Background: Previously, we detected that chloride intracellular channel 1 (CLIC1) was
involved in the pathogenesis of atopic dermatitis (AD).
Objective: In this study, we aimed to use high-throughput screening (HTS) approaches to identify
critical factors associated with the function of CLIC1 in knock-down cells.
Methods: We down-regulated CLIC1 in human A549 cells via siRNA and then conducted serial
HTS studies, including proteomics integrated with a microarray and the implementation of bioinformatics
Results: Together, these approaches identified several important proteins and genes associated
with the function of CLIC1. These proteins and genes included tumor rejection antigen (gp96) 1,
nucleophosmin, annexin I, keratin 1 and 10, FLNA protein, enolase 1, and metalloprotease 1,
which were found using two-dimensional electrophoresis (2-DE) proteomics. Separately, NTNG1,
SEMA5A, CLEC3A, GRPR, GNGT2, GRM5, GRM7, DNMT3B, CXCR5, CCL11, CD86, IL2,
MNDA, TLR5, IL23R, DPP6, DLGAP1, CAT, GSTA1, GSTA2, GSTA5, CYP2E1, ADH1A, ESR1,
ARRDC3, A1F1, CCL5, CASP8, DNTT, SQSTM1, PCYT1A, and SLCO4C1 were found using
a DNA microarray integrated with PPI mapping.
Conclusion: CCL11 is thought to be a particularly critical gene among the candidate genes detected
in this study. By integrating the datasets and utilizing the strengths of HTS, we obtained new insights
into the functional role of CLIC1, including the use of CLIC1-associated applications in the
treatment of human diseases such as AD.