Increasing cell apoptosis is one of the major causes of intervertebral disc degeneration (IDD). β-ecdysterone has been demonstrated to protect PC12 cells against neurotoxicity. A previous study revealed that β-ecdysterone may be involved in the regulation of autophagy in osteoblasts. Therefore, we hypothesized that β-ecdysterone may possess therapeutic effects on IDD via autophagy stimulation. The effect of β-ecdysterone on IDD was explored by in vitro experiments. The results demonstrated that β-ecdysterone attenuated the apoptosis induced by tert-butyl hydroperoxide via promoting autophagy in nucleus pulposus cells. Beclin-1, an indispensable protein for the stimulation of autophagy, is upregulated and stabilized by β-ecdysterone in a dose-and time-dependent manner in nucleus pulposus cells. Inhibition of autophagy with 3-methyladenine partially abrogated the protective function of β-ecdysterone against apoptosis of nucleus pulposus cells, indicating that autophagy participated in the protective effect of β-ecdysterone on IDD. Additionally, β-ecdysterone promoted the expression of anabolic genes while inhibiting the expression of catabolic genes in nucleus pulposus cells. Collectively, the present study demonstrated that β-ecdysterone may protect nucleus pulposus cells against apoptosis by autophagy stimulation and ameliorate disc degeneration, which indicates that β-ecdysterone may be a potential therapeutic agent for IDD.
SV40 Tag not only is expressed in brain tumors; it also can form specific complexes with tumor suppressors p53 and pRb. SV40 is correlated with brain tumorigenesis. The inactivation of p53 and pRb due to the formation of Tag-p53 and Tag-pRb complexes possibly is a significant mechanism in the etiopathogenesis of brain tumors.
Background:The present study aimed to investigate the functions and regulation mechanism of the transmembrane protease, serine 3 (TMPRSS3), which plays an important role in sensorineural hearing loss.
Methods:House Ear Institute-Organ of Corti 1 (HEI-OC1) cells, comprising auditory-related cells, were used in the present study. An overexpression vector and small hairpin RNA target on TMPRSS3 were designed and transfected into HEI-OC1 cells.Circular RNA (circRNA) sequencing was conducted and expression profiles were obtained. The circular structure of circRNAs was validated with a polymerase chain reaction and Sanger sequencing using convergent and divergent primers.
Results: Overexpression of TMPRSS3 increased cell viability, whereas suppression of TMPRSS3 increased the percentage of apoptotic cells and decreased cell viability, compared to the control group. circRNA sequencing provided expression profiles indicating that the overexpression of TMPRSS3 increased the expression level of 195 circRNAs. Results of GO (Gene Ontology) and KEGG (Kyoto Encyclopedia of Genes and Genomes) studies indicated that the circRNAs are focused on the RAS signaling pathway. The pathway, circ-Slc41a2 (chr10: 82744115|82767120), miR-182 and Akt, might comprise one of the key cascades of TMPRSS3. Conclusions: TMPRSS3 is an important molecule in the regulation of cell viability and cell apoptosis of HEI-OC1 cells. Its functions are dependent on the circ-Slc41a2, miR-182 and Akt cascade.
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