Search

Trichinella spiralis (T. spiralis) muscle larvae (ML) excretory/secretory products (ESPs) are antitumor substances extracted from the culture medium of T. spiralis ML. The ESPs inhibit tumor growth and induce tumor cell apoptosis. To explore the effects of these products on the non-small-cell lung cancer (NSCLC) line A549, logarithmically growing A549 cells were co-cultured with different concentrations of T. spiralis ML ESPs for 24, 36 and 48 h. Our results showed that T. spiralis ML ESPs significantly inhibited A549 cells proliferation, which was dose-and time-dependent. To evaluate the inhibition by T. spiralis ML ESPs of the growth of A549 cells, we assayed their apoptosis and cell-cycle distribution by flow cytometry (FCM). To determine whether ESPs induced apoptosis of A549 cells via the mitochondrial pathway, we evaluated the levels of mitochondrion-related factors by Western blotting. The FCM indicated a clear trend toward apoptosis of A549 cells co-cultured with ESPs for 24 h. The cells were blocked in S-phase. Western blotting revealed that the expression levels of the genes encoding Bax, caspase-3, and caspase-9 increased (compared to a control group), and the Bcl-2 gene expression level decreased. Our results suggest that T. spiralis ML ESPs induce apoptosis of the NSCLC line A549 via the mitochondrial pathway; the cells become arrested in S-phase. This may explain the antineoplastic activity of T. spiralis ML ESPs., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Osteoarthritis (OA) acts as the most common type of degenerative joint disease. Long noncoding RNA (lncRNA) has been identified to regulate the apoptosis and proliferation of chondrocyte. However, the deepgoing mechanism involved in the regulation is still unclear. This research aims to investigate the role and molecular mechanism by which lncRNA LINC00511 regulates the OA biology. Functionally, the functional experiments found that LINC00511 expression was upregulated in the IL-1β-stimulated chondrocyte (ATDC5). Knockdown of LINC00511 facilitated proliferation, and repressed the apoptosis and extracellular matrix (ECM) synthesis of chondrocyte. Mechanically, LINC00511 functioned as sponge of miR-150-5p and then interacted with the 3'-UTR of transcription factor (SP1). In turn, transcription factor SP1 bound with the promoter region of LINC00511 and thus upregulated LINC00511 expression. In conclusion, our findings highlight the function and prognostic value of LINC00511/miR-150-5p/SP1 feedback loop in OA and extend the importance of lncRNA epigenetics in OA biology.