Chunlin Ke , Peirong Wang , Biao Chen , Xianhui Cheng , Xinyi Zhang , Rongmu Xia , Feng Dong , Jiancheng Li
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引用次数: 0
Abstract
Colorectal cancer (CRC), the most common gastrointestinal malignancy, has incompletely understood underlying developmental mechanisms. LincRNA, a subclass of long non-coding RNAs (LncRNAs), is implicated in the pathogenesis of multiple cancers, including CRC. In this study, qPCR analysis revealed that Linc00960 expression was significantly upregulated in CRC tissues compared to adjacent non-tumor tissues and correlated with poor patient prognosis. Functional assays (including cell proliferation, colony formation, flow cytometry, Transwell assay and xenograft experiments) demonstrated that high Linc00960 expression enhanced CRC cell proliferation, whereas Linc00960 knockdown markedly suppressed cell proliferation, migration and invasion. To investigate the mechanism, dual-luciferase reporter assays were performed; there revealed that Linc00960 directly bound to hsa-miR-107 (miR-107) and negatively regulated its expression, thereby upregulating CDK6 expression and promoting CRC cell proliferation. In conclusion, our findings indicated that the Linc00960/miR-107/CDK6 axis served as a crucial signaling pathway in CRC progression, providing novel potential targets and biomarkers for CRC diagnosis and therapy.
期刊介绍:
Our scope includes but is not limited to areas such as: Chromosome biology; Chromatin and epigenetics; DNA repair; Gene regulation; Nuclear import-export; RNA processing; Non-coding RNAs; Organelle biology; The cytoskeleton; Intracellular trafficking; Cell-cell and cell-matrix interactions; Cell motility and migration; Cell proliferation; Cellular differentiation; Signal transduction; Programmed cell death.