Yan Zhang1, Rong Yu2, Lei Li1. 1. Department of Obstetrics, the Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, Shandong, China. 2. Department of Obstetrics and Gynecology, Yantai Yuhuangding Hospital Laishan Branch, Yantai, Shandong, China.
Abstract
BACKGROUND: LINC00641 was found to act in anti-tumor manner in several types of cancers. Nonetheless, the detailed functions of LINC00641 have not been determined in cervical cancer (CC). METHODS: The expression of LINC00641, miR-378a-3p and CPEB3 was examined using a quantitative reverse transcriptase-polymerase chain reaction. The relationships between LINC00641 and its downstream mechanism were illustrated by RNA pull-down and luciferase reporter experiments. RESULTS: LINC00641 was found to be under-expressed in CC cell lines. By overexpressing LINC00641, cell proliferative, migratory and invasive abilities, as well as epithelial mesenchymal transition (EMT) characteristics, were inhibited, whereas the rate of apoptosis was increased. Next, a starBase search (http://starbase.sysu.edu.cn) was applied to select microRNAs that had binding sequences with LINC00641. By up-regulating LINC00641 expression, miR-378a-3p expression displayed the strongest decline. Moreover, miR-378a-3p was found to be up-regulated in CC cell lines. In addition, LINC00641 hindered the progression of CC by decreasing miR-378a-3p expression. CPEB3 was discovered as a downstream target of miR-378a-3p and was under-expressed in CC cells. Furthermore, knockdown of CPEB3 could counter the influence of an overexpression of LINC00641 with respect to CC progression. CONCLUSIONS: LINC00641 suppressed the progression of CC by targeting miR-378a-3p/CPEB3, suggesting that LINC00641 may have positive therapeutic impact for treatment for CC.
BACKGROUND:LINC00641 was found to act in anti-tumor manner in several types of cancers. Nonetheless, the detailed functions of LINC00641 have not been determined in cervical cancer (CC). METHODS: The expression of LINC00641, miR-378a-3p and CPEB3 was examined using a quantitative reverse transcriptase-polymerase chain reaction. The relationships between LINC00641 and its downstream mechanism were illustrated by RNA pull-down and luciferase reporter experiments. RESULTS:LINC00641 was found to be under-expressed in CC cell lines. By overexpressing LINC00641, cell proliferative, migratory and invasive abilities, as well as epithelial mesenchymal transition (EMT) characteristics, were inhibited, whereas the rate of apoptosis was increased. Next, a starBase search (http://starbase.sysu.edu.cn) was applied to select microRNAs that had binding sequences with LINC00641. By up-regulating LINC00641 expression, miR-378a-3p expression displayed the strongest decline. Moreover, miR-378a-3p was found to be up-regulated in CC cell lines. In addition, LINC00641 hindered the progression of CC by decreasing miR-378a-3p expression. CPEB3 was discovered as a downstream target of miR-378a-3p and was under-expressed in CC cells. Furthermore, knockdown of CPEB3 could counter the influence of an overexpression of LINC00641 with respect to CC progression. CONCLUSIONS:LINC00641 suppressed the progression of CC by targeting miR-378a-3p/CPEB3, suggesting that LINC00641 may have positive therapeutic impact for treatment for CC.