected by immunohistochemistry. Real-time PCR and Western Blot were used to screen CDH12 high-expression cell lines. CCK-8 assay was used to detect the proliferation ability of CRC cells being transfected by shRNAs against CDH12. The wound assay and transwell assay were performed to test migration and invasion ability. The importance of CDH12 in cell-cell junctions was detected by cell adhesion assay and cell aggregation assay. Endothelial tube formation assay was used to test the influence of CDH12 on angiogenesis.

RESULTS

Statistical analysis of clinical cases revealed that the positive rate of CDH12 was higher in the CRC tumor tissues compared with the adjacent non-tumor tissues. The expression levels of CDH12 in CRC patients are significantly correlated with invasion depth. Consistently, the ability of proliferation, migration and invasion were suppressed when CDH12 was decreased in CRC cells transfected with shRNAs. Cell adhesion assay and cell aggregation assay presented that tumor cells tend to disperse with the lack of CDH12. Endothelial tube formation assay showed that down-regulation of CDH12 could obviously inhibit the process of angiogenesis, implying that CDH12 may play an important role in tumor metastasis

CONCLUSION

Our results showed that CDH12 promotes proliferation, migration, invasion, adhesion and angiogenesis, suggesting that CDH12 may be an oncogene in colorectal cancer. CDH12 is expected to become a new diagnostic and prognostic marker and a novel target of the treatment of colorectal cancer.

摘要

背景

钙黏蛋白12（CDH12）编码钙黏蛋白超家族中的II型经典钙黏蛋白，可能介导钙依赖性细胞黏附。已证明CDH12在涎腺腺样囊性癌的侵袭和转移中起重要作用。我们决定研究CDH12表达水平与结直肠癌（CRC）患者临床病理变量之间的关系，并探讨CDH12在CRC肿瘤发生中的作用。

方法

采用免疫组织化学法检测结直肠癌组织中CDH12的表达水平。采用实时荧光定量PCR和蛋白质免疫印迹法筛选CDH12高表达细胞系。采用CCK-8法检测针对CDH12的短发夹RNA（shRNAs）转染的CRC细胞的增殖能力。进行划痕实验和Transwell实验以检测迁移和侵袭能力。通过细胞黏附实验和细胞聚集实验检测CDH12在细胞间连接中的重要性。采用内皮管形成实验检测CDH12对血管生成的影响。

结果

临床病例统计分析显示，与相邻非肿瘤组织相比，CRC肿瘤组织中CDH12的阳性率更高。CRC患者中CDH12的表达水平与侵袭深度显著相关。同样，在用shRNAs转染的CRC细胞中，当CDH12表达降低时，其增殖、迁移和侵袭能力受到抑制。细胞黏附实验和细胞聚集实验表明，缺乏CDH12时肿瘤细胞倾向于分散。内皮管形成实验表明，CDH12的下调可明显抑制血管生成过程，这意味着CDH12可能在肿瘤转移中起重要作用。

结论

我们的结果表明，CDH12促进增殖、迁移、侵袭、黏附和血管生成，提示CDH12可能是结直肠癌中的一个癌基因。CDH12有望成为结直肠癌新的诊断和预后标志物以及新的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f52b/3879717/a54d381347cc/1479-5876-11-288-7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f52b/3879717/a172f6cb24f4/1479-5876-11-288-1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f52b/3879717/c8ecc4fbfe87/1479-5876-11-288-3.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f52b/3879717/7e4300429f9e/1479-5876-11-288-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f52b/3879717/79de0c70dcab/1479-5876-11-288-6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f52b/3879717/a54d381347cc/1479-5876-11-288-7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f52b/3879717/a172f6cb24f4/1479-5876-11-288-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f52b/3879717/e2d526f99f37/1479-5876-11-288-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f52b/3879717/c8ecc4fbfe87/1479-5876-11-288-3.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f52b/3879717/a54d381347cc/1479-5876-11-288-7.jpg

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