Hai-Xia Liang1, Yu-Hong Li2. 1. Department of Gynaecology and Obstetrics, The 986th Hospital of Chinese People's Liberation Army Air Force, No. 269 of You-Yi East Road, Xi'an, 710054, Shaanxi, People's Republic of China. 2. Department of Gynaecology and Obstetrics, The 986th Hospital of Chinese People's Liberation Army Air Force, No. 269 of You-Yi East Road, Xi'an, 710054, Shaanxi, People's Republic of China. Lianghx1128@163.com.
Abstract
BACKGROUND: Cervical cancer (CC) remains a large burden in the developing countries. The tumor inhibitory role of miR-873 has been verified in a variety of cancers, however, whether miR-873 has a suppressive effect on CC remains unclear. OBJECTIVE: The purpose of this study was to investigate the functional role of miR-873 in CC, as well as explore the underlying molecular mechanism. METHODS: The prognostic values of miR-873 were assessed by Kaplan-Meier methods and cox regression models using the data which were downloaded from TCGA database. The expression of miR-873 was measured by RT-qPCR. Cell counting Kit-8, clone formation, and Transwell assays were used to assess the cell viability and metastasis, appropriately. The targeting relationship between miR-873 and ULBP2 was predicted by biological software and confirmed by dual luciferase reporter assay. Rescue assays were conducted to investigate whether miR-873 affects the phenotype of CC cells via regulating ULBP2. RESULTS: We observed that miR-873 was low-expressed in CC. Up-regulation of miR-873 notably restrained the proliferation, invasion and migration of C33a cells. Meanwhile, down-regulation of miR-873 in SiHa cells presented the opposite outcomes. ULBP2 was forecasted and certified as a target of miR-873. The results of rescue assays showed that overexpression of ULBP2 could restore the proliferation and motility of CC cells that inhibited by miR-873. CONCLUSION: MiR-873 suppressed the CC cells proliferation, invasion and migration via negatively regulating ULBP2, suggesting that miR-873 could serve as a valuable therapeutic target for CC therapy.
BACKGROUND: Cervical cancer (CC) remains a large burden in the developing countries. The tumor inhibitory role of miR-873 has been verified in a variety of cancers, however, whether miR-873 has a suppressive effect on CC remains unclear. OBJECTIVE: The purpose of this study was to investigate the functional role of miR-873 in CC, as well as explore the underlying molecular mechanism. METHODS: The prognostic values of miR-873 were assessed by Kaplan-Meier methods and cox regression models using the data which were downloaded from TCGA database. The expression of miR-873 was measured by RT-qPCR. Cell counting Kit-8, clone formation, and Transwell assays were used to assess the cell viability and metastasis, appropriately. The targeting relationship between miR-873 and ULBP2 was predicted by biological software and confirmed by dual luciferase reporter assay. Rescue assays were conducted to investigate whether miR-873 affects the phenotype of CC cells via regulating ULBP2. RESULTS: We observed that miR-873 was low-expressed in CC. Up-regulation of miR-873 notably restrained the proliferation, invasion and migration of C33a cells. Meanwhile, down-regulation of miR-873 in SiHa cells presented the opposite outcomes. ULBP2 was forecasted and certified as a target of miR-873. The results of rescue assays showed that overexpression of ULBP2 could restore the proliferation and motility of CC cells that inhibited by miR-873. CONCLUSION:MiR-873 suppressed the CC cells proliferation, invasion and migration via negatively regulating ULBP2, suggesting that miR-873 could serve as a valuable therapeutic target for CC therapy.
Entities:
Keywords:
Cervical cancer; Migration and invasion; Proliferation; ULBP2; miR-873
Authors: D Cosman; J Müllberg; C L Sutherland; W Chin; R Armitage; W Fanslow; M Kubin; N J Chalupny Journal: Immunity Date: 2001-02 Impact factor: 31.745
Authors: Konstantina Eleme; Sabrina B Taner; Björn Onfelt; Lucy M Collinson; Fiona E McCann; N Jan Chalupny; David Cosman; Colin Hopkins; Anthony I Magee; Daniel M Davis Journal: J Exp Med Date: 2004-03-29 Impact factor: 14.307