Lu Zhou1, Zhi Li1, Xinye Shao1, Bowen Yang1, Jing Feng1, Lu Xu1, Yuee Teng2. 1. Department of Medical Oncology, The First Hospital of China Medical University, Shenyang 110001, China; Key Laboratory of Anticancer Drugs and Biotherapy of Liaoning Province, The First Hospital of China Medical University, Shenyang 110001, China. 2. Department of Medical Oncology, The First Hospital of China Medical University, Shenyang 110001, China; Key Laboratory of Anticancer Drugs and Biotherapy of Liaoning Province, The First Hospital of China Medical University, Shenyang 110001, China. Electronic address: yeteng@cmu.edu.cn.
Abstract
BACKGROUND: Although increasing evidence has revealed that FOXD2-AS1 overexpression exists in various solid tumors, the value of FOXD2-AS1 as a prognostic marker in such cancers remains uncertain. Accordingly, the present research aimed to assess the association of FOXD2-AS1 with cancer prognosis and predict the biological function of FOXD2-AS1. METHODS: We systematically retrieved PubMed, PMC, Web of Science, EMBASE and Wiley Online Library databases for eligible articles published up to December 2018. Pooled hazard ratios (HRs) and odds ratios (ORs) with 95% confidence intervals (95%CIs) were calculated to evaluate the correlation of FOXD2-AS1 expression with overall survival (OS), disease free survival (DFS) and clinicopathological characteristics. We also used five Gene Expression Omnibus (GEO) datasets from breast cancer patients to explore the relationship between FOXD2-AS1 expression and prognosis. Finally, we validated FOXD2-AS1 expression in various carcinomas and predicted its biological function based on the public databases. RESULTS: A total of 13 studies with 2502 tumor patients were included. The pooled HRs demonstrated that FOXD2-AS1 overexpression was significantly associated with unfavorable OS (HR = 1.39, 95%CI: 1.23-1.57, p < 0.001) and DFS (HR = 2.24, 95%CI: 1.55-3.23, p < 0.001) in tumor patients. The pooled ORs indicated that FOXD2-AS1 upregulation was related to large tumor size (OR = 1.53, 95%CI: 1.26-1.85, p < 0.001), deep invasion depth (OR = 1.99, 95%CI: 1.53-2.58, p < 0.001), distant metastasis (OR = 2.03, 95%CI: 1.69-2.43, p < 0.001) and advanced TNM stage (OR = 1.35, 95%CI: 1.06-1.72, p = 0.0150), but not to lymph node metastasis nor differentiation. Moreover, a similar pooled result for the OS of breast cancer patients was obtained (HR = 1.55, 95%CI: 1.14-2.11, p = 0.0052) by analyzing GEO data. Finally, elevated FOXD2-AS1 expression in various solid tumor tissues was verified based on The Cancer Genome Atlas (TCGA) data. Further functional prediction demonstrated that FOXD2-AS1 may participate in some cancer-related pathways. CONCLUSION: Elevated FOXD2-AS1 expression was associated with poor survival in patients with solid tumors and may serve as a potential prognostic biomarker for a variety of cancers.
BACKGROUND: Although increasing evidence has revealed that FOXD2-AS1 overexpression exists in various solid tumors, the value of FOXD2-AS1 as a prognostic marker in such cancers remains uncertain. Accordingly, the present research aimed to assess the association of FOXD2-AS1 with cancer prognosis and predict the biological function of FOXD2-AS1. METHODS: We systematically retrieved PubMed, PMC, Web of Science, EMBASE and Wiley Online Library databases for eligible articles published up to December 2018. Pooled hazard ratios (HRs) and odds ratios (ORs) with 95% confidence intervals (95%CIs) were calculated to evaluate the correlation of FOXD2-AS1 expression with overall survival (OS), disease free survival (DFS) and clinicopathological characteristics. We also used five Gene Expression Omnibus (GEO) datasets from breast cancerpatients to explore the relationship between FOXD2-AS1 expression and prognosis. Finally, we validated FOXD2-AS1 expression in various carcinomas and predicted its biological function based on the public databases. RESULTS: A total of 13 studies with 2502 tumorpatients were included. The pooled HRs demonstrated that FOXD2-AS1 overexpression was significantly associated with unfavorable OS (HR = 1.39, 95%CI: 1.23-1.57, p < 0.001) and DFS (HR = 2.24, 95%CI: 1.55-3.23, p < 0.001) in tumorpatients. The pooled ORs indicated that FOXD2-AS1 upregulation was related to large tumor size (OR = 1.53, 95%CI: 1.26-1.85, p < 0.001), deep invasion depth (OR = 1.99, 95%CI: 1.53-2.58, p < 0.001), distant metastasis (OR = 2.03, 95%CI: 1.69-2.43, p < 0.001) and advanced TNM stage (OR = 1.35, 95%CI: 1.06-1.72, p = 0.0150), but not to lymph node metastasis nor differentiation. Moreover, a similar pooled result for the OS of breast cancerpatients was obtained (HR = 1.55, 95%CI: 1.14-2.11, p = 0.0052) by analyzing GEO data. Finally, elevated FOXD2-AS1 expression in various solid tumor tissues was verified based on The Cancer Genome Atlas (TCGA) data. Further functional prediction demonstrated that FOXD2-AS1 may participate in some cancer-related pathways. CONCLUSION: Elevated FOXD2-AS1 expression was associated with poor survival in patients with solid tumors and may serve as a potential prognostic biomarker for a variety of cancers.