Background
We aimed to evaluate the role of long non-coding RNA (LncRNA) gastric carcinoma proliferation-enhancing transcript 1 (GHET1) on thyroid cancer (TC) behavior in vitro.
Conclusions
LncRNA GHET1 dysregulation might be involved in the carcinogenesis of thyroid cancer. LncRNA GHET1 could be used as a potential molecular marker and molecular target for TC.
Methods
TC tissues and paired adjacent normal tissues were obtained after surgical excision from 43 patients with TC. The expression of LncRNA GHET1 was analyzed by real-time (RT) PCR. Human papillary thyroid cancer cell lines (TPC-1, BCPAP) were used to examine the role of LncRNA GHET1 in vitro. Cell proliferation was determined by CCK8 and cell colony formation assays. Transwell and wound-healing assays were used to detect the invasion and migration of thyroid cancer cells.
Results
Our results showed that LncRNA GHET1 was significantly more upregulated in TC tissues than in adjacent normal tissues. LncRNA GHET1 was also increased in thyroid cancer cell lines compared to normal thyroid cell lines. The upregulation of LncRNA GHET1 was significantly associated with tumor invasion, gender, and lymph node metastasis in patients with thyroid cancer. The in vitro studies showed that silencing LncRNA GHET1 in BCPAP cells inhibited cell proliferation, cell invasion, and migration. Silencing of LncRNA GHETI also promoted the cell apoptotic rate, caused an increase in the cell population at the G0/G1 phase, and decreased the cell population at the S phase. In contrast, the overexpression of LncRNA GHET1 promoted cell proliferation, invasion, and migration, inhibited cell apoptosis, and increased cell population at the S phase in TPC cells. Conclusions: LncRNA GHET1 dysregulation might be involved in the carcinogenesis of thyroid cancer. LncRNA GHET1 could be used as a potential molecular marker and molecular target for TC.