PARProceedings of Anticancer Research2208-35452208-3553Bio-Byword Scientific Publishing Pty. Ltd.10.26689/par.v6i6.4452ArticleThe Mechanism of Long Non-Coding RNA SNHG7 in Cholangiocarcinoma Cell Proliferation, Migration, and Epithelial-Mesenchymal Transitionhttps://artdesignp.com/journal/PAR/6/6/10.26689/par.v6i6.4452ZhaoJisen,YuYang,ZhouYuanlong,WangYuan,ChenSheng,ChengShujie2022662022-11-29Objective: To investigate the mechanism of long non-coding RNA SNHG7 and its regulatory effect on the proliferation, migration, and epithelial-mesenchymal transition of cholangiocarcinoma cells. Methods: A total of 20 pairs of cholangiocarcinoma and adjacent non-tumor bile duct tissues were collected from patients with cholangiocarcinoma who underwent surgery in the Affiliated Hospital of Hebei University (Hebei, China). Cholangiocarcinoma cell lines CCLP-1, QBC939, RBE, and HCC-9810 as well as normal human biliary epithelial cell line HIBEC were purchased for cell culture. We performed cell transfection, quantitative real-time polymerase chain reaction (qRT-PCR) to detect gene expression, Cell Counting Kit-8 (CCK-8) experiment to determine cell proliferation ability, scratch test to determine cell migration ability, and Transwell test to detect cell invasion ability. Results: The expression of lncRNA SNHG7 in cholangiocarcinoma cell lines CCLP-1, QBC939, RBE, and HCCC-9810 was 3.21 ± 1.01, 3.03 ± 1.02, 2.98 ± 1.21, and 3.12 ± 1.14, respectively, while its expression in normal cell line HIBEC was 3.21 ± 1.21; the expression of lncRNA SNHG7 in CCLP-1 was the highest; compared with HIBEC, the p values were all less than 0.05, indicating that the difference was statistically significant. The expression of miR-520f-3p in CCLP-1, QBC939, RBE, and HCCC-9810 was 1.45 ± 0.75, 1.55 ± 0.71, 1.54 ± 0.73, and 1.61 ± 0.72, respectively, while its expression in normal cell line HIBEC was 3.21 ± 1.21; the expression of miR-520f-3p in CCLP-1 was the lowest, and compared with HIBEC, the p values were all less than 0.05, indicating that the difference was statistically significant. In qRT-PCR, the expression of lncRNA SNHG7 of si-NC (3.21±1.11) was significantly higher than that of si-SNHG7 (1.14±0.76), and the p value was less than 0.05, indicating that the difference was statistically significant. In the CCK-8 experiment, the proliferation ability of CCLP-1 cells of the si-NC group at 24 h, 48 h, and 72 h was 0.61±0.59, 0.75±0.68, and 1.36±0.71, respectively; the proliferation ability of CCLP-1 cells of the si-SNHG7 group at 24 h, 48 h, and 72 h was 0.51±0.64, 0.59±0.59, and 0.63±0.61, respectively; there was a significant decrease in the proliferation ability, and the p value was less than 0.05, indicating a statistically significant difference. After 24 h of scratch treatment, compared with the si-NC group, the migration ability of CCLP-1 cells of the si-SNHG20 group was reduced (t = 6.356, P = 0.026). The results of Transwell test showed that the cell invasion ability of CCLP-1 in the si-SNHG20 group was significantly reduced compared with the si-NC group (t = 7.845, P = 0.032). Conclusion: Exploring the gene expression mechanism in relation to the occurrence and development of cholangiocarcinoma is beneficial to future clinical work in terms of diagnosis, treatment, and prognosis. The knockdown of lncRNA SNHG7 can effectively inhibit the proliferation, migration, and invasion of cholangiocarcinoma.

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