Basic helix-loop-helix (bHLH) transcription factors (TFs) participate in many physiological and cellular processes in eukaryotes. However, their functions remain unclear in the macro basidiomycete Ganoderma lucidum (G. lucidum).In this study, a gene encoding bHLH TF, GlbHLH, was identified in G. lucidum. The knockdown of GlbHLH by RNA interference reduced hyphal growth, hyphal branching, and resistant to osmotic, oxidative, and cell wall stress. The content of cell wall components β-1,3 glucan and chitin and the expression of their synthesis genes were decreased in the GlbHLH knockdown strains. The knockdown of GlbHLH led to an increase of intracellular reactive oxygen species by decreasing the enzyme activity and gene expression of antioxidant enzymes. Furthermore, the production of intracellular polysaccharides and extracellular polysaccharides was greatly decreased in the GlbHLH mutants. These results suggested that GlbHLH is involved in hyphal growth, stress response, and polysaccharide biosynthesis in G. lucidum.
Synovial sarcoma is an aggressive soft-tissue malignancy with poor prognosis and lack of response to conventional cytotoxic chemotherapy. The regulatory mechanisms for the rapid proliferation of synovial sarcoma cells and the particular aggressiveness of this sarcoma remain poorly understood. In this study, we investigate the effect of epigallocatechin-3-gallate (EGCG) on growth and apoptosis of chondrosarcoma cells. The MTT assay and DAPI staining indicated that EGCG effectively inhibited cellular proliferation and induces apoptosis of the synovial sarcoma cells and induced apoptosis as confirmed by flow cytometry. Furthermore, Bcl-2 and Mcl-1 levels significantly decreased, Bax levels significantly increased, whereas expression levels of the proteins Bcl-XL were unchanged in response to EGCG treatment in SW982. In conclusion, our findings demonstrate that EGCG is effective for growth inhibition of synovial sarcoma cell lines in vitro and suggest that EGCG may be a new therapeutic option for patients with synovial sarcoma.
There is concrete evidence that lncRNA-MINCR is involved in tumorigenesis of a number of human cancers through modulation of Wnt/β-catenin signaling pathway. However, the characterization of regulatory role of lncRNA-MINCR has not been worked out in osteosarcoma yet. The present study was undertaken to explore the role of lncRNA-MINCR in human osteosarcoma. The osteosarcoma tissues and cell lines were found to exhibit significant (P<0.05) over-expression of lncRNA-MINCR. Silencing of lncRNA-MINCR in osteosarcoma cells suppressed their cell viability through the induction of apoptosis. The Saos-2 osteosarcoma cells exhibited significant (P<0.05) decline in migration and invasion rate together with inhibition of EMT under transcriptional knockdown of lncRNA-MINCR. Western blot analysis revealed that lncRNA-MINCR operated through Wnt/β-catenin signaling pathway to control the growth and metastasis of osteosarcoma cells. In vivo mice tumorigenesis was significantly (P<0.05) restricted under lncRNA-MINCR repression. The study clearly indicated that lncRNA-MINCR exhibits crucial growth regulatory role in osteosarcoma together with its ability to control the metastasis of cancer cells through Wnt/β-catenin signal.
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