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. 2009 May;57(5):513-21.
doi: 10.1369/jhc.2009.953257. Epub 2009 Feb 2.

Lipocalin2 expressions correlate significantly with tumor differentiation in epithelial ovarian cancer

HanByoul Cho  1 , Jae-Hoon Kim
Affiliations

Lipocalin2 expressions correlate significantly with tumor differentiation in epithelial ovarian cancer

HanByoul Cho et al. J Histochem Cytochem. 2009 May.

Abstract (V体育2025版)

We recently identified lipocalin2 (LCN2) as being upregulated in ovarian cancer cell lines. The purpose of this study was to validate LCN2 upregulation in ovarian cancers and to investigate its potential as a serum biomarker. We assayed LCN2 expression in ovarian cancers using real-time PCR and IHC. To evaluate the potential of LCN2 as a biomarker, we measured serum LCN2 levels in 54 ovarian cancers, 15 borderline and 53 benign ovarian tumors, and 90 healthy controls. SYBR green PCR and IHC showed LCN2 overexpression in ovarian cancers. LCN2 immunoreactivity was significantly associated with tumor differentiation (p=0. 009), as well-differentiated tumors showed the highest LCN2 expression VSports手机版. Serum LCN2 level in ovarian cancer was significantly higher than in the other study groups (p<0. 001), and in accordance with IHC results, it also correlated with tumor differentiation, with well-differentiated tumors having the highest value. The sensitivity and specificity of LCN2 in detecting ovarian cancer was 72. 2% and 50. 4%, respectively. By Cox univariate analysis, LCN2 positivity was an independent prognostic factor for overall survival (hazard ratio = 1. 47, p=0. 012). In conclusion, LCN2 expressions are upregulated and related to tumor differentiation in ovarian cancers and should be included in future research assessing potential biomarkers for ovarian cancer. .

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Figures

Figure 1
Figure 1
Relative quantitation of lipocalin2 (LCN2) in healthy ovarian epithelial cell cultures, borderline ovarian tumor tissues, ovarian cancer cell lines, and cancer tissues. Independent t-tests showed statistically significant differences between study groups (p<0.001). Each value is expressed as the mean of duplicate. The reference tissue, HOSE 186, was considered to have a value of 1.
Figure 2
Figure 2
Evaluation of LCN2 IHC staining. The staining intensity (A, no evidence of staining, 0; B, weak staining, 1+; C, moderate staining, 2+; D, strong positive staining in most cells, 3+) and the percentage of positive cells (E, no cells staining positive, 0; F, <25% of cells staining positive, 1+; G, 25%–50% of cells staining positive, 2+; H, >50% of cells staining positive, 3+) were scored. Representative fields were photographed in serous type. Bars: A–D = 50 mm; E–H = 100 mm.
Figure 3
Figure 3
IHC staining score of LCN2 in ovarian cancer samples. (A) IHC staining score of LCN2 in ovarian cancer samples was significantly higher than that in benign ovarian tumors and healthy controls. (B) The mean scores associated directly with tumor grade; well-differentiated tumors stained more strongly than poorly differentiated tumors. The Kruskal-Wallis ANOVA and a post hoc Dunn method were used to compare the staining score among the groups.
Figure 4
Figure 4
Pretreatment serum LCN2 levels in study subjects. The differences in diagnostic categories were statistically significant (p=0.021), as were the differences in tumor differentiation (p=0.038). The Kruskal-Wallis ANOVA and a post hoc Dunn method were used to compare the serum LCN2 level among the groups.
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