Y-T Gao1, Y-C Zhou. 1. College of Traditional Chinese Medicine, Southern Medical University, Guangzhou, China. weareone989@outlook.com.
Abstract
OBJECTIVE: The abnormal expression of lncRNA small nucleolar RNA host gene 7 (SNHG7) has been found in various kinds of cancers but its expression and role in breast cancer are unknown. We conducted this study to identify the expression, the function, and to underline the mechanism of SNHG7 in breast cancer. PATIENTS AND METHODS: The expression of SNHG7 was evaluated in clinical breast cancer tissues and adjacent normal tissues by qPCR assays. The expression was also detected in breast cancer cell lines and normal cell line. CCK8 assays were used to determine the biological functions of SNHG7 on breast cancer cells' proliferation. The transwell assays were applied for the exploration of the effects of SNHG7 on breast cancer cells' invasion. The direct target of SNHG7 was predicted by bioinformatics algorithm and verified by the Luciferase reporter assays. RESULTS: SNHG7 was found to be significantly upregulated in breast cancer tissues when compared with normal tissues. Breast cancer cell lines showed higher levels of SNHG7 than normal breast epithelial cell line. The knockdown of SNHG7 by siRNA could remarkably repress breast cancer cell proliferation and invasion. Moreover, miRNA-381 was newly confirmed as a direct target of SNHG7 and it mediated the suppressing effects of SNHG7 on breast cancer cells. CONCLUSIONS: SNHG7 was significantly upregulated in breast cancer and acted as an oncogene to promote breast cancer cell proliferation and invasion by directly sponging miRNA-381.
OBJECTIVE: The abnormal expression of lncRNA small nucleolar RNA host gene 7 (SNHG7) has been found in various kinds of cancers but its expression and role in breast cancer are unknown. We conducted this study to identify the expression, the function, and to underline the mechanism of SNHG7 in breast cancer. PATIENTS AND METHODS: The expression of SNHG7 was evaluated in clinical breast cancer tissues and adjacent normal tissues by qPCR assays. The expression was also detected in breast cancer cell lines and normal cell line. CCK8 assays were used to determine the biological functions of SNHG7 on breast cancer cells' proliferation. The transwell assays were applied for the exploration of the effects of SNHG7 on breast cancer cells' invasion. The direct target of SNHG7 was predicted by bioinformatics algorithm and verified by the Luciferase reporter assays. RESULTS:SNHG7 was found to be significantly upregulated in breast cancer tissues when compared with normal tissues. Breast cancer cell lines showed higher levels of SNHG7 than normal breast epithelial cell line. The knockdown of SNHG7 by siRNA could remarkably repress breast cancer cell proliferation and invasion. Moreover, miRNA-381 was newly confirmed as a direct target of SNHG7 and it mediated the suppressing effects of SNHG7 on breast cancer cells. CONCLUSIONS:SNHG7 was significantly upregulated in breast cancer and acted as an oncogene to promote breast cancer cell proliferation and invasion by directly sponging miRNA-381.
Authors: Sajad Najafi; Soudeh Ghafouri-Fard; Bashdar Mahmud Hussen; Hazha Hadayat Jamal; Mohammad Taheri; Mohammad Hallajnejad Journal: Front Cell Dev Biol Date: 2022-01-17