2016年2月cellular physiology and biochemistry杂志（JCR 生理学分类下的3 区期刊）发表了朱广伟题目为“LPS Upregulated VEGFR-3 Expression PromoteMigration and Invasion in Colorectal Cancer via a Mechanism of Increased NF-κBBinding to the Promoter of VEGFR-3”的研究论文，揭示了LPS上调VEGFR-3促进结肠癌侵袭迁移。

在中国结肠癌是女性的第四大恶性肿瘤，是男性的第五大恶性肿瘤。尽管手术根治后患者处于无淋巴结转移状态，仍有10-30%的患者会发生肿瘤复发和远处转移。结肠癌复发和转移的机制仍不清楚。炎症和肿瘤密切相关，炎症会促进肿瘤的发生和发展。LPS是革兰性阴性菌的重要抗原，其能导致结肠部位局部炎症和广泛炎症，在结肠癌进展中起着重要作用。本研究在此基础上，探讨LPS对于结肠癌发生侵袭迁移的影响及其可能机制。

研究发现VEGFR-3在结肠癌肿瘤组织中高表达，且与临床上的TNM分期和淋巴结转移密切相关。LPS能够促进结肠癌细胞的迁移侵袭，其作用能被VEGFR-3的中和抗体减弱。启动子分析发现，在-159 nt 到 +65 nt部分是VEGFR-3启动子的关键位点，LPS能够增加NF-kB结合到此位点，从而提高VEGFR-3的表达。

叶建新为本文的通讯作者，黄强，黄永健，郑伟，华进，杨树刚，庄金福，王锦洲，常俊轩，徐杰参与了该课题的研究。该项目得到了福建省科学技术研究重点项目计划，j9九游会苗圃科研基金，中国非干预胃癌登记调查临床研究项目，卫生部医学科学技术的发展和研究项目，国家临床重点专科建设项目(普通外科) 等基金资助。

Fig. 5. Activity analysis of VEGFR-3 promoterand effects of LPS to VEGFR-3 promoter activity. (A) sw480 cells weretransfected with plasmids that included different VEGFR-3 promoter fragments asfollows: pGL3B-1659, pGL3B-1159, pGL3B-834, pGL3B-609, pGL3B-334, andpGL3B-159, pGL3B-59 and pGL3-Ba-sic. And the renilla luciferase expressionvector pRL-TK was used for normalization, and the promoterless vectorpGL3-Basic served as the negative control. After transfection 48 h luciferaseactivities were mea-sured. The relative luciferase units were obtained bycomparison with the longest of VEGFR-3 promo-ter(pGL3B-1659), which was set to1. Each transfection was carried out in duplicate and the data were ex-pressionas the mean ± SD of three times. (*P<0.05). (B) Nucleotide sequence of -159nt to +65 nt fragment of VEGFR-3 promoter is shown on the Figure. Thetranscription start site is ATG and A set +1 indicating by the arrow. The NF-κBbinding sites in the nucleotide region -137 nt to -128 nt are framed. (C) Effectof mutation of the NF-κB binding site on the activity of the VEGFR-3 promoter.NF-κB mutant plasmid was construction and depicted as pGL3B-159-mut. And thepGL3B-159-mut plasmid and pRL-TK plasmid was co-transfected into sw480 cells.pGL3-Basic vector serve as the negative control. Relative luciferaseactivi-ties were tested 48 h after transfection. The relative luciferase unitswere obtained by comparison with the wild vector of pGL3B-159, which was set to1. Each transfection was carried out in duplicate and the data were expressionas the mean ± SD of three times.(*P<0.05). (D) LPS enhanced VEGFR-3 promoteractivi-ties. Used the different concentration of LPS(0 ng/ml, 200 ng/ml, 500ng/ml, and 800 ng/ml) treated with sw480 cells. And pGL3B-159 and pRL-TK whichwas used to nornalize the transfection efficiency plasmids co-transfected thesecells. After transfection 48 h, the relative luciferase units were tests andthe pGL3B-159 luciferase activity( LPS 0 ng/ml) was set 1. Each transfectionwas carried out in duplicate and the data were expression as the mean± SD ofthree times. (*P<0.05). (E) Used LPS-800 ng/ml to treated with sw480 cellswhich was transfected with pGL3B-159 and pGL3B-59, and pRL-TK which was used tonornalize the trans-fection efficiency plasmids co-transfected these cells.After transfection 48 h, the relative luciferase units were tests and thepGL3B-159 luciferase activity( LPS 0 ng/ml) was set 1. Each transfect wascarried out in duplicate and the data were expression as the mean ± SD of threetimes. (*P<0.05).