CD95 is the first death receptor identified and characterized in recent years, and it plays important roles in the molecular network regulating cell death and survival. CD95 rs1800682 polymorphism is a common genetic polymorphism identified in the CD95 gene. Many publications evaluated the association between CD95 rs1800682 polymorphism and cervical cancer risk, but the association remained inconclusive. To provide a more precise estimate on the association, a meta-analysis was carried out. The association between CD95 rs1800682 polymorphism and cervical cancer risk was assessed by calculating the pooled odds ratio (OR) with its 95% confidence intervals (95% CI). On the basis of our inclusion criteria, ten studies with a total of 5,481 individuals were included into the meta-analysis. There was obvious heterogeneity among the included studies. Meta-analysis of the ten studies suggested that there was no association between CD95 rs1800682 polymorphism and cervical cancer risk under all four genetic models (allele model: OR = 1.05, 95% CI 0.92-1.18, P = 0.478; homozygous model: OR = 1.08, 95% CI 0.83-1.41, P = 0.550; dominant model: OR = 1.12, 95% CI 0.88-1.42, P = 0.347; recessive model: OR = 1.00, 95% CI 0.76-1.31, P = 0.978). Subgroup analysis by ethnicity suggested that there was no association between CD95 rs1800682 polymorphism and cervical cancer risk in Asians, Caucasians, and Africans. Thus, the meta-analysis suggests that CD95 rs1800682 polymorphism is not associated with cervical cancer risk.

The role of vitamin D receptor (VDR) BsmI polymorphism in ovarian cancer development has been studied in various populations, but those results are discordant controversial and ambiguous. Thus, we performed a meta-analysis to assess the association between VDR BsmI polymorphism and susceptibility to ovarian cancer more precisely. Odds ratio (OR) and its 95% confidence interval (95% CI) were used for statistical analysis. Nine individual studies with a total 2,331 cases and 3,301 controls were included into this meta-analysis. There was no heterogeneity among those nine studies. Meta-analysis of total nine studies suggested that there was no association between VDR BsmI polymorphism and susceptibility to ovarian cancer (B vs. b, OR = 1.02, 95% CI = 0.94-1.10, P = 0.616, I(2) = 0%; BB vs. bb, OR = 1.02, 95 % CI = 0.87-1.20, P = 0.810, I(2) = 0 %; BB/Bb vs. bb, OR = 1.05, 95% CI = 0.94-1.18, P = 0.391, I(2) = 0 %; BB vs. bb/Bb, OR = 0.99, 95% CI = 0.85-1.14, P = 0.853, I(2) = 0 %). Meta-analysis of seven studies from Caucasians also showed that there was no association between VDR BsmI polymorphism and susceptibility to ovarian cancer. This meta-analysis suggests that there is no association between VDR BsmI polymorphism and susceptibility to ovarian cancer in Caucasians. Future studies from Asians or Africans are needed to further assess the above association.

Objective LINC01354 has been defined as a tumor driver in several cancers. Nevertheless, whether LINC01354 involves in endometrial cancer (EC) has been little navigated. Thus, the mechanism of LINC01354 was explored in the disease. Methods Measurements of LINC01354, microRNA (miR)-216b and kirsten rat sarcoma viral oncogene (KRAS) levels in EC tissues and cells were performed. LINC01354 low expression and miR-216b overexpression vectors were introduced into EC cells (lshikawa), thereby their effects on cell viability, apoptosis, migration and invasion were manifested. Rescue experiments were also carried out by down-regulating LINC01354 and miR-216b spontaneously. Tumorigenesis in vivo was also assessed. The relationships of LINC01354/miR-216b/KRAS were analyzed. Results Increased LINC01354 and KRAS and reduced miR-216b levels were measured in EC. Silencing LINC01354 or overexpressing miR-216b retarded EC cellular development. LINC01354 counteracted with miR-216b to target KRAS. Suppression of miR-216b antagonized silenced LINC01354-induced impacts on EC cell development. LINC01354/miR-216b/KRAS axis enhanced tumorigenesis in mice with EC. Conclusion It is testified that silencing LINC01354 inhibits KRAS by up-regulating miR-216b, thereby discouraging cell malignant phenotype in EC.