Stanniocalcin 2 (STC2) 是一种在癌细胞中被识别为糖基化肽激素和雌激素响应基因。STC2在癌症的发展过程中参与血管生成、细胞发育、细胞保护以及钙和磷的调节。STC2在子宫内膜癌（EC）中的作用尚不清楚。生物信息学和免疫组织化学分析的数据表明，在EC组织中，STC2的表达上调。将EC细胞用17β-雌二醇（E2）处理，0.1 μmol/L的E2增加了EC细胞中STC2的表达。E2还增加了细胞的存活率、促进了增殖，抑制了EC细胞的凋亡。然而，STC2的敲降减少了E2刺激的EC细胞的存活率，减少了细胞增殖，促进了凋亡。此外，静默STC2削弱了E2诱导的EC细胞中磷酸--AMP-激活蛋白激酶（AMPK）的下调。STC2的丧失减少了E2刺激的EC肿瘤生长。总之，STC2缺陷通过激活AMPK信号抑制了E2刺激的EC增殖和肿瘤生长。

Stanniocalcin 2 (STC2) is identified as a glycosylated peptide hormone and estrogen-responsive gene in cancer cells. STC2 participates in angiogenesis, cell development, cytoprotection, and calcium and phosphate regulation during the development of cancer. The role of STC2 in endometrial cancer (EC) remains unclear. The data from the bioinformatic and immunohistochemical analysis showed that STC2 was upregulated in the EC tissues. The EC cells were treated with 17β-estradiol (E2), and 0.1 μmol/L E2 increased the expression of STC2 in the EC cells. E2 also increased cell viability, promoted proliferation, and inhibited apoptosis of EC. However, the knockdown of STC2 decreased cell viability, reduced proliferation, and promoted apoptosis of E2-stimulated EC. Moreover, silencing of STC2 attenuated E2-induced downregulation of phosphorylated-AMP-activated protein kinase (AMPK) in the EC cells. The loss of STC2 reduced E2-stimulated tumor growth EC in vivo. In conclusion, STC2 deficiency suppressed E2-stimulated proliferation and tumor growth of EC through the activation of AMPK signaling.