ABSTRACT
BACKGROUND: Gastric cancer (GC) is the most common malignant tumor of the digestive tract and its molecular mechanism is not clear. HOXD9 plays an important role in tumor progression as transcription factor. In the current study, we explored the role of HOXD9 in GC. METHODS: We predicted the expression and potential mechanism of HOXD9 in GC through an online database. The expression of HOXD9 was detected in GC and adjacent tissues, and then we analyzed the relationship between HOXD9 and the prognosis of patients with GC. In vitro, we investigated the effects of HOXD9 on malignant biological behaviors such as proliferation, migration, and invasion of the GC cell line MCG-803. In addition, we have initially studied the underlying mechanism by Western blot. RESULTS: High expression of HOXD9 in GC was predicted by online database prediction and implied poor prognosis. In the clinical sample, we confirmed the above predictions. In vitro, we found that knockdown of HOXD9 could effectively inhibit the proliferation, migration, and invasion of GC cells. In terms of mechanism, HOXD9 may activate the TGF-ß/Smad signaling pathway. CONCLUSION: HOXD9 promotes the malignant biological process of GC, which may be a potential therapeutic target for GC.
ABSTRACT
BACKGROUND: GTPase-activating protein SH3 domain-binding protein 1 (G3BP1) is involved in various biological functions, including cell growth, metastasis, differentiation, apoptosis, and RNA metabolism. In current study, we aimed to investigate the effect of G3BP1 on gastric cancer (GC). METHODS: The expression of G3BP1 in GC tissues and cell lines was assessed by immunohistochemistry and Western blotting. Correlations of G3BP1 expression with clinicopathological and prognosis of GC patients were evaluated. The functions of G3BP1 in regulating proliferation, migration and invasion of GC cell were investigated using small interfering RNA (siRNA) strategies. Preliminary exploration of its underlying mechanism using Western blotting. RESULTS: G3BP1 expression was upregulated in GC tissues compared with adjacent tissues, and the higher G3BP1 expression was correlated with poor prognosis. G3BP1 knockdown decreased GC cell proliferation, migration and invasion. Mechanistically, silencing of G3BP1 inhibits the activation of the transforming growth factor (TGF)-ß/Smad signaling pathway in GC cells. CONCLUSION: G3BP1 plays an important role in the progression of GC as an oncogene and may become a new therapeutic target.
