Downregulated LINC00460 inhibits cell proliferation and promotes cell apoptosis in prostate cancer.

OBJECTIVE: LINC00460 has been confirmed to contribute to cancer development. However, the role and function of LINC00460 in prostate cancer is not identified. The purpose of this study was to evaluate the expression and effect of LINC00460 on prostate cancer cell malignant behaviors. PATIENTS AND METHODS: The expression of LINC00460 in cancer tissues and cell lines were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) assay. The LINC00460 expression was downregulated by siRNA. The cell counting kit-8 (CCK-8) assay was used to detect cell proliferation. The cell migration and invasion were detected by migration and Matrigel invasion assays. The Western blot assay was used to detect the altered expression levels of Ki67, Cyclin D1, PI3K, p-AKT, T-AKT, Bcl2, and Bax. RESULTS: LINC00460 was increased in human prostate cancer tissues and cell lines. LINC00460 high expression was related to Tumor Size (T1-T2/T3-T4; p=0.004), and high Gleason Score (≤8/>8, p=0.000). Downregulation of LINC00460 by siRNA could inhibit cancer cell proliferation and decreased Ki67 and Cyclin D1 expression. Meanwhile, downregulation of LINC00460 promoted apoptosis of cell lines and was related to PI3K/AKT pathway. CONCLUSIONS: LINC00460 could regulate cell proliferation and cell apoptosis, which might be a novel marker in prostate cancer.

Bryostatin-1 promotes long-term potentiation via activation of PKCα and PKCε in the hippocampus.

Activation of protein kinase C (PKC) by bryostatin-1 affects various functions of the central nervous system. We explored whether bryostatin-1 influenced synaptic plasticity via a process involving PKC. Our purpose was to examine whether bryostatin-1 affected the induction of hippocampal long-term potentiation (LTP) in Schaffer-collateral fibers (CA1 fibers) of the hippocampus, and/or influenced the intracellular Ca(2+) level of hippocampal neurons. We also determined the PKC isoforms involved in these processes. We found that bryostatin-1 strongly facilitated LTP induction, in a dose-dependent manner, upon single-theta burst stimulation (TBS). Further, intracellular Ca(2+) levels also increased with increasing concentration of bryostatin-1. The facilitative effects of bryostatin-1 in terms of LTP induction and enhancement of intracellular Ca(2+) levels were blocked by specific inhibitors of PKCα and PKCε, but not of PKCδ. Our results suggest that bryostatin-1 is involved in neuronal functioning and facilitates induction of LTP via activation of PKCα and/or PKCε.