Rong Hu1, Zongming Zhu2. 1. Department of Obstetrics and Gynecology, Xiangya Hospital, Central South University, Changsha, Hunan Province, China. 2. Changsha University, Changsha, Hunan Province, China.
Abstract
BACKGROUND: Long non-coding RNA (lncRNA) is reported to be involved in multiple biological processes in numerous human tumors. Furthermore, an increasing number of studies have confirmed the involvement of lncRNA in the initiation and development of human cancers, including cervical cancer (CC). METHODS: The present study explored the potential role of lncRNA glypican 3 antisense transcript 1 (GPC3-AS1) with respect to regulating CC cell proliferation and migration. RESULTS: A quantitative reverse transcriptase-polymerase chain reaction confirmed that GPC3-AS1 was up-regulated in CC cells compared to normal CRL-2614 cells. Loss-of-function assays demonstrated the negative effect of GPC3-AS1 depletion on CC cell proliferation and migration. GPC3-AS1 positively regulated its nearby gene glypican 3 (GPC3). Significant up-regulation of GPC3 was also observed in CC cells, consistently with GPC3-AS1. In addition, GPC3-AS1 and GPC3 synergistically promoted the proliferative and migratory abilities of CC cells. Mechanistic investigation showed that ELK1 acted as the transcription activator of GPC3-AS1 and GPC3, thus contributing to their up-regulation in CC cells. Rescue assays indicated that the ELK1-induced GPC3-AS1/GPC3 axis promoted cell proliferation and migration in CC. CONCLUSIONS: The results of the present study have revealed a novel molecular pathway that can regulate CC cell proliferation and migration, thus providing a new basis for investigating the molecular mechanism associated with CC progression.
BACKGROUND: Long non-coding RNA (lncRNA) is reported to be involved in multiple biological processes in numerous human tumors. Furthermore, an increasing number of studies have confirmed the involvement of lncRNA in the initiation and development of humancancers, including cervical cancer (CC). METHODS: The present study explored the potential role of lncRNA glypican 3 antisense transcript 1 (GPC3-AS1) with respect to regulating CC cell proliferation and migration. RESULTS: A quantitative reverse transcriptase-polymerase chain reaction confirmed that GPC3-AS1 was up-regulated in CC cells compared to normal CRL-2614 cells. Loss-of-function assays demonstrated the negative effect of GPC3-AS1 depletion on CC cell proliferation and migration. GPC3-AS1 positively regulated its nearby gene glypican 3 (GPC3). Significant up-regulation of GPC3 was also observed in CC cells, consistently with GPC3-AS1. In addition, GPC3-AS1 and GPC3 synergistically promoted the proliferative and migratory abilities of CC cells. Mechanistic investigation showed that ELK1 acted as the transcription activator of GPC3-AS1 and GPC3, thus contributing to their up-regulation in CC cells. Rescue assays indicated that the ELK1-induced GPC3-AS1/GPC3 axis promoted cell proliferation and migration in CC. CONCLUSIONS: The results of the present study have revealed a novel molecular pathway that can regulate CC cell proliferation and migration, thus providing a new basis for investigating the molecular mechanism associated with CC progression.