TRPC1 and lip and oral cavity carcinoma: Our working hypothesis is that oral cancer cells treated with CIDD-99 undergo apoptosis due to either 1) inhibition of mitochondrial function or 2) induction of ER stress, which are both modulated by calcium entry via TRPC1 channels (Singh and LiuAmbudkar, 2005; Selvaraj et al., 2012; Sukumaran et al., 2016).