Xiaodong Yin1, Xilan Gu1, Fenjun Li1, Fei Ye1, Fang Liu1, Wenbin Wang2. 1. Department of Otolaryngology (ENT), the Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Suzhou 215000, China. 2. Department of Otolaryngology (ENT), the Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Suzhou 215000, China. Electronic address: wangwenbin215@163.com.
Abstract
OBJECTIVES: Long noncoding RNAs (lncRNAs) have been reported to be involved in multiple cancer progression, yet the biological role of lncRNA SNHG6 in nasopharyngeal carcinoma (NPC) is still unclear. This research aims to explore the molecular mechanism of SNHG6 in the development and progression of NPC. DESIGN: Prospective feasibility study. SETTING: The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital. Long noncoding RNAs (lncRNAs) have been reported to be involved in multiple cancer progression, yet the biological role of lncRNA SNHG6 in nasopharyngeal carcinoma (NPC) is still unclear. This research aims to explore the molecular mechanism of SNHG6 in the development and progression of NPC. RT-qPCR assay was used to examine the expression of SNHG6, miR-26a-5p, and ARPP19 in NPC. CCK-8 and transwell assays were employed to detect NPC cell viability, migration, and invasion. The interaction between miR-26a-5p and SNHG6 or ARPP19 was determined by the luciferase reporter, RIP and RNA pull-down assays. We observed that SNHG6 expression was enhanced in NPC tissues and cells. SNHG6 deletion attenuated NPC cell viability and metastasis. MiR-26a-5p was predicted and validated to interact with SNHG6, and miR-26a-5p expression was markedly elevated in NPC after SNHG6 silence. Moreover, miR-26a-5p inhibitor rescued the suppressive effect of SNHG6 depletion on NPC cell viability, migration and invasion. Besides, ARPP19 was a target of SNHG6 and positively regulated by SNHG6. ARPP19 overexpression neutralized the repressive effect of SNHG6 knockdown on NPC progression. Our results indicated that SNHG6 regulated NPC progression through modulating miR-26a-5/ARPP19 axis, which might provide new insights into NPC diagnosis and treatment.
OBJECTIVES: Long noncoding RNAs (lncRNAs) have been reported to be involved in multiple cancer progression, yet the biological role of lncRNA SNHG6 in nasopharyngeal carcinoma (NPC) is still unclear. This research aims to explore the molecular mechanism of SNHG6 in the development and progression of NPC. DESIGN: Prospective feasibility study. SETTING: The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital. Long noncoding RNAs (lncRNAs) have been reported to be involved in multiple cancer progression, yet the biological role of lncRNA SNHG6 in nasopharyngeal carcinoma (NPC) is still unclear. This research aims to explore the molecular mechanism of SNHG6 in the development and progression of NPC. RT-qPCR assay was used to examine the expression of SNHG6, miR-26a-5p, and ARPP19 in NPC. CCK-8 and transwell assays were employed to detect NPC cell viability, migration, and invasion. The interaction between miR-26a-5p and SNHG6 or ARPP19 was determined by the luciferase reporter, RIP and RNA pull-down assays. We observed that SNHG6 expression was enhanced in NPC tissues and cells. SNHG6 deletion attenuated NPC cell viability and metastasis. MiR-26a-5p was predicted and validated to interact with SNHG6, and miR-26a-5p expression was markedly elevated in NPC after SNHG6 silence. Moreover, miR-26a-5p inhibitor rescued the suppressive effect of SNHG6 depletion on NPC cell viability, migration and invasion. Besides, ARPP19 was a target of SNHG6 and positively regulated by SNHG6. ARPP19 overexpression neutralized the repressive effect of SNHG6 knockdown on NPC progression. Our results indicated that SNHG6 regulated NPC progression through modulating miR-26a-5/ARPP19 axis, which might provide new insights into NPC diagnosis and treatment.