Xia Zheng1, Min Liu2, YingChun Song3, ChunHua Feng4. 1. 1 Department of Gynaecology and Obstetrics, Fifth Hospital of Xi'an, Xi'an, China. 2. 2 Department of Oncology, Affiliated Hospital of Yan'an University, Yan'an, Yan'an, China. 3. 3 Department of Gynaecology and Obstetrics, First Hospital of Xi'an, Xi'an, China. 4. 4 Department of Obstetrics and Gynecology, Tongchuan People's Hospital, Tongchuan, China.
Abstract
OBJECTIVE: Long non-coding RNA-ATB (Lnc-ATB) have been reported to promote tumor proliferation and metastasis via regulation of tumor suppressive miRNA-related signals. Patients with endometrial cancer (EC) have advanced stage disease or metastasis have poor prognosis. We here investigated the role of Lnc-ATB in endometrial cancer. METHODS: Endometrial cancer tissues and normal tissues (n = 35) were collected to determine the expression and clinical significance of Lnc-ATB, and bioinformatics analysis was used to predict the miRNA target. siRNA was used to estimate the function of Lnc-ATB in EC cell lines and in vivo. RESULT: The expression of Lnc-ATB is up-regulated in tumor tissues and EC cell lines. Patients with high expressed Lnc-ATB have high FIGO stage and poor tumor differentiation. The tumor suppressor miR-126 interacted with Lnc-ATB. Down-regulated miR-126 negative correlated with FIGO stage and tumor differentiation. Knockdown of Lnc-ATB in RL95 and HEC1A cell lines increased the miR-126 level and impaired the cell vitality, induced caspase-3-related tumor apoptosis and G1/S arrest. However, abrogation of miR-126 by its inhibitors counteracted Lnc-ATB knockdown-induced tumor inhibition via regulation of miR-126 target gene PIK3R2 and Sox2-related apoptosis and cell cycle pathway. Meanwhile, Lnc-ATB knockdown also suppressed the migration and invasion and inhibited TGF-β-induced epithelial-mesenchymal transition (EMT) phenotype via miR-126. Knockdown of Lnc-ATB in vivo remarkably induced tumor regression via restoration of tumor suppressor miR-126, leading to deceased tumor volume, reduced expression of PCNA and PIK3R2/Sox2 signals and EMT phenotype in tumor tissues. CONCLUSION: These data demonstrate the tumorigenic role of Lnc-ATBs in endometrial cancer via abrogation of tumor suppressor miR-126 signals.
OBJECTIVE: Long non-coding RNA-ATB (Lnc-ATB) have been reported to promote tumor proliferation and metastasis via regulation of tumor suppressive miRNA-related signals. Patients with endometrial cancer (EC) have advanced stage disease or metastasis have poor prognosis. We here investigated the role of Lnc-ATB in endometrial cancer. METHODS:Endometrial cancer tissues and normal tissues (n = 35) were collected to determine the expression and clinical significance of Lnc-ATB, and bioinformatics analysis was used to predict the miRNA target. siRNA was used to estimate the function of Lnc-ATB in EC cell lines and in vivo. RESULT: The expression of Lnc-ATB is up-regulated in tumor tissues and EC cell lines. Patients with high expressed Lnc-ATB have high FIGO stage and poor tumor differentiation. The tumor suppressor miR-126 interacted with Lnc-ATB. Down-regulated miR-126 negative correlated with FIGO stage and tumor differentiation. Knockdown of Lnc-ATB in RL95 and HEC1A cell lines increased the miR-126 level and impaired the cell vitality, induced caspase-3-related tumor apoptosis and G1/S arrest. However, abrogation of miR-126 by its inhibitors counteracted Lnc-ATB knockdown-induced tumor inhibition via regulation of miR-126 target gene PIK3R2 and Sox2-related apoptosis and cell cycle pathway. Meanwhile, Lnc-ATB knockdown also suppressed the migration and invasion and inhibited TGF-β-induced epithelial-mesenchymal transition (EMT) phenotype via miR-126. Knockdown of Lnc-ATB in vivo remarkably induced tumor regression via restoration of tumor suppressor miR-126, leading to deceased tumor volume, reduced expression of PCNA and PIK3R2/Sox2 signals and EMT phenotype in tumor tissues. CONCLUSION: These data demonstrate the tumorigenic role of Lnc-ATBs in endometrial cancer via abrogation of tumor suppressor miR-126 signals.