Knockdown of long noncoding RNA DLX6-AS1 inhibits migration and invasion of thyroid cancer cells by upregulating UPF1.

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "Knockdown of long noncoding RNA DLX6-AS1 inhibits migration and invasion of thyroid cancer cells by upregulating UPF1, by Z.-B. Zhong, Y.-J. Wu, J.-N. Luo, X.-N. Hu, Z.-N. Yuan, G. Li, Y.-W. Wang, G.-D. Yao, X.-F. Ge, published in Eur Rev Med Pharmacol Sci 2019; 23(24): 10867-10873-DOI: 10.26355/eurrev_201912_19790-PMID: 31858555" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/19790.

Knockdown of long noncoding RNA DLX6-AS1 inhibits migration and invasion of thyroid cancer cells by upregulating UPF1.

OBJECTIVE: Recently, long non- coding RNAs (lncRNAs) have attracted much attention for their roles in tumor progression. The aim of this study was to investigate the exact role of lncRNA DLX6 antisense RNA 1 (DLX6-AS1) in the development of thyroid cancer (TC), and to explore the underlying mechanism. PATIENTS AND METHODS: DLX6-AS1 expression in both TC cells and tissue samples was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Moreover, transwell assay and wound healing assay were conducted. QRT-PCR and Western blot assay were used to explore the underlying mechanism. Furthermore, the function of DLX6-AS1 was identified in vivo. RESULTS: DLX6-AS1 expression level in TC tissues was significantly higher than that of the corresponding normal tissues. Moreover, TC cell migration and invasion were markedly inhibited after DLX6-AS1 was knocked down in vitro. The mRNA and protein expressions of UPF1 were both remarkably up-regulated after knockdown of DLX6-AS1. Meanwhile, the expression level of UPF1 was negatively correlated with the expression of DLX6-AS1 in TC tissues. Furthermore, knockdown of DLX6-AS1 significantly inhibited tumor metastasis in vivo. CONCLUSIONS: Knockdown of DLX6-AS1 could inhibit TC cell migration and invasion via upregulating UPF1, which might be a potential therapeutic target in TC.

Over-expression of lncRNA SBF2-AS1 is associated with advanced tumor progression and poor prognosis in patients with non-small cell lung cancer.

OBJECTIVE: Emerging evidence suggest that long non-coding RNAs (lncRNAs) may play important roles in human cancers. The aim of this study was to investigate the expression of SBF2-AS1 in non small cell lung cancer (NSCLC) and its correlation with clinicopathological features and prognosis in NSCLC. PATIENTS AND METHODS: The expression of lncRNA SBF2-AS1 was measured in 174 NSCLC samples and their matched non-tumor tissues by using RT-PCR. Association of SBF2-AS1 expression with clinicopathological features was analyzed in NSCLC. Kaplan-Meier analysis was performed to evaluate the overall survival of NSCLC patients. RESULTS: The expression of SBF2-AS1 was higher in NSCLC tissues compared with adjacent non-tumor tissues (p < 0.01). Additionally, high expression level of SBF2-AS1 was significantly associated with NSCLC histological grade, and lymph node metastasis. Furthermore, a higher SBF2-AS1 expression was demonstrated to be associated with poor overall survival times in NSCLC patients (p < 0.001). Multivariate analysis suggested that SBF2-AS1 expression was an independent prognostic factor for overall survival of patients with NSCLC (p = 0.013). CONCLUSIONS: Our data suggest that SBF2-AS1 could represent a novel prognostic marker and potential therapeutic target in patients with NSCLC.

MEK inhibitor CI-1040 induces apoptosis in acute myeloid leukemia cells in vitro.

OBJECTIVE: MEK1/2 (mitogen-activated protein kinase 1 and 2)/ERK1/2 (extracellular signal-regulated kinase 1 and 2) is important transducers of external signals for cell growth, survival, and apoptosis in acute myeloid leukemia cells (AML). In this study, we analyzed the effect of MEK inhibitor CI-1040 on the survival of AML cells. MATERIALS AND METHODS: Using ELISA and MTT we studied the cytotoxic effects of CI-1040 on AML U-937 cells. We studied the changes induced by CI-1040 on PUMA and p53 expression in U-937 cells by Western blotting assay. Moreover, we analyzed the cytotoxic effect of CI-1040 in U-937 cells with deleted PUMA, wt-p53 by wt-p53 siRNA and PUMA siRNA transfection. RESULTS: CI-1040 induced apoptosis and inhibited proliferation in U-937 cells in a dose and time-dependent manner. CI-1040 induced a significant increase in PUMA mRNA and protein levels. Importantly, we show that knockdown of PUMA by PUMA siRNA transfection inhibited CI-1040-induced apoptosis and proliferation inhibition in U-937 cells. Moreover, CI-1040 induced apoptosis and proliferation inhibition was irrespective of wt-P53 status. CONCLUSIONS: These results demonstrate that CI-1040 induce apoptosis of U-937 cells and might be a new therapeutic option for the treatment of AML.