Knockdown of long non-coding RNA LINC00324 inhibits proliferation, migration and invasion of colorectal cancer cell via targeting miR-214-3p.

OBJECTIVE: Increasing evidence demonstrated that long non-coding RNA (lncRNA) played a vital role in human tumorigenesis and progression, including colorectal cancer (CRC). However, the underlying mechanisms are still largely unknown. The aim of this study was to investigate the function of lncRNA LINC00324 on the development of CRC and explore the possible mechanisms. MATERIALS AND METHODS: The expression level of LINC00324 and miR-214-3p was measured by quantitative real time polymerase chain reaction (qRT-PCR) in CRC cells. The effects on cell proliferation, migration and invasion were assessed by MTT and transwell assays, respectively. In addition, the protein levels of cyclin D1, p21, p27 and three MMPs were detected by Western blot analysis. The target of LINC00324 was predicted by online software and confirmed by luciferase reporter assay. RESULTS: We first detected the expression of LIN00324 was increased while miR-214-3p was decreased in CRC cells. Knockdown of LIN00324 suppressed proliferation, migration and invasion in SW620 and HCT15 cells. Moreover, overexpression of miR-214-3p also inhibited CRC cell proliferation, migration and invasion. Then, we identified miR-214-3p as directly target of LINC00324 and the expression of miR-214-3p was downregulated by LINC00324. In addition, inhibiting miR-214-3p reversed the effects of LINC00324 on CRC cell proliferation, migration and invasion. CONCLUSIONS: Our results proved that LINC00324 regulated CRC cell proliferation, migration and invasion by sponging miR-214-3p, suggesting that it might be a potential therapeutic target for CRC therapy.

Long noncoding RNA HOTTIP contributes to the progression of prostate cancer by regulating HOXA13.

Prostate cancer is a leading cause of cancer-related mortality in men worldwide and there is a lack of effective treatment options for advanced (metastatic) prostate cancer. Long non-coding RNAs (lncRNAs) play important roles in diverse biological processes, such as cell growth, apoptosis and migration. However, little is known about the molecular mechanism of lncRNA-HOTTIP-mediated prostate cancer cell proliferation and apoptosis. The aim of this study was to elucidate the involvement of lncRNA HOTTIP in prostate cancer tumorigenesis and further investigate the role of HOXA13 in this process. Here, we showed that HOTTIP silencing inhibited cell survival pathway in vitro and in vivo by reducing the protein expression of Bcl-2 and enhancing Bax. We further demonstrated that knockdown of HOTTIP inhibited the expression of cell cycle regulatory protein Cyclin D1 and induced cell cycle arrest in G0/G1 phase. Additionally, depletion of HOXA13 by RNA interference (si-HOXA13) revealed that HOTTIP silencing suppressed cell growth at least partly through regulating HOXA13. In conclusion, down-regulation of HOTTIP and HOXA13 was associated with cell growth and cell cycle, and exerts tumor-suppressive functions in the genesis and progression of prostate cancer, providing a potential attractive therapeutic approach for this malignancy.

Stationary multifaceted asymmetric radiation from the edge and improved confinement mode in a superconducting tokamak.

Stationary multifaceted asymmetric radiation from the edge (MARFE) is studied by gas-puffing feedback control according to an empirical MARFE critical density ( approximately 1.8 x 10(13) cm(-3)) in the HT-7 Ohmic discharges (where the plasma current I(p) is about 170 kA, loop voltage V(loop)=2-3 V, toroidal field B(T)=1.9 T, and Z(eff)=3-4). It is observed that an improved confinement mode characterized by D(alpha) line emissions drops and the line-averaged density increase is triggered in the stationary MARFE discharges. The mode is not a symmetric "detachment" state, because the quasi-steady-state poloidally asymmetric radiation (e.g., C III line emissions) still exists. This phenomenon has not been predicted by the current MARFE theory.