Long non-coding RNA small nucleolar RNA host gene 20 (SNHG20) has been demonstrated to play crucial regulatory roles in many types of cancer. However, the biological function of long ncRNA (lncRNA) SNHG20 in ovarian cancer is still unclear. In the present study, we found that lncRNA SNHG20 was significantly increased in ovarian cancer. In addition, lncRNA SNHG20 knockdown suppressed the ovarian cancer progression, whereas overexpression of SNHG20 showed the opposite effects. Moreover, our results also revealed that lncRNA SNHG20 knockdown inhibited Wnt/β-catenin signaling activity by suppressing β-catenin expression and reversing the downstream target gene expression. Taken together, lncRNA SNHG20 plays an pivotal role in ovarian cancer progression by regulating Wnt/β-catenin signaling.

PurposeTo establish a prognostic index model for advanced pancreatic cancer patients receiving palliative chemotherapy based on clinical variables.MethodsThe clinical data of 118 patients with advanced pancreatic cancer who received palliative chemotherapy between January 2006 and August 2013 in our center were retrospectively analyzed. Prognostic factors for overall survival were identified using Cox proportional hazards model. A prognostic index model was established by these pretreatment factors to predict prognosis. Kaplan–Meier estimation and log-rank test were performed to compare the overall survival difference between low-risk and high-risk group of patients.ResultsMedian overall survival time for all patients was 8.8 months [95 % confidence interval (CI) 7.0–10.6 months]. Multivariate analysis identified ECOG score = 2 (hazard ratio 2.03; 95 % CI 1.07–3.85; P = 0.030), CA19-9 levels of ≥1000 U/mL (hazard ratio 2.07; 95 % CI 1.09–3.92; P = 0.026), and CRP levels of ≥5 mg/L (hazard ratio 2.05; 95 % CI 1.06–3.96; P = 0.033) as independent poor prognostic factors for overall survival. For the three factors, ECOG score = 2, CA19-9 levels of ≥1000 U/mL, and CRP levels of ≥5 mg/L were allocated 1 point each. There were 84 (71.2 %) patients allocated to low-risk group with total score 0–1 point, and 34 (28.8 %) patients were categorized as high-risk group with total scores 2–3 points. The median overall survival for low-risk group and high-risk group was 9.9 months (95 % CI 6.8–13.0) and 5.3 months (95 % CI 4.1–6.5), respectively (hazard ratio 0.27; 95 % CI 0.14–0.52; P < 0.001). The estimated 1-year survival rates for low-risk group and high-risk group were 40.5 and 5.9 %, respectively (P < 0.05).ConclusionsA novel prognostic index model based on three clinical parameters was established to predict the prognosis of patients with advanced pancreatic cancer receiving palliative chemotherapy.

Cisplatin resistance is frequently occurred in ovarian cancer therapy, understanding its regulatory mechanisms is critical for developing novel treatment methods and drugs. Here, we found ovarian cancer patients with low FAM83B levels had shorter survival time, tissues with cisplatin resistance also had low FAM83B levels, suggesting FAM83B might inhibit cisplatin resistance. FAM83B overexpression inhibits cisplatin resistance showed in increased ovarian cancer cell proliferation and growth rate, and reduced apoptosis rate, while FAM83B knockdown promotes cisplatin resistance. Mechanism analysis showed FAM83B interacted with APC to inhibit Wnt pathway activity, causing ovarian cancer cisplatin resistance. We also found FAM83B levels were negative with Wnt pathway activity in clinic samples, confirming FAM83B inhibited Wnt pathway activity. In summary, we found FAM83B inhibits ovarian cancer cisplatin resistance through inhibiting Wnt pathway, providing a new target for ovarian cancer therapy.

Chemotherapy resistance is a bottleneck for ovarian cancer treatment; therefore, revealing its regulatory mechanism is critical. In the present study, we found that prostate tumor overexpressed-1 (PTOV1) was upregulated significantly in ovarian cancer cells and tissues. Patients with high PTOV1 levels had a poor outcome. In addition, PTOV1 overexpression increased CDDP (cisplatin) resistance, while PTOV1 knockdown inhibited CDDP resistance, as determined using cell viability assays, apoptosis assays, and an animal model. Mechanistic analysis showed that PTOV1 increased nuclear factor kappa B (NF-κB) pathway activity, reflected by increased nuclear translocation of its p65 subunit and the phosphorylation of inhibitor of nuclear factor kappa-B kinase subunits alpha and beta, which are markers of NF-κB pathway activation. Inhibition of the NF-κB pathway in PTOV1 -overexpressing ovarian cancer cells increased CDDP-induced apoptosis, suggesting that PTOV1 promoted chemotherapy resistance by activating the NF-κB pathway. In summary, we identified PTOV1 as a prognostic factor for patients with ovarian cancer. PTOV1 might be a target for inhibition of chemotherapy resistance.