Ca2+ influx induces various physiological events such as contraction, exocytosis, gene expression, and cell growth and death. Transient receptor potential (TRP) and store-operated Ca2+ (SOC) channels are the representative of non-voltage-gated Ca2+ entry channels, and serve as major Ca2+ entry routes for non-excitable cells. Many reports indicate that Ca2+ influx through these channels is causally associated with cell cycle progression or growth, but the mechanism underlying it seems to vary depending on the cell type. To question how the proliferative potential and cell cycle progression of adult stem cells are controlled is an attractive theme for regenerative medicine and bioengineering, but the implication of non-voltage-gated Ca2+ entry channels therein is poorly elucidated. In this study, we investigated the roles of TRP and STIM/Orai channels on cell cycle progression of bone marrow stromal cells (BMSCs) from adult rat which include mesenchymal stem cells. Cultured BMSCs were synchronized in G1, S, G2 or M phases, and the mRNA levels of respective TRPC and STIM/Orai subtypes were assessed by the quantitative real-time PCR. In the S phase, the expression levels of TRPC1, STIM and Orai were significantly enhanced. On the other hand, that of TRPC6 was greatly reduced in the S phase and significantly enhanced in the G1 phase. In experiments measuring the intracellular Ca2+ concentration with Fura 2, SOC-mediated Ca2+ influx, which was evoked by thapsigargin or cyclopiazonic acid, was inhibited by 1μM Gd3+. The Ca2+ influx was significantly enhanced in the S phase. Gd3+ (1μM), SKF96365 or pyrazole compound (Pyr2) suppressed cell proliferation. To seek a role of TRPC6 channels for cell cycle progression, we evaluated the resting membrane potential (RMP) of cells using a voltage-sensitive dye DiBAC4(3) or by the current-clamp mode of patch clamp technique. siRNA knockdown of TRPC6 expression but not of TRPC1 produced a significant negative shift of RMP. RMP in the S phase was deeper than in the other cell cycle stages. From these observations, we speculate that TRPC6 channels may work as a modulator of RMP thereby controlling the driving force for Ca2+ influx in the S phase. Cell cycle analysis by the flow cytometry revealed that siRNA knockdown of TRPC1, TRPC6 or STIM/Orai expression differentially affected the distribution of cell cycle stages. The fraction of cells residing in the G0/G1 phase was increased by siRNA of STIM/Orai but decreased by siRNA of TRPC1 or TRPC6. siRNA of TRPC6 significantly increased the fraction of cells in the G2/M phase. To elucidate these observations more explicitly, the correlation between cell cycle-regulating molecules such as cyclins and the functions of TRPC1/C6 and STIM/Orai will need to be investigated.