Emerging evidence has shown that long non-coding RNAs (lncRNAs) play an important role in inhibiting tumor cell proliferation and inducing differentiation. In this study, integrative analysis of whole transcriptome sequencing data demonstrated that lncRNA-Gm31932 is significantly decreased in all-trans retinoic acid (ATRA)-induced and sodium 4-phenylbutanoate (PB-4)-induced mouse melanoma B16 cells. Silencing lncRNA-Gm31932 could inhibit B16 cell proliferation, with cell cycle arrest at the G0/G1 phase and obvious differentiation characteristics, e.g., increased cell volume, melanin content and tyrosinase (Tyr) activity. Furthermore, a series of experiments (luciferase reporter assay, RNA pull-down assay, and western blotting) showed that lncRNA-Gm3932 down-regulated Prc1 and Nuf2 by competitively sponging miR-344d-3-5p, which subsequently reduced the expression of cell cycle-related proteins CDK2, CDC2, and Cyclin B1, and increased the expression of P21 and P27. Moreover, silencing lncRNA-Gm31932 could significantly inhibit tumor growth in B16 melanoma-bearing mice. Taken together, these results indicate that as a possible signaling pathway for ATRA and PB-4, lncRNA-Gm31932 can induce cell cycle arrest and differentiation via miR-344d-3-5p/Prc1 (and Nuf2) axis.
A synergetic strategy was proposed to address the critical issue in the brand characterization of Colla corii asini (Ejiao, CCA), a precious traditional Chinese medicine (TCM). In all brands of CCA, Dong’e Ejiao (DEEJ) is an intangible cultural heritage resource. Seventy-eight CCA samples (including forty DEEJ samples and thirty-eight samples from other different manufacturers) were detected by laser-induced breakdown spectroscopy (LIBS) and near-infrared spectroscopy (NIR). Partial least squares discriminant analysis (PLS-DA) models were built first considering individual techniques separately, and then fusing LIBS and NIR data at low-level. The statistical parameters including classification accuracy, sensitivity, and specificity were calculated to evaluate the PLS-DA model performance. The results demonstrated that two individual techniques show good classification performance, especially the NIR. The PLS-DA model with single NIR spectra pretreated by the multiplicative scatter correction (MSC) method was preferred as excellent discrimination. Though individual spectroscopic data obtained good classification performance. A data fusion strategy was also attempted to merge atomic and molecular information of CCA. Compared to a single data block, data fusion models with SNV and MSC pretreatment exhibited good predictive power with no misclassification. This study may provide a novel perspective to employ a comprehensive analytical approach to brand discrimination of CCA. The synergetic strategy based on LIBS together with NIR offers atomic and molecular information of CCA, which could be exemplary for future research on the rapid discrimination of TCM.
Hepatocellular carcinoma (HCC) is a malignant tumor with a high rate of recurrence and a poor prognosis. Here, we investigated the effect and the potential antitumor mechanism of Gamabufotalin (CS-6) against HCC. Our results show that CS-6 strikingly reduced cell viability, inhibited colony formation, and promoted apoptosis in Hep3B and Huh7 cells. In vivo, CS-6 inhibited HCC xenograft tumor growth with no toxicity to normal tissues. Mechanistically, we found that CS-6 could induce cytoprotective autophagy through the mTOR–ULK1 signaling pathway through downregulation of p62 and upregulation of LC3 II/LC3 I. Meanwhile, CS-6 activated caspase-3 and PARP mediated apoptosis, and the caspase inhibitor Z-VAD-FMK blocked the CS-6-induced cell death in HCC cells. Moreover, autophagy and apoptosis were found to have antagonistic effects in Hep3B and Huh7 cells. Both the autophagy inhibitor chloroquine (CQ) and the mTOR activator MHY1485 blocked autophagy and further enhanced CS-6-induced apoptosis. Taken together, we demonstrated for the first time that CS-6 promotes apoptosis and cytoprotective autophagy through the mTOR signaling pathway in HCC, which proposes a novel strategy for HCC therapy.
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