Abstract
The incidence and mortality rate of cancer continues to gradually increase, although considerable research effort has been directed at elucidating the molecular mechanisms underlying biomarkers responsible for tumorigenesis. Accumulated evidence indicates that the long non-coding RNAs (lncRNAs), which are transcribed but not translated into functional proteins, contribute to cancer development. Recently, linc00152 (an lncRNA) was identified as a potent oncogene in various cancer types, and shown to be involved in cancer cell proliferation, invasiveness, and motility by sponging tumor-suppressive microRNAs acting as a competing endogenous RNA, binding to gene promoters acting as a transcriptional regulator, and binding to functional proteins. In this review, we focus on the oncogenic role of linc00152 in tumorigenesis and provided an overview of recent clinical studies on the effects of linc00152 expression in human cancers.
Highlights
Cancers are diseases caused by abnormal cell growth
Another study presented that linc00152 directly bound to epidermal growth factor receptor (EGFR) and increased the activity of EGFR to promote the EGFR/phosphoinositide 3-kinase/Akt pathway, which contributed to the inductions of tumorigenic features [30,31]
Many studies have investigated the association between linc00152 and human cancers
Summary
Cancers are diseases caused by abnormal cell growth. Unlike benign tumors where cells grow abnormally but do not spread, malignant tumors can migrate to other parts of the body. Linc00152 might enhance the invasion and migration capacities of cancer cells by sponging miR-138 and upregulating hypoxia-inducible factor-1α (HIF-1α) expression [18]. Linc00152 may interact directly with miR-139-5p, which is associated with the expressional upregulation of protein kinase AMP-activated catalytic subunit alpha 1, which is involved in the promotion of aerobic glycolysis for metabolic reprogramming [19]. These results suggest the associations between linc00152 and HIF-1α activation and increased aerobic glycolysis might be linked to cancer cell survival against intratumoral hypoxia, and contribute to tumor aggressiveness and malignant development
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