Suppression of long non-coding RNA UCA1 inhibits proliferation and invasion and induces apoptosis in human lung cancer cells.

OBJECTIVE: Lung cancer is one of the deadliest cancers responsible for significant mortality and morbidity across the globe. The unavailability of efficient treatments, lack of reliable biomarkers and potent therapeutic targets, limit the treatment of lung cancer. In this study, we explored the potential of long non-coding RNA (lncRNA) urothelial carcinoma-associated 1 (UCA1) as the therapeutic target for lung cancer. MATERIALS AND METHODS: The expression analysis was carried out by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Cell viability was monitored by cell counting kit 8 (CCK-8) assay. The 4',6-diamidino-2-phenylindole (DAPI), annexin-V/Propidium iodide staining and comet assays were used to detect apoptosis. Boyden chamber and wound heal assays were used for cell to asses cell invasion and migration respectively. Protein expression was determined by immunoblotting. RESULTS: The expression of lncRNA UCA1 was determined by qRT-PCR in six different types of lung cancer cell lines. It was observed that lncRNA UCA1 was significantly (p < 0.05) upregulated in all the lung cancer cell lines. To investigate the role of lncRNA UCA1 in lung cancer, its expression was suppressed by transfection of the lung cancer NCI-H23 cells by si-UCA1. The results showed that suppression of lncRNA UCA1 significantly (p < 0.05) reduced the viability of NCI-H23 cancer cells via induction of the apoptosis. Furthermore, the lncRNA UCA1 suppression (p < 0.05) significantly inhibited the migration and invasion of the NCI-H23 lung cancer at least in part via inhibition of mitogen-activated protein kinase 1 (MAPK1). Additionally, the suppression of MAPK1 exhibited similar effects on the proliferation, migration, and invasion of the NCI-H23 cells as that of UCA1 silencing. Finally, the co-suppression of lncRNA UCA1 and MAPK1 exhibited synergistic effects on cell proliferation, migration, and invasion. CONCLUSIONS: We demonstrated that lncRNA UCA1 could be an important therapeutic target for curbing lung cancer.

Long non-coding RNA UCA1 regulates the proliferation, migration and invasion of human lung cancer cells by modulating the expression of microRNA-143.

OBJECTIVE: Accounting for 25% of all the cancers and 20% of the cancer-related mortality, lung cancer is one of the devastating types of cancers. Due to an increase in the incidence of lung cancer and limited treatment options, there is a pressing need to look for novel drug options and to identify potential therapeutic targets. Long non-coding RNAs (LncRNAs) have been considered to be important therapeutic targets due to their plethora of cellular roles. Herein, we investigated the therapeutic potential of UCA1 in lung cancer and also attempted to examine the underlying mechanism through UCA1 exerts its growth inhibitory effects on cancer cells. MATERIALS AND METHODS: The quantitative Reverse-Transcriptase Polymerase Chain Reaction (qRT-PCR) was used to perform the expression analysis. The CCK-8 assay was used to monitor the growth of the cells. The AO/EB assay was used to check apoptosis and flow cytometry was used for cell cycle distribution. The wound heal and transwell assays were used to monitor the cell migration and invasion. RESULTS: It was found that the lncRNA UCA was significantly (p < 0.05) upregulated in the lung cancer cells and silencing of UCA1 could inhibit the proliferation of the SK-MES-1 lung cancer cells via induction of G2/M cell cycle arrest and apoptosis. Moreover, UCA1 silencing could also suppress the migration and invasion of the SK-MES-1 cells. The LncRNA UCA1 was also found to upregulate the expression of miR-143, and overexpression of miR-143 could also suppress the proliferation, migration, and invasion of the SK-MES-1 lung cancer cells. Both UCA1 silencing and miR-143 overexpression could cause a significant decrease in the expression of mitogen-activated protein kinase 1 (MAPK1). Therefore, it is concluded that UCA1 regulates the growth of the SK-MES-1 lung cancer by inhibition of MAPK1 via miR-143 upregulation. CONCLUSIONS: UCA1, as well as miR-143, may be essential therapeutic targets for the management of lung cancer and warrant further investigations.

[Effects of different training methods on cardiovascular autonomic regulation during bedrest].

Objective. To investigate the effects of different training methods on cardiovascular autonomic regulation under bedrest. Method. 15 healthy male volunteers aged 19-22 participated tests in head-down tilt (HDT) -6 degrees bedrest in order to observe the changes of cardiovascular system under simulated weightlessness. They were divided into control (5 men), hypoxia training (5 men) and Fangsong training (5 men) groups. 24 h dynamic ECG were recorded on the 2nd day of pre-bedrest, on the 3rd, 14th and 18th day of bedrest and on the 7th day of the post- bedrest. All spectra were estimated from entire 24 h HRV, before, during and after Fangsong and hypoxia training by autoregressive (AR) modeling method. Normalized low-frequency (LF%) was a quantitative marker of cardiac sympathetic activity, normalized high-frequency (HF%) reflected the changes in cardiac vagal activity, and LF/HF was considered to be related to sympathovagal balance or sympathetic activity. Result. In control group, LF% and HF% were all significantly reduced (P<0.05), LF/HL showed no significant changed during bedrest. In Fangsong group, HF% increased markedly (P< 0.05), while in hypoxia group, LF% increased markedly (P< 0.05). Conclusion. Fangsong training counteracted markedly the reduction in vagal activity, while hypoxia training counteracted markedly the decrease in sympathetic activity. It was possible that HRV indices could be used to evaluate the efficiency of countermeasures counteracting the adverse effects of weightlessness.