Previously, we showed that CACNA2D3 (voltage-dependent subunit alpha 2 delta 3 of a calcium channel complex) was significantly downregulated and functioned as a tumor suppressor in ESCC, but its role in the chemosensitivity of ESCC to cisplatin remained unknown.
Ectopic expression of CACNA2D3 inhibited cell proliferation, migration, invasion, and tumor growth in vitro and in vivo, whereas CACNA2D3 depletion inhibited cell viability and invasion.
Our study also warrants further exploration in the potential therapeutic use of existing epigenetic targeting drugs (e.g., 5-azacytidine, SAHA) to reconstitute CACNA2D3-associated tumor suppression in NPC.
Inverse effects were seen by CACNA2D3 small interfering RNA treatment in the CACNA2D3-positive cell lines, indicating that CACNA2D3 may have tumor suppressive functions.