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Abstract
Gastric cancer (GC) is one of the most common malignancies and its prognosis is extremely poor. This study identifies a novel oncogene, microfibrillar-associated protein 2 (MFAP2) in GC. With integrative reanalysis of transcriptomic data, we found MFAP2 as a GC prognosis-related gene. And the aberrant expression of MFAP2 was explored in GC samples. Subsequent experiments indicated that silencing and exogenous MFAP2 could affect motility of cancer cells. The inhibition of silencing MFAP2 could be rescued by another FAK activator, fibronectin. This process is probably through affecting the activation of focal adhesion process via modulating ITGB1 and ITGA5. MFAP2 regulated integrin expression through ERK1/2 activation. Silencing MFAP2 by shRNA inhibited tumorigenicity and metastasis in nude mice. We also revealed that MFAP2 is a novel target of microRNA-29, and miR-29/MFAP2/integrin α5β1/FAK/ERK1/2 could be an important oncogenic pathway in GC progression. In conclusion, our data identified MFAP2 as a novel oncogene in GC and revealed that miR-29/MFAP2/integrin α5β1/FAK/ERK1/2 could be an important oncogenic pathway in GC progression.
Highlights
Gastric cancer (GC) is one of the most common and lethal malignant cancer throughout the world, in Eastern Asian and South American countries[1]
We validated that microfibrillar-associated protein 2 (MFAP2) was upregulated in GC tissue, and it was implicated in the malignant behavior of GC cells, such as proliferation, migration, and invasion. We demonstrated that it activated focal adhesion kinase (FAK), paxillin, and extracellular signal-regulated kinase 1/2 (ERK1/2) through the MFAP2/integrin α5β1/FAK/ERK1/2 pathway
We found that a previous study had verified that MFAP2 was upregulated in GC among 168 paired samples by immunohistochemistry[24]
Summary
Gastric cancer (GC) is one of the most common and lethal malignant cancer throughout the world, in Eastern Asian and South American countries[1]. In the subsequent wound healing assays, AGS cells treated with fibronectin (10 μg/ml) showed stronger motility than the control group even after MFAP2 knockdown (Fig. 4h). (see figure on previous page) Fig. 4 MFAP2 modulates proliferation, migration, and invasion of GC cells through integrin-stimulated focal adhesion kinase activation.
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