RESUMO
Laryngeal squamous cell carcinoma (LSCC) is one of the most aggressive cancers that affect the head and neck region. Recent researches have confirmed that long non-coding RNAs (lncRNAs) present an emerging role in diversiform diseases including cancers. Prostate cancer-associated ncRNA transcript 6 (PCAT6) is an oncogene in lung cancer, cervical cancer, colon cancer and gastric cancer, but its role in LSCC is still unknown. In the current study, we attempted to figure out the role of PCAT6 in LSCC. RT-qPCR was to analyze PCAT6 expression in LSCC cells. Functional assays were to uncover the role of PCAT6 in LSCC. Mechanism assays were to explore the regulatory mechanism behind PCAT6 in LSCC. PCAT6 exhibited higher expression in LSCC cells and PCAT6 strengthened cell proliferation and inhibited cell apoptosis. Furthermore, lncRNA PCAT6 modulated notch receptor 3 expression and activated NOTCH signaling pathway via serving as a sponge for miR-4731-5p. Taken together, lncRNA PCAT6 was identified as an oncogene in LSCC, which revealed that PCAT6 might be used as potential therapeutic target for LSCC.
Assuntos
Apoptose , Proliferação de Células , Regulação Neoplásica da Expressão Gênica , Neoplasias Laríngeas , MicroRNAs , RNA Longo não Codificante , Receptor Notch3 , Transdução de Sinais , Humanos , RNA Longo não Codificante/genética , RNA Longo não Codificante/metabolismo , Neoplasias Laríngeas/genética , Neoplasias Laríngeas/patologia , Neoplasias Laríngeas/metabolismo , MicroRNAs/metabolismo , MicroRNAs/genética , Linhagem Celular Tumoral , Receptor Notch3/metabolismo , Receptor Notch3/genética , Carcinoma de Células Escamosas/genética , Carcinoma de Células Escamosas/metabolismo , Carcinoma de Células Escamosas/patologia , Sequência de BasesRESUMO
Previous case-control studies on the association of interleukin-17F (IL-17F) T7488C polymorphism and cancer risk have yielded conflicting and inconclusive findings. We performed a meta-analysis by pooling all currently available data to acquire a more precise estimation of the association. A comprehensive literature screening from the PubMed, Embase, Web of Science, and Wanfang databases was performed for eligible publications without language restrictions. The pooled odds ratios (ORs) with corresponding 95 % confidence intervals (95 % CIs) were calculated. According to the inclusion criteria, a total of nine case-control studies with 3,034 cases and 3,694 controls were included. Overall, the pooled ORs showed that IL-17F T7488C polymorphism was associated with neither increased nor decreased risk of cancer. However, the IL-17F T7488C polymorphism exerted risk effect on cancer in population-based case-control studies when stratifying analysis by source of controls (C vs T OR = 1.24, 95 % CI, 1.10-1.40, pooled OR (POR) < 0.001; TC vs TT OR = 1.28, 95 % CI, 1.11-1.48, POR = 0.001; CC + TC vs TT OR = 1.29, 95 % CI, 1.12-1.48, POR < 0.001). Additionally, the variant genotypes of IL-17F T7488C could alter the risk of gastric cancer under the following comparisons (C vs T OR = 1.29, 95 % CI, 1.13-1.47, POR < 0.001; TC vs TT OR = 1.35, 95 % CI, 1.14-1.60, POR < 0.001; CC + TC vs TT OR = 1.35, 95 % CI, 1.15-1.58, POR < 0.001). Sensitivity analysis by sequential omission of single study did not materially alter the pooled findings. The present meta-analysis suggests that the IL-17F T7488C polymorphism may modify the risk of cancer, particularly gastric cancer. However, the precise association needs to be elucidated by more individual studies with sufficient statistical power.