Here, we report that calcium release-activated calcium modulator 2 (ORAI2), a poorly characterized store-operated calcium (SOC) channel subunit, predominantly upregulated in the lymph node metastasis of gastric cancer, supports cell proliferation and migration.
First-pass extracted concept
ORAI2
Aliases
calcium release-activated calcium modulator 2
Evidence Snippets
Supporting Sources
Linked Claims
A high frequency of ORAI2-positive cells in gastric cancer tissues significantly correlates with poor differentiation, invasion, lymph node metastasis, and worse prognosis.
Clinical data reveal that a high frequency of ORAI2-positive cells in gastric cancer tissues significantly correlated with poor differentiation, invasion, lymph node metastasis, and worse prognosis.
ORAI2 is predominantly upregulated in lymph node metastasis of gastric cancer.
ORAI2, a poorly characterized store-operated calcium (SOC) channel subunit, predominantly upregulated in the lymph node metastasis of gastric cancer
Gain- and loss-of-function experiments show that ORAI2 promotes cell motility, tumor formation, and metastasis in gastric cancer cell lines and mice.
Gain- and loss-of-function showed that ORAI2 promotes cell motility, tumor formation, and metastasis in both gastric cancer cell lines and mice.
ORAI2 enhances metastatic ability of gastric cancer cells by inducing FAK-mediated MAPK/ERK activation and promoting focal adhesion disassembly at the rear edge of the cell.
Moreover, ORAI2 enhanced the metastatic ability of gastric cancer cells by inducing FAK-mediated MAPK/ERK activation and promoted focal adhesion disassembly at rear-edge of the cell.
ORAI2 mediates store-operated calcium activity and regulates tumorigenic properties through activation of PI3K/Akt signaling.
Mechanistically, ORAI2 mediated SOC activity and regulated tumorigenic properties through the activation of the PI3K/Akt signaling pathways.