Store-Operated Ca²⁺ Entry Does Not Control Proliferation in Primary Cultures of Human Metastatic Renal Cellular Carcinoma

Figure 7

InsP₃-dependent signalling in mRCC cells and endothelial progenitor cells. (a) Thimerosal triggered a brief train of intracellular Ca²⁺ spikes in mRCC cells when applied at 50 μM (black tracing), while it was almost ineffective at 25 μM (grey tracing). (b) Prolonged oscillations in intracellular Ca²⁺ levels stimulated by thimerosal (same solution as that used in (a), recording performed on the same day) in EPCs isolated from mRCC patients. (c) Percentage of mRCC cells and EPCs responding to thimerosal. ^∗𝑃<0.05 (Student’s 𝑡-test). (d) 100 μM ATP stimulated InsP₃-dependent Ca²⁺ mobilization from EPCs (black tracing), but not from mRCC cells (grey tracing). The same solution was used in both experiments and the recordings were conducted on the same day. (e) Fraction of mRCC cells and EPCs responding to ATP. ^∗𝑃<0.05 (Student’s 𝑡-test). (f) InsP₃R transcripts in primary mRCC cells. ^∗𝑃<0.05 versus InsP₃R1, ^∘𝑃<0.05 versus InsP₃R2. The inset illustrates InsP₃R expression detected by an InsP₃R-I/II/III antibody. A major band that corresponds to the sum of the three single 313/260/250 kDa bands for InsP₃R1/2/3 was found.

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