Identification of MAD2L1 and BUB1B as Potential Biomarkers Associated with Progression and Prognosis of Ovarian Cancer.

Ovarian cancer develops insidiously and is frequently diagnosed at advanced stages. Screening for ovarian cancer is an effective strategy for reducing mortality. This study aimed to investigate the molecular mechanisms underlying the development of ovarian cancer and identify novel tumor biomarkers for the diagnosis and prognosis of ovarian cancer. Three databases containing gene expression profiles specific to serous ovarian cancer (GSE18520, GSE12470, and GSE26712) were acquired. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes were analyzed for the differentially expressed gene (DEGs). The protein-protein interaction (PPI) network was constructed using the STRING database. The pivotal genes in the PPI network were screened using the Cytoscape software. Survival curve analysis was performed using a Kaplan-Meier Plotter. The cancer genome atlas and Gene Expression Omnibus databases were used to find the relationship between Hub gene and serous ovarian cancer. PCR and immunohistochemistry were used to detect the expression of Hub gene in serous ovarian cancer tissues and cells. Downstream pathways of the candidate tumor marker genes were predicted using Gene Set Enrichment Analysis. In this study, 252 DEGs were screened for pathway enrichment. 20 Hub genes were identified. Survival analysis suggested that Aurka, Bub1b, Cenpf, Cks1b, Kif20a, Mad2l1, Racgap1, and Ube2c were associated with the survival of patients with serous ovarian cancer. MAD2L1 and BUB1B levels were significantly different in serous ovarian cancer at different stages. Finally, Mad2l1 was found to play a role in the cell cycle, oocyte meiosis, and ubiquitin-mediated proteolysis. Meanwhile, Bub1b may play a role in the cell cycle, ubiquitin-mediated proteolysis, and spliceosome processes. Mad2l1 and Bub1b could be used as markers to predict ovarian carcinogenesis and prognosis, providing candidate targets for the diagnosis and treatment of serous ovarian cancer.

Investigating the influence of primary uterine tumor site on pelvic and para-aortic lymph node metastatic pattern and evaluating the risk factors for lymph node metastases in endometrial carcinoma: A retrospective study.

To assess the metastatic pattern in pelvic and para-aortic lymph nodes in relation with the primary uterine tumor site and to evaluate risk factors for lymph node metastases. 212 patients with endometrial cancer who underwent surgical treatment from December 2014 to December 2019 were selected. The clinical and pathological data were retrospectively analyzed. The factors and uterine primary tumor site related to lymph node metastasis were analyzed by univariate and multivariate analysis. Among the 212 patients with endometrial cancer, 17 cases had lymph node metastasis, and thus the metastasis rate was 8.02%. Univariate analysis revealed that lymph node metastasis was significantly correlated with Federation of Gynecology and Obstetrics stage, depth of myometrial invasion, tumor size, pathological grade, and lymphovascular space invasion (P < .05) and was not correlated with age, pathological type, and cervical involvement (P > .05). Primary uterine tumor site (fundus, horns, body or lower uterine segment) with or without cervical involvement was associated with different lymph nodes' metastatic sites. The lymph node metastatic pathways of endometrial cancer mainly include obturator lymph nodes and para-aortic lymph nodes, and skip metastasis may occur; endometrial carcinoma may jump and metastasize to para-aortic lymph nodes, specially when the lesion is located in the uterine fundus and uterine horns (cornua of uterus); there is a significant correlation between the location of lymph node metastasis and the location of primary uterine malignant tumor.

[Expression of prostaglandin transporter in colorectal cancer tissues and its relationship with clinicopathological features].

OBJECTIVE: To investigate the expression of prostaglandin transporter (PGT) in colorectal cancer (CRC) tissues and its relationship with clinicopathological features. METHODS: The mRNA and protein levels of PGT were determined by real-time PCR, Western blot and immunohistochemical methods in cancer tissues and adjacent normal tissue from 80 patients with colorectal cancer and their relationship with clinicopathological features was analyzed. RESULTS: Compared with the adjacent normal tissue of colorectal cancer, the PGT mRNA relative expression (0.57 ± 0.33 vs. 2.33 ± 1.20) and the PGT protein expression in cancer tissues decreased significantly [PGT/GAPDH 0.45 ± 0.16 vs. 0.78 ± 0.23, integral A 718.7 ± 359.4 vs. 10412.0 ± 6423.3, average A 0.03 ± 0.01 vs. 0.12 ± 0.09, all P<0.01]. Lower mRNA and protein expressions of PGT in colorectal cancer were associated with depth of invasion T3 to T4 and TNM stage III( to IIII( (P<0.01), while not associated with gender, age, tumor location and differentiation degree (all P>0.05). CONCLUSION: Expression levels of PGT mRNA and protein in colorectal cancer tissue are significantly down-regulation. PGT expression is associated with invasion depth and late stages.

[Clinical significance of the detection of serum neutrophil gelatinase-associated lipocalin in human colorectal cancer].

OBJECTIVE: To explore the feasibility and clinical significance of the detection of serum neutrophil gelatinase-associated lipocalin (NGAL) in human colorectal cancer. METHODS: Levels of NGAL in serum samples from 133 healthy people, 125 colorectal polyps patients and 100 colorectal cancer patients respectively were determined by sandwich ELISA assay. Relationship of NGAL level with clinicopathological features of colorectal cancer patients was analyzed. The optimal cut-off value of serum NGAL for diagnosing colorectal cancer was determined by ROC curve and compared with CEA and CA19-9. Univariate and multivariate analyses were performed to examine the relationship of NGAL level with the prognosis of patients with colorectal cancer. RESULTS: The median serum NGAL protein level in 100 colorectal cancer cases was 67.96 (53.30-79.86) µg/L, significantly higher than that in healthy people and colorectal polyps patients. The differences were statistically significant (all P<0.01). Serum NGAL protein level was significantly associated with tumor diameter, TNM stage, lymph node metastasis and vascular involvement (P<0.05). The optimal cut-off point of serum NGAL protein level for diagnosing colorectal cancer was 49.78 µg/L, and the sensitivity and specificity were 88% and 81% respectively. As for colorectal cancer patients with stage I, the sensitivity of serum NGAL (78.9%) was significantly higher as compared to CA19-9 (31.6%) and CEA (36.8%); as for those with stage II, the sensitivity of serum NGAL(88.0%) was also significantly higher compared to CA19-9 (48.0%) and CEA (52.0%). Kaplan-Meier analysis showed that patients with positive NGAL (≥49.78 µg/L) had worse survival than those with negative NGAL (P=0.002). Multivariate analysis showed that NGAL was an independent prognostic factor (HR=2.060, 95%CI:1.023-4.150, P=0.043). CONCLUSIONS: NGAL can be served as the novel malignant biological phenotype marker for human colorectal cancer and can be used for the risk stratification. NGAL may be an independent prognostic factor in colorectal cancer.