H Liu1, S-Y Zeng, Y Xie, C-Q Fei, L Sun. 1. Department of Oncology, Jiangxi Maternal and Child Health Hospital, Nanchang, China. 435110492@qq.com.
Abstract
OBJECTIVE: To elucidate the role of linc-UBC1 in regulating the metastasis and progression of ovarian cancer (OC) by downregulating the p53 level. PATIENTS AND METHODS: Relative levels of linc-UBC1 in OC tissues and paracancerous tissues were determined by quantitative Real-Time Polymerase Chain Reaction (qRT-PCR). Differential expressions of linc-UBC1 in OC tissues with different tumor staging or tumor sizes were detected as well. Receiver operating characteristic (ROC) curves were introduced for assessing the diagnostic value of linc-UBC1 in OC. After silence of linc-UBC1, proliferative and migratory abilities of HO8910 and HEY cells were evaluated. Subcellular distribution of linc-UBC1 was analyzed. The interaction between linc-UBC1 and p53 was explored through the RNA immunoprecipitation (RIP) assay. At last, rescue experiments were conducted to uncover the role of linc-UBC1/p53 regulatory loop in influencing the progression of OC. RESULTS: Linc-UBC1 was upregulated in OC and its level negatively correlated to that of p53. Linc-UBC1 level was higher in OC patients with advanced TNM staging or larger tumor size. Linc-UBC1 was mainly distributed in the nucleus. Silence of linc-UBC1 attenuated proliferative and migratory abilities of HO8910 and HEY cells. RIP assay verified that linc-UBC1 could inhibit the transcription of p53. Knockdown of p53 could partially reverse the regulatory effects of linc-UBC1 on regulating the progression of OC. CONCLUSIONS: Linc-UBC1 is upregulated in OC tissues and cells. It stimulates the proliferation and metastasis of OC by downregulating p53 level, thus exerting a carcinogenic role.
OBJECTIVE: To elucidate the role of linc-UBC1 in regulating the metastasis and progression of ovarian cancer (OC) by downregulating the p53 level. PATIENTS AND METHODS: Relative levels of linc-UBC1 in OC tissues and paracancerous tissues were determined by quantitative Real-Time Polymerase Chain Reaction (qRT-PCR). Differential expressions of linc-UBC1 in OC tissues with different tumor staging or tumor sizes were detected as well. Receiver operating characteristic (ROC) curves were introduced for assessing the diagnostic value of linc-UBC1 in OC. After silence of linc-UBC1, proliferative and migratory abilities of HO8910 and HEY cells were evaluated. Subcellular distribution of linc-UBC1 was analyzed. The interaction between linc-UBC1 and p53 was explored through the RNA immunoprecipitation (RIP) assay. At last, rescue experiments were conducted to uncover the role of linc-UBC1/p53 regulatory loop in influencing the progression of OC. RESULTS:Linc-UBC1 was upregulated in OC and its level negatively correlated to that of p53. Linc-UBC1 level was higher in OCpatients with advanced TNM staging or larger tumor size. Linc-UBC1 was mainly distributed in the nucleus. Silence of linc-UBC1 attenuated proliferative and migratory abilities of HO8910 and HEY cells. RIP assay verified that linc-UBC1 could inhibit the transcription of p53. Knockdown of p53 could partially reverse the regulatory effects of linc-UBC1 on regulating the progression of OC. CONCLUSIONS:Linc-UBC1 is upregulated in OC tissues and cells. It stimulates the proliferation and metastasis of OC by downregulating p53 level, thus exerting a carcinogenic role.