WISP2 exhibits its potential antitumor activity via targeting ERK and E-cadherin pathways in esophageal cancer cells
WISP2 exhibits its potential antitumor activity via targeting ERK and E-cadherin pathways in esophageal cancer cells
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DOI：
10.1186/s13046-019-1108-0
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发表时间：
2019-02-26
影响因子：
11.3
通讯作者：
Tao, Yi-Sheng
中科院分区：
文献类型：
--
作者：
Chai, Da-Min;Qin, Yan-Zi;Tao, Yi-Sheng
研究背景新的证据表明WISP 2在肿瘤细胞的增殖、迁移、侵袭和转移中起重要作用。然而，WISP 2在食管鳞状细胞癌（ESCC）中的功能在很大程度上尚不清楚。本研究旨在探讨WISP 2对食管鳞癌细胞增殖、运动和侵袭能力的影响及其可能机制。方法采用MTT法检测WISP 2下调和过表达后食管鳞癌细胞的增殖，流式细胞仪检测WISP 2下调和过表达后食管鳞癌细胞的凋亡。伤口愈合实验和transwell迁移实验检测细胞迁移和侵袭能力。Western blot检测ERK-1/2、Slug和E-cadherin的表达。采用免疫组化法检测WISP 2在食管鳞癌组织中的表达。WISP 2过表达可抑制食管鳞癌细胞的生长、诱导细胞凋亡、抑制细胞迁移和侵袭。此外，WISP过表达在小鼠模型中延缓肿瘤生长。WISP 2下调可促进食管鳞癌细胞生长、抑制凋亡、促进细胞迁移和侵袭。机制上，WISP 2发挥其肿瘤抑制功能，通过调节ERK 1/2，Slug，和E-cadherin在ESCC cells.ConclusionsOur研究结果表明，激活WISP 2可能是一个有用的治疗策略，用于治疗ESCC。
BackgroundsEmerging 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.MethodsCell 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.ResultsWISP2 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.ConclusionsOur findings suggest that activation of WISP2 could be a useful therapeutic strategy for the treatment of ESCC.