Exploring the downstream mechanism of CCDC86 regulating the progression of glioma. (IMAGE)
Caption
(A) The volcano plot depicting the differential expression of genes in SHG-44 cells following CCDC86 knockdown, as revealed by GeneChip PrimeView Human PathArray™ analysis. (B) The heat map illustrating the top 20 significantly down-regulated genes in SHG-44 cells treated with shCCDC86. (C) Quantitative reverse transcription PCR validation of the top 13 down-regulated genes post-CCDC86 knockdown. (D) The correlation between CCDC86 and ATF3 based on the glioma samples from the CGGA database. (E, F) Validation of ATF3 through quantitative reverse transcription PCR (E) and western blotting (F) experiments in SHG-44 cells and U251 cells with CCDC86 knockdown. (G) Flow chart of downstream molecular relationship construction. (H) Co-immunoprecipitation experiments confirmed the endogenous interaction between CCDC86 and BHLHE40. (I) The levels of BHLHE40 were detected in the nucleus and cytoplasm of CCDC86-depleted SHG-44 and U251 cells. (J) Chromatin immunoprecipitation experiments were performed to detect the binding of ATF3 promoter to BHLHE40 in BHLHE40-overexpressed SHG-44 and U251 cells. (K) Chromatin immunoprecipitation experiments were performed to detect the binding of ATF3 promoter to BHLHE40 in CCDC86-overexpressed SHG-44 and U251 cells. ***P < 0.001. CCDC86, coiled-coil domain-containing 86; ATF3, activating transcription factor 3; BHLHE40, basic helix-loop-helix family member E40; ns, not significant.
Credit
Jinping Liu, Dingyu Du, Yukai Huang, Jie Tian, Xuhui Wang, Longyi Chen, Feng Wang
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CC BY-NC-ND