WISP2 通过靶向食管癌细胞中的 ERK 和 E-钙黏蛋白通路发挥其潜在的抗肿瘤活性。
WISP2 exhibits its potential antitumor activity via targeting ERK and E-cadherin pathways in esophageal cancer cells.
机构信息
Department of Pathology, the First Affiliated Hospital of Bengbu Medical University, Bengbu Medical College, Changhuai road 287#, Bengbu, Anhui, 233000, People's Republic of China.
Department of Biochemistry and Molecular Biology, School of Laboratory Medicine, Bengbu Medical College, Anhui, 233030, China.
出版信息
J Exp Clin Cancer Res. 2019 Feb 26;38(1):102. doi: 10.1186/s13046-019-1108-0.
BACKGROUNDS
Emerging evidence has demonstrated that WISP2 is critically involved in cell proliferation, migration, invasion and metastasis in cancers. However, the function of WISP2 in esophageal squamous cell carcinoma (ESCC) is largely unclear. Therefore, we aim to explore the effects and the potential mechanism of WISP2 on proliferation and motility and invasion of ESCC cells.
METHODS
Cell proliferation was detected by MTT assay and apoptosis was measured by FACS in ESCC cells after WISP2 downregulation and overexpression. Cell migration and invasion were analyzed by wound healing assay and transwell migration assay, respectively. The expression of ERK-1/2, Slug and E-cadherin was measured by Western blot respectively. IHC was performed to measure the expression of WISP2 in ESCC tissues.
RESULTS
WISP2 overexpression is associated with survival in ESCC patients. WISP2 overexpression inhibited cell growth and induced cell apoptosis, suppressed cell migration and invasion in ESCC cells. Moreover, WISP overexpression retarded tumor growth in mouse model. WISP2 downregulation enhanced cell growth, inhibited apoptosis, promoted cell migration and invasion in ESCC cells. Mechanistically, WISP2 exerts its tumor suppressive functions via regulation of ERK1/2, Slug, and E-cadherin in ESCC cells.
CONCLUSIONS
Our findings suggest that activation of WISP2 could be a useful therapeutic strategy for the treatment of ESCC.
背景
新出现的证据表明，WISP2 在内皮细胞增殖、迁移、侵袭和转移中起关键作用。然而，WISP2 在食管鳞状细胞癌（ESCC）中的功能在很大程度上尚不清楚。因此，我们旨在探讨 WISP2 对 ESCC 细胞增殖、迁移和侵袭的影响及其潜在机制。
方法
下调和过表达 WISP2 后，通过 MTT 测定法检测 ESCC 细胞的增殖，通过 FACS 检测细胞凋亡。通过划痕愈合实验和 Transwell 迁移实验分别分析细胞迁移和侵袭。通过 Western blot 分别检测 ERK-1/2、Slug 和 E-cadherin 的表达。通过免疫组织化学（IHC）检测 ESCC 组织中 WISP2 的表达。
结果
WISP2 过表达与 ESCC 患者的生存相关。WISP2 过表达抑制细胞生长并诱导细胞凋亡，抑制 ESCC 细胞的迁移和侵袭。此外，WISP2 过表达在小鼠模型中抑制肿瘤生长。下调 WISP2 增强细胞生长，抑制细胞凋亡，促进 ESCC 细胞的迁移和侵袭。机制上，WISP2 通过调节 ESCC 细胞中的 ERK1/2、Slug 和 E-cadherin 发挥其肿瘤抑制功能。
结论
我们的研究结果表明，激活 WISP2 可能是治疗 ESCC 的一种有用的治疗策略。
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