Key result
Caveolin-1 promotes anchorage-independent growth and anoikis resistance in gastric cancer cells via Src-dependent signaling.
Why the study?
The role of Caveolin-1 in the acquisition of anoikis resistance in gastric cancer cells had not been explored.
Caveolin-1 promotes anoikis resistance and anchorage-independent growth in gastric cancer cells via Src-dependent EGFR-integrin β signaling.
Does not support clinical targeting of Caveolin-1 in gastric cancer; leaves open its role pending in vivo validation.
Anoikis resistance is considered to be an essential prerequisite of tumor metastasis and which is an important mechanism in the metastatic process of gastric cancer (GC). Caveolin-1 (CAV-1), a protein component of caveolae, has been reported to regulate several cancer cell behaviors including anoikis resistance. However, the role of CAV-1 in the acquisition of anoikis resistance in GC cells has never been explored. In this study, we investigated the promoting effect of CAV-1 on anchorage-independent growth and anoikis resistance, and the involvement of the related signaling pathways in such process in SGC-7901 cells. The results showed that CAV-1 could promote anchorage-independent growth and anoikis resistance in detached SGC-7901 cells, which was associated with the activation of Src-dependent epidermal growth factor receptor-integrin β signaling as well as the phosphorylation of PI3K/Akt and MEK/ERK signaling pathways. The data from this study might contribute to the in-depth understanding of the metastatic mechanism for GC.
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Wang et al. (2018) studied Gastric cancer. Caveolin-1 (CAV-1) was evaluated on Anchorage-independent growth and anoikis resistance. Caveolin-1 promoted anchorage-independent growth and anoikis resistance in detached SGC-7901 gastric cancer cells via activation of Src-dependent EGFR-integrin β and PI3K/Akt and MEK/ERK signaling.
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