lncRNA TINCR participates in ALA‐PDT‐induced apoptosis and autophagy in cutaneous squamous cell carcinoma

自噬 细胞凋亡 基底细胞 癌症研究 生物 医学 病理 生物化学
作者
Wu Zhou,Shoumin Zhang,Jianguo Li,Zhenlu Li,Yuping Wang,Xueli Li
出处
期刊:Journal of Cellular Biochemistry [Wiley]
卷期号:120 (8): 13893-13902 被引量:36
标识
DOI:10.1002/jcb.28662
摘要

Abstract This study aims to investigate whether terminal differentiation‐induced ncRNA (TINCR) has an effect on apoptosis and autophagy induced by ALA‐PDT in cutaneous squamous cell carcinoma (CSCC). A431 cells were treated with 5‐aminolevulinic acid (ALA) solution at different concentrations and for different duration time. A431 cell viability was detected by Cell Counting Kit‐8 (CCK‐8) assay, relative TINCR messenger RNA expression was detected by quantitative reverse‐transcription polymerase chain reaction (qRT‐PCR). A431 cell apoptosis was examined by flow cytometry. Relative apoptosis/autophagy‐related protein expression was analyzed by Western blot analysis. The effect of TINCR on cell autophagy was detected by RFP‐LC3 immunofluorescence assay. Reactive oxygen species concentration was detected by 2′,7′‐dichlorodihydrofluorescein diacetate (DCFH‐DA) fluorescent probe. Relative expressions of ERK1/2 and specificity protein 3 (Sp3) in A43 cells were detected by Western blot analysis and qRT‐PCR. Sp3 binding sites were analyzed by ChIP‐qPCR. The relative transcription activity was measured with luciferase reporter assay. ALA‐PDT treatment at 3.2 mmol/L for 120 minutes significantly promoted TINCR expression in CSCC A431 cells, and TINCR promoted ALA‐PDT‐induced apoptosis and cell autophagy. Furthermore, ALA‐PDT promoted TINCR expression through ERK1/2‐SP3 pathway. Sp3 promoted TINCR transcription by binding TINCR promoters. Our data indicated that TINCR involves in ALA‐PDT‐induced apoptosis and autophagy in CSCC.
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