S100A8 promotes the proliferation, migration and invasion in bladder cancer cells

There is mounting evidence that S100 calcium-binding A8 (S100A8) is involved in inflammation and cancer. However, whether S100A8 promotes the proliferation, invasion and migration of bladder cancer (BC) is still not completely clear. To investigate the influence of S100A8 on the proliferation, migration and invasion of BC.

In this study, the bioinformatics and in vitro experiments revealed that S100A8 could promote the proliferation, invasion and migration of BC cells. Consequently, S1008A emerges as a promising diagnostic and therapeutic target for BC.

Based on Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) databases, genes related to the grading, staging, proliferation, migration and invasion of BC were screened, and S100A8 was selected as the target gene for further studies. Immunohistochemical staining were employed to examine the protein expression levels of S100A8 on adjacent tissues and BC tissues. The gene expression level of S100A8 in Pan cancer cell lines was analyzed through the Cancer Cell Line Encyclopedia (CCLE) database, and the HT-1376 cell line was selected for subsequent experiments. Overexpression recombinant lentivirus and short hairpin RNA-encoding lentivirus were used to overexpress and knock down S100A8 in HT-1376 cells via infection. The mRNA and protein expression levels of S100A8 were detected by reverse transcription-quantitative PCR and western blotting. The proliferation of BC cells was analyzed using Cell Counting Kit-8 and 5-ethynyl-2'-deoxyuridine assays. The Wound‑healing assay and Transwell assay were used to estimate the migration and invasion of BC cells.

The results demonstrated that S100A8 was highly expressed in BC based on the GEO and TCGA databases. In addition, compared with those of HT-1376 cells and the negative control group, the proliferation, migration and invasion of S100A8-overexpressing HT-1376 cells were enhanced, while those of S100A8-knockdown HT-1376 cells were reduced. Furthermore, S100A8 was differentially expressed in non-muscle invasive BC and muscle invasive BC, and in low- and high-grade BC. Conclusions: In this study, the bioinformatics and in vitro experiments revealed that S100A8 could promote the proliferation, invasion and migration of BC cells. Consequently, S1008A emerges as a promising diagnostic and therapeutic target for BC.