SHUN-FA YANGTSUNG-HO YINGJIUNN-LIANG KO2026-10-162026-10-162011-05-01Pure ID: 15087666Pure UUID: 7d437245-d937-4f8a-a73b-e24954910c1510.1177/1933719110395407https://www.scopus.com/pages/publications/84864531516https://scholars.csmu.edu.tw/handle/123456789/23601To investigate the novel role of lipocalin 2 and its concernment with human nonmetastatic clone 23 type 1 (nm23-H1) and p53 in cervical carcinogenesis, SiHa cervical cancer cells were knocked down for nm23-H and lipocalin 2 or overexpressed by lipocalin 2 genes. We found that the overexpression of lipocalin 2 or knockdown of nm23-H1 genes increased the proliferation of SiHa cancer cells, while knocking down of lipocalin 2 decreased the proliferation of SiHa. Furthermore, knockdown of nm23-H1 or overexpression of lipocalin 2 was associated with reduced expression of p53 and its downstream gene p21. Using tissue microarrays, lipocalin 2 immunoreactivity was significantly elevated in cancer tissues as compared with it in high-or low-grade dysplasia or normal tissues. Serum secreted form lipocalin 2 from patients with cervical cancer increased in comparison with normal controls. Conclusively, secreted form lipocalin 2 reflects its implication in cervical cancer tissues and may be utilized as an adjuvant biomarker.9enjournal article