结直肠癌
基因敲除
癌症研究
长非编码RNA
细胞生长
细胞迁移
生物
肿瘤进展
大肠癌小鼠模型的建立
癌症
核糖核酸
细胞
细胞培养
基因
遗传学
作者
Zhe Liu,Liang Ma,Yuchen Gu,Yingying Huang,Xin Liang,Lingyun Kong,Yiming Sun
标识
DOI:10.1016/j.prp.2022.153843
摘要
Increasing evidences demonstrated that long non-coding RNAs (lncRNAs) participates in the occurrence and development of cancer. In this study, we explored the function and molecular mechanism of LINC01123 in colorectal cancer progression.Analyze the expression level of LINC01123 in gastrointestinal tumors via TCGA database. Colorectal tumor tissues and normal tissues were collected to detect the expression of LINC01123 by RT-qPCR. CCK-8 assay, clone formation assay, transwell assay, and wound healing assays were used to explore the effects of LINC01123 on the proliferation, invasion and migration of colorectal cancer cells. Coomassie blue staining, RNA pull-down and mass spectrometry were used to screen the protein interacted with LINC01123. Xenograft model was used to explore the effect of LINC01123 in vivo.LINC01123 was up-regulated in colorectal cancer tumor tissues. The proliferation, invasion and migration ability of colorectal cancer cells were decreased significantly after LINC01123 knockdown, and it may inhibit its expression by interacted with SRSF7, thereby promoting colorectal cancer progression.LINC01123 can promote the proliferation, invasion and migration of colorectal cancer cells by regulating SRSF7, suggesting that it may be an important regulator of colorectal cancer progression.
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