Hepatocellular carcinoma (HCC) is one of the most common subtypes of malignant liver tumors, characterized by high morbidity and mortality. Due to its poor diagnosis strategy and inefficient clinical intervention, HCC has brought terrible life experiences for patients worldwide. Finding novel curative agents for HCC is urgently needed. In the current study, we hypothesized that lncRNA PANTR1 participates in HCC initiation or progression. Our study found that lncRNA PANTR1 was upregulated in HCC tumor tissues and abundantly expressed in HCC cell lines. PANTR1 knockdown inhibited cell growth and migration, promoted cell apoptosis in vitro, and suppressed tumor cell growth in vivo. Moreover, our results suggest that downregulated PANTR1 inhibited the Warburg effect in HCC cells. Underlying mechanisms of PANTR1 in HCC progression were investigated. PANTR1 acted as a competent sponge for miR-587 and downregulated miR-587 expression in HCC cells. Further, MiR-587 directly targets BCL2A1. lncRNA PANTR1 promotes HCC progression via mediating the miR-587-BCL2A1 axis. Our study identified a novel lncRNA PANTR1/miR-587/BCL2A1 axis in HCC progression. We might provide a new target for HCC basic research and clinical management.

The interaction between circRNAs and atherosclerosis has been extensively studied. However, more novel circRNAs need to be explored to help establish a perfect regulatory network. In the present research, hsa_circ_0000345 was demonstrated to regulate cellular development of oxygenized low-density lipoprotein (ox-LDL)-treated aortic smooth muscle cells (ASMCs), which was closely related to the occurrence and progress of atherosclerosis. Ox-LDL exposure remarkably decreased hsa_circ_0000345 expression in ASMCs. Transfection-induced hsa_circ_0000345 overexpression activated cell viability (detected by an MTT assay) and restrained cellular apoptosis (analysed by flow cytometry) in the atherosclerosis cellular model. While down-regulation of hsa_circ_0000345 reduced cell viability and promoted cell apoptosis. In addition, the data of the cell cycle distribution analysis and trans-well assay indicated that cell cycle progression was arrested at the G1 phase while cell invasion was enhanced in ASMCs following treatment of ox-LDL in the context of hsa_circ_0000345 OE plasmids. In addition, up-regulation of hsa_circ_0000345 supported HIF-1 alpha at both the mRNA and protein level, and down-regulation of hsa_circ_0000345 reduced HIF-1 alpha expression. Overall, the above findings revealed that hsa_circ_0000345 was a dramatic regulator of ASMCs proliferation, apoptosis and invasion in response to ox-LDL treatment. Hsa_circ_0000345 was identified as a protector of cell viability during ox-LDL induced cell development.

Chronic inflammation is part of the pathological process during atherosclerosis (AS). Due to the abundance of monocytes/macrophages within the arterial plaque, monocytes/macrophages have become a critical cellular target in AS studies. In recent decades, a number of long noncoding RNAs (lncRNAs) have been found to exert regulatory roles on the macrophage metabolism and macrophage plasticity, consequently promoting or suppressing atherosclerotic inflammation. In this review, we provide a comprehensive overview of lncRNAs in macrophage biology, highlighting the potential role of lncRNAs in AS based on recent findings, with the aim to identify disease biomarkers and future therapeutic interventions for AS.

Corrigendum: Functioning of Long Noncoding RNAs Expressed in Macrophage in the Development of Atherosclerosis