Reduced SPOCK1 expression inhibits non-small cell lung cancer cell proliferation and migration through Wnt/β-catenin signaling.

OBJECTIVE

Accumulating evidence suggests that SPARC/osteonectin, cwcv, and kazal-like domain proteoglycan 1 (SPOCK1) contributes to the initiation and progression of human cancers. However, little is known about the function mechanisms of SPOCK1 in non-small cell lung cancer (NSCLC). The aim of this study was to investigate the molecular mechanism of SPOCK1 in NSCLC.

PATIENTS AND METHODS

The expression levels of SPOCK1 in NSCLC tissues and cell lines were analyzed by qRT-PCR and Western blotting. The proliferative activity of NSCLC cells was determined by MTT and colony formation assays. The transwell assay was used to examine the cell migration and invasive ability. To study the impact of SPOCK1 on Wnt/β‑catenin signaling, we further performed Western blotting for related proteins in this pathway.

RESULTS

We observed that the expression of SPOCK1 at both protein and mRNA levels was also increased in human NSCLC tissues and cell lines. Functionally, down-regulation of SPOCK1 in NSCLC cells markedly suppressed cell proliferation, colony formation, migration and invasion in vitro. Mechanistically, we found that indicated the activation of Wnt/β-catenin pathway was suppressed by SPOCK1 silencing.

CONCLUSIONS

The expression of SPOCK1 served as a tumor promoter, possibly through the Wnt/β-catenin signaling pathway in NSCLC. Targeting SPOCK1 could be a potential therapeutic strategy in NSCLC.