Clinical significance of ascites in epithelial ovarian cancer.

The prognostic significance of ascites in the dissemination of metastases in epithelial ovarian cancer (EOC) is unclear. Our study aimed to investigate the association between clinicopathological factors and the development of ascites, as well as its prognostic significance. Three hundred and thirty three patients with primary EOC were suitable for inclusion. We analyzed the correlation between clinicopathological factors, including the extent of metastases, and ascitic volume. The prognostic significance of ascites was assessed using the Kaplan-Meier method and multivariate Cox's regression analysis. The average ascitic volume was 1,800 ml. Significantly, more patients with advanced FIGO stage disease presented with ascites. The volume of ascites increased significantly when metastatic disease was present in more than three regions (p<0.05), and this was the sole factor identified as associated with ascitic volume by multiple linear regression analysis. Median survival was significantly different between those with an ascitic volume less than 1,800 ml (median survival = 58 months), and those with a volume greater than 1,800 ml (median survival = 28.6 months) (p<0.05). Subgroup analysis of stage III and IV patients also revealed a poor prognosis in the presence of massive ascites (p = 0.03). Multivariate analyses found that massive ascites and poor differentiation were independent poor prognostic factors for stage III and IV EOC patients by Cox regression, using a backward elimination procedure. The volume of ascites increased significantly with the extent of metastastic disease. Massive ascites and poor tumor differentiation were associated with a worse prognosis in patients with advanced stage ovarian cancer.

Sam68 expression and cytoplasmic localization is correlated with lymph node metastasis as well as prognosis in patients with early-stage cervical cancer.

BACKGROUND: This study was aimed at investigating the role and molecular mechanism of Sam68 in cervical cancer lymph node metastasis. MATERIALS AND METHODS: Sam68 expression profile was detected by quantitative polymerase chain reaction, western blotting and immunohistochemical staining. Short hairpin RNA interfering approach was employed to suppress endogenous Sam68 expression in cervical cancer cells to determine its role in metastasis and the possible mechanism. RESULTS: Sam68 expression in cervical cancer was significantly up-regulated at both messenger RNA and protein levels compared with that in normal cervical tissues. The high expression level of Sam68 and its cytoplasmic localization were significantly associated with risk factors including pelvic lymph node metastasis (P < 0.001), and served as independent prognostic factors for predicting shortening of the overall survival time and disease-free survival time in patients with early-stage cervical cancer. Moreover, down-regulation of Sam68 in cervical cancer cells remarkably inhibited cellular motility and invasion. In addition, down-regulation of Sam68 reversed epithelial-mesenchymal transition through inhibiting the Akt/ GSK-3ß/Snail pathway. CONCLUSION: This study demonstrated that Sam68 could induce cervical cancer lymph node metastasis through regulating epithelial-mesenchymal transition, and Sam68 expression profile possessed the potential to serve as predictors of pelvic lymph node metastasis in cervical cancer patients.

IMP3 promotes TNBC stem cell property through miRNA-34a regulation.

OBJECTIVE: To explore the expression and function of insulin-like growth factor II (IGFII) mRNA binding protein (IMP3) in the Triple Negative Breast Cancer (TNBC). MATERIALS AND METHODS: According to previously reported gene expression array, we found that IMP3 had significantly higher expression in the CD44+CD24-ESA+ cell cluster, tumor initiating cell or cancer stem cell (CSCs), compared to other tumor cells. Based on the GEO database (GEO accession No. GSE6883), we detected the mRNA levels of IMP 1,2 and 3 by quantitative polymerase chain reaction (q-PCR) in CD44+CD24-ESA+ cell cluster and other breast tumor cell clusters. Besides, we measured IMP3 expression in microsphere of breast cancer, which exerted more significant tumor stem cell properties. The effects of IMP3 on breast cancer cell stem cell properties were studied by RNA interference and overexpression approaches in vitro. Furthermore, we predicted and identified microRNA, which could target and regulate IMP3 from bioinformatics analysis, and verified the interaction by luciferase assays and rescue experiments. RESULTS: Previously reported data showed that IMP3 expression was significantly upregulated in CD44+CD24-ESA+ cell cluster from breast cancer tissues. Besides, we found IMP3 had higher expression in mesenchymal cells rather than epithelial cells, which was also significantly elevated in SUM159 and T49D cell lines cultured as microsphere rather than adherent cells or differentiated cells. CD44+CD24-ESA+ cell cluster proportion was significantly decreased after silencing IMP3 in SUM1315, and its ability to develop into microsphere was significantly inhibited. By re-expressing IMP3 in SUM315, we restored the self-renewal capacity and tumorigenesis potential of SUM315. Through relative predicting website, we found several miRNAs which could regulate IMP3. miR-34a with highest score was chosen for further analysis. Mimicking miR-34a significantly downregulated IMP3 expression and inhibited its ability to develop into microsphere, while overexpressing IMP3 could rescue this process. CONCLUSIONS: IMP3 plays a vital role in maintaining stem cell properties of breast cancer cells, which could be regulated by mir-34a.

Relationship between IL-1ß polymorphisms and obstructive sleep apnea syndrome.

OBJECTIVE: To explore the relationship between obstructive sleep apnea syndrome (OSAS) and polymorphism in the IL-1ß gene. PATIENTS AND METHODS: We recruited 164 OSAS patients to the observation group and 146 healthy people to the control group during the same period. Using RFLP (Restriction Fragment Length Polymorphism), we detected higher G/G and C/C rates on locus 154 of the IL-1ß gene in the OSAS patients compared with the control group. RESULTS: Quantitative fluorescence PCR results showed no significant differences in the mRNA expression between the OSAS patients and the healthy people. ELISA results showed that levels of IL-1ß in people with the G/G and C/C genotypes were lower than those with the G/C genotype. The frequencies of T/A and T/T on locus 468 of IL-1ß was increased in the OSAS patients compared with the control group. ELISA and Western blot results indicated that individuals with the T/T and T/T genotypes at locus 468 had lower expression of IL-1ß than those with A/A. CONCLUSIONS: This observation suggests that IL-1ß polymorphisms at 154 and 468 contribute to the incidence of OSAS, possibly, by altering the protein expression of IL-1ß.