Gliomas are the most common and aggressive types of tumors in human brain, of which the prognosis remains dismal because of their biological behavior. The involvement of miRNAs in tumorigenesis of various kinds of cancers drives us to explore new miRNAs related to gliomas. We measured expression level of miR‑95‑3p by qRT-PCR in human glioma and non-neoplasm brain tissues and found that higher level of miR‑95‑3p in glioma tissues of higher grade. Biological functions of miR‑95‑3p on glioma cells were investigated by MTT assay, flow cytometry and transwell assay. We discovered the cell lines transfected with miR‑95‑3p ASO (antisense oligonucleotide) had retarded proliferation and invasion but enhanced apoptosis ability. We searched on-line tool Targetscan and selected CELF (CUGBP- and ETR-3-like family 2) as a putative target. Luciferase reporter was employed to confirm the binding sites in 3'UTR region of CELF2 for miR‑95‑3p. The correlation between expression of CELF2 and miR‑95‑3p was determined by western blotting and qRT-PCR both in cell lines and human samples. Results showed CELF2 was a direct target of miR‑95‑3p and expression levels of CELF2 and miR‑95‑3p were negatively correlated. Finally, CELF2 largely abrogated the effects of miR‑95‑3p on proliferation, invasion and apoptosis of glioma cells in rescue experiments, which verified the role of CELF2 in miR‑95‑3p regulating glioma biological behavior. In conclusion, our data suggest the expression level of miR‑95‑3p is positively related to glioma grade and downregulation of miR‑95‑3p affects proliferation, invasion and apoptosis of glioma cells by targeting CELF2. We identified miR‑95‑3p as a putative therapeutic target and CELF2 as a potential tumor suppressor.
Background: Keratinocyte is a key component of the skin barrier and maintains skin homeostasis. As an environmental pathogenic factor, PM2.5 can cause epidermal cell damage, but the mechanism remains to be elucidated. The present study aimed to evaluate the effect caused by PM2.5 in HaCaT cells and investigate the underlying mechanisms.Methods: HaCaT cells were treated with PM2.5 for 12 h or 24 h, either alone or combined with UVB irradiation. A Cell Counting Kit (CCK-8) assay was carried out to detect the effect of PM2.5 on HaCaT cell viability. Flow cytometry, Western Blot, and AO staining were employed to detect the changes of apoptosis and autophagy. The changes of cytotoxicity and apoptosis in HaCaT cells were analyzed by CCK-8 and flow cytometry after pretreatment with autophagy inhibitor 3-MA.
Results:The results showed that PM2.5 induced cytotoxicity by increasing cell apoptosis and activating autophagy. Apoptosis was determined to be increased significantly after autophagy inhibition. Moreover, solar radiation intensified PM2.5-induced damage in HaCaT cells, which further enhanced the autophagy.However, there was no significant difference in apoptosis after inhibition of autophagy in combined treatment.Conclusions: Our data reveals that PM2.5 induces damage in HaCaT cells, and autophagy plays a protective role to promote cell survival.
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