Mechanism of long noncoding RNA RP11-97C16.1 regulating the proliferation of bladder cancer cells
10.3760/cma.j.cn115396-20231222-00175
- VernacularTitle:长链非编码RNA RP11-97C16.1调控膀胱癌细胞增殖的作用机制
- Author:
Jinlun FU
1
;
Zhihua YE
;
Dan PAN
;
Shuai LUO
;
Geng HUANG
Author Information
1. 黄石市中心医院（湖北理工学院附属医院）泌尿外科，黄石 435000
- Keywords:
Long noncoding RNA;
RP11-97C16.1;
Bladder neoplasms;
miR-3687;
Cell proliferation
- From:
International Journal of Surgery
2025;52(2):93-98
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To observe the expression level of long noncoding RNA RP11-97C16.1 in bladder cancer tissues and its relationship with the survival time of bladder cancer patients, and to explore the role and potential molecular mechanism of RP11-97C16.1 in the proliferation of bladder cancer cells.Methods:The expression difference of RP11-97C16.1 in bladder cancer tissue and adjacent tissue was analyzed by TCGA database, and the relationship between the expression level of RP11-97C16.1 and the survival time of bladder cancer patients was analyzed by GEPIA database. The expression of RP11-97C16.1 in four bladder cancer cell lines (T24, MGH-U3, J82, UM-UC-3) was detected by real-time fluorescence quantitative polymerase chain reaction (RT-qPCR). The UM-UC-3 cells were divided into RP11-97C16.1 group and control group, and the transfectants were pcDNA-RP11-97C16.1 plasmid and negative control plasmid, respectively. The expression levels of RP11-97C16.1 and miR-3687 were detected by RT-qPCR. The viability and proliferation ability of UM-UC-3 cells were detected by cell counting kit-8 (CCK8) and colony formation assay. The complementary relationship between RP11-97C16.1 and miR-3687 was verified by dual-luciferase reporter gene assay. The expression levels of Cyclin E2, CDK2, CDK4, CDK6 and Cyclin D2 were detected by Western blotting. Measurement data were expressed as mean ± standard deviation ( ± s), independent sample t-test was used for comparison between two groups, and one-way analysis of variance was used for comparison between multiple groups. Results:Compared with adjacent tissues, the expression of RP11-97C16.1 in bladder cancer tissues was significantly decreased ( P<0.01). Compared with patients with lower expression of RP11-97C16.1, patients with higher expression of RP11-97C16.1 had longer overall survival time ( P<0.01). Compared with the SV-HUC-1 cell line, the expression of RP11-97C16.1 was significantly decreased in the four bladder cancer cell lines ( P<0.01). In UM-UC-3 cells in which RP11-97C16.1 was upregulated, the expression of miR-3687 was decreased ( P<0.01). Compared with the control group, up-regulation of RP11-97C16.1 could significantly reduce the proliferation ability of UM-UC-3 cells ( P<0.05), and decrease the number of bladder cancer cell colonies ( P<0.01). RP11-97C16.1 could target and bind miR-3687 ( P<0.01). Compared with the control group, overexpression of RP11-97C16.1 could significantly decreased the expression of Cyclin E2, CDK2, CDK4, CDK6, and Cyclin D2 proteins. Conclusions:The expression of RP11-97C16.1 is low in bladder cancer tissue, and patients with higher expression of RP11-97C16.1 have a longer survival time. Up-regulation of RP11-97C16.1 can down-regulate the expression of miR-3687, thereby inhibiting the proliferation of bladder cancer cells UM-UC-3.
