Abstract
BackgroundPrevious studies indicated CRNDE to have a pivotal part within tumorigenesis. Notwithstanding, precise details on CRNDE activities within NPC are still uncertain. The investigation described in this article served to focus in greater depth on the mechanistics regarding CRNDE, together with all associated regulatory networks, on nasopharyngeal carcinoma (NPC) and its treatment possibilities.MethodsQuantitative real-time polymerase chain reaction (RT-qPCR) analyzed CRNDE, miR-545-5p and CCND2 expression within NPCs and representative cell lineages. CCK-8 cell counting-, EdU-, wound-healing-/transwell-assays analyzed cellular proliferation, migrative, together with invasive properties. Apoptosis/cell cycle progression were scrutinized through flow cytometry. Dual-luciferase reporter assays validated CRNDE/miR-545-5p/CCND2 interplay. Proteomic expression of apoptosis-related protein, EMT-related protein and CCND2 protein were evaluated through Western blotting. In addition, Ki67 expression was evaluated through immunohistochemical staining. The effect of CRNDE in vivo was assessed by nude murine xenograft model studies.ResultsThis study demonstrated up-regulated expression of CRNDE and CCND2 within NPC tissues/cell lines. Meanwhile, miR-545-5p was down-regulated. CRNDE knock-down or miR-545-5p over-expression drastically reduced NPC proliferative, migrative and invasive properties, promoted apoptosis/altered cell cycle, and inhibited CCND2 expression. However, miR-545-5p down-regulation had opposing effects. All inhibiting functions generated by CRNDE down-regulation upon NPC progression could be counterbalanced or synergistically exacerbated, depending on miR-545-5p down-regulation or up-regulation, respectively. Multiple-level investigations revealed CRNDE to serve as a sponge for miR-545-5p, and can target CCND2 within NPCs.ConclusionsCRNDE increases CCND2 expression by competitive binding with miR-545-5p, thus accelerating the development of NPC. This provides potential therapeutic targets and prognostic markers against NPC.
Highlights
Previous studies indicated Colorectal neoplasia differential expression (CRNDE) to have a pivotal part within tumorigenesis
Down‐regulation of CRNDE inhibits nasopharyngeal carcinoma (NPC) proliferative, migrative and invasive properties RT-qPCR was employed for gene expression analysis of CRNDE within 32 NPC and matching adjacent tissues
CRNDE expression in NPC tissues was found to be highly up-regulated in comparison to adjacent tissue levels (p < 0.01) (Fig. 1a)
Summary
Previous studies indicated CRNDE to have a pivotal part within tumorigenesis. Notwithstanding, precise details on CRNDE activities within NPC are still uncertain. Long non-coding RNAs (lncRNAs) are > 200 bp and lack an open reading frame that cannot encode proteins [3]. Due to their vast spectrum of expression profiles and tissue-linked expression specificity, lncRNAs can be used as tumor markers and therapeutic targets [4]. Dysregulated expression/mutations in lncRNAs influences tumorigenesis and metastasis, with this trend occurring within multiple tumor models including colon [5], prostate [6] and oral cancer [7]. Studies have found that CRNDE plays an oncogenic role in the development of TSCC by inhibiting the expression of miR-384 [12]. The mechanism/s employed by CRNDE to influence NPC malignancy is lacking
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