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DC - SIGNR通过影响长链非编码RNA HNRNPKP2上调胃癌肝转移中CXCR4的表达。

DC - SIGNR by influencing the lncRNA HNRNPKP2 upregulates the expression of CXCR4 in gastric cancer liver metastasis.

作者信息

Zhang Yu, Zhang Qianshi, Zhang Mengyang, Yuan Menglang, Wang Zhaohui, Zhang Jingbo, Zhou Xu, Zhang Yinan, Lin Fang, Na Heya, Ren Shuangyi, Zuo Yunfei

机构信息

Department of Clinical Biochemistry, College of Laboratory Diagnostic Medicine, Dalian Medical University, lvshun South Road West 9, Dalian, 116044, China.

Department of General Surgery, The Second Affiliated Hospital of Dalian Medical University, Dalian, Shahekou District Zhongshan Road no. 467, 116023, Dalian, China.

出版信息

Mol Cancer. 2017 Apr 13;16(1):78. doi: 10.1186/s12943-017-0639-2.

DOI:10.1186/s12943-017-0639-2
PMID:28403883
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5390362/
Abstract

BACKGROUND

Profiling evidences of selectin demonstrate that they play an crucial role in cancer progression and metastasis. However, DC-SIGNR as a family member of selectin participates in gastric cancer liver metastasis remains unknown.

METHODS

The serum level of DC-SIGNR was evaluated in gastric cancer patients by ELISA. Manipulation DC-SIGNR expression in BGC823 and SGC7901 cell lines was mediated by lentivirus. Investigation the biological effects of DC-SIGNR were verified by MTT, wounding and transwell in vitro and experiments on animals to confirm gastric cancer liver metastasis by IVIS. Insights of the mechanism were employed microarray and bioinformatic analysis. Further to confirm the results were conducted by qRT-PCR, western blot and by flow cytometry.

RESULTS

DC-SIGNR serum level was significantly increased in gastric cancer patients compared with healthy group. Additionally, DC-SIGNR level was associated with an advanced pathological stage in gastric cancer patients. DC-SIGNR knockdown inhibited the proliferation, migration and invasion of gastric cancer cells in vitro and suppressed the liver metastasis in vivo. While, DC-SIGNR overexpression promoted cell proliferation, migration and invasion. In mechanism, HNRNPKP2 as a lncRNA was upregulated after DC-SIGNR knockdown. Importantly, STAT5A promoted HNRNPKP2 expression after knockdown DC-SIGNR. Furthermore after HNRNPKP2 depletion, the downstream target gene CXCR4 was downregulated.

CONCLUSIONS

DC-SIGNR promoted gastric cancer liver metastasis mediated with HNRNPKP2 which expression was regulated by STAT5A. And HNRNPKP2 decreased the expression of downstream target gene CXCR4. These findings indicated potential therapeutic candidates for gastric cancer liver metastasis.

摘要

背景

选择素的分析证据表明它们在癌症进展和转移中起关键作用。然而，作为选择素家族成员的DC-SIGNR参与胃癌肝转移的情况仍不清楚。

方法

通过ELISA评估胃癌患者血清中DC-SIGNR的水平。慢病毒介导BGC823和SGC7901细胞系中DC-SIGNR表达的调控。通过MTT、划痕实验和Transwell体外实验以及IVIS动物实验验证DC-SIGNR的生物学效应以确认胃癌肝转移。采用基因芯片和生物信息学分析探究其机制。通过qRT-PCR、蛋白质印迹法和流式细胞术进一步确认结果。

结果

与健康组相比，胃癌患者血清中DC-SIGNR水平显著升高。此外，DC-SIGNR水平与胃癌患者的晚期病理分期相关。DC-SIGNR基因敲低抑制了胃癌细胞的体外增殖、迁移和侵袭，并抑制了体内肝转移。而DC-SIGNR过表达促进细胞增殖、迁移和侵袭。机制上，lncRNA HNRNPKP2在DC-SIGNR基因敲低后上调。重要的是，DC-SIGNR基因敲低后STAT5A促进了HNRNPKP2的表达。此外，HNRNPKP2缺失后，下游靶基因CXCR4表达下调。

结论

DC-SIGNR通过HNRNPKP2介导促进胃癌肝转移，HNRNPKP2的表达受STAT5A调控。且HNRNPKP2降低了下游靶基因CXCR4的表达。这些发现为胃癌肝转移提供了潜在的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa85/5390362/16824d6187a4/12943_2017_639_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa85/5390362/8b4c12eac43a/12943_2017_639_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa85/5390362/2df081527772/12943_2017_639_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa85/5390362/4a42ec3703a7/12943_2017_639_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa85/5390362/b376df703439/12943_2017_639_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa85/5390362/b73c61e34e8d/12943_2017_639_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa85/5390362/0948c19d3352/12943_2017_639_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa85/5390362/9b06e7c00bad/12943_2017_639_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa85/5390362/16824d6187a4/12943_2017_639_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa85/5390362/8b4c12eac43a/12943_2017_639_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa85/5390362/2df081527772/12943_2017_639_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa85/5390362/4a42ec3703a7/12943_2017_639_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa85/5390362/b376df703439/12943_2017_639_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa85/5390362/b73c61e34e8d/12943_2017_639_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa85/5390362/0948c19d3352/12943_2017_639_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa85/5390362/9b06e7c00bad/12943_2017_639_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa85/5390362/16824d6187a4/12943_2017_639_Fig8_HTML.jpg

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