In this study, we identified CTCs using the previously reported CanPatrol CTC enrichment technique from peripheral blood samples of 126 patients with colorectal cancer (CRC) and found that CTCs could be classified into three subpopulations based on expression of epithelial cell adhesion molecule (EpCAM) (E-CTCs), the mesenchymal cell marker vimentin (M-CTCs), or both EpCAM and vimentin (biphenotypic E/M-CTCs). Circulating tumor microemboli (CTMs) were also identified in peripheral blood samples. Meanwhile, E-CTCs, M-CTCs, E/M-CTCs, and CTMs were detected in 76.98%, 42.06%, 56.35%, and 36.51% of the 126 patients, respectively. Interestingly, the presence of CTMs and each CTC subpopulation was significantly associated with blood lymphocyte counts and tumor-node-metastasis stage (P < 0.001). Lymphocyte counts and the neutrophil-to-lymphocyte ratio (NLR) in patients lacking CTCs were significantly different from those in patients testing positive for CTMs and each CTC subpopulation (P < 0.001). Our results indicate that tumor metastasis is more significantly associated with the presence of CTMs and M-CTCs than with other CTC subpopulations and suggest that EMT may be involved in CTC evasion of lymphocyte-mediated clearance.
Evidence indicates that long non-coding RNAs (lncRNAs) serve a critical role in the regulation of non-small cell lung cancer (NSCLC) progression. LncRNA Ubiquitin-like with PHD and RING finger domains 1 (UHRF1) protein associated transcript (UPAT) has been identified to be overexpressed in a variety of types of cancer. The present study demonstrated that lncRNA UPAT expression was upregulated in NSCLC tissues and significantly associated with tumor size and Tumor-Node-Metastasis stage. Additionally, UPAT promoted NSCLC cell proliferation and G1-S phase transition in vitro. Furthermore, UPAT promoted NSCLC cell proliferation, partly via increasing UHRF1 expression and consequently epigenetically silencing RASSF1 and CDH13 transcription. In addition, the knockdown of UHRF1 partially decreased the promotion of cell growth and G1-S phase transition caused by UPAT overexpression. In conclusion, these data suggest that the lncRNA UPAT promotes the NSCLC cell proliferation and may be a potential therapeutic target of NSCLC.
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