LLLT enhance cyclophosphamide induced TRPM2 channel activation in human colon cancer cells

Abstract

AIM: Transient receptor potential (TRP) channels expression is enhanced signifi cantly in colon cancer cells and Low Lever Laser Treatment (LLLT), is known to have effects and is used clinically in the treatment ofmany diseases, including colon cancer. We aimed to reveal the effects of (LLLT) on apoptosis of colon cancer and on the effi cacy of cyclophosphamide via Transient receptor potential melastatin 2 (TRPM2) channels. METHOD: Human colon cancer cells (Caco-2) were cultured and cells were divided into seven main groups. Cells were incubated with cyclophosphamide, TRPM2 channel inhibitor, stimulator and low level laser exposure separately and together. The effects of cyclophosphamide and low level laser were investigated on apoptosis. RESULTS: It was found that the levels of apoptosis in cyclophosphamide group were signifi cantly increased in cancer cells compared to the control group. TRPM2 channel stimulator administration resulted in signifi cantly increased apoptosis levels compared to the control group, in cyclophosphamide + low level laser group the apoptosis level was signifi cantly increased compared to the cyclophosphamide-only group. CONCLUSIONS: It has been shown that apoptotic effects of cyclophosphamide on colon cancer cells were directly related to TRPM2 channels, low level laser increased apoptosis in colon cancer cells through TRPM2 channels and induced apoptotic effect of cyclophosphamide (Fig. 5, Ref. 26).

Effect of TRPM2-Mediated Calcium Signaling on Cell Proliferation and Apoptosis in Esophageal Squamous Cell Carcinoma

“…TRPM2 has numerous functions in a variety of cell types and has been shown to be involved in neurological disorders, insulin release, cell motility, and cell death. [6][7][8][9][10] The TRPM2 channel is activated by intracellular adenosine diphosphate ribose, hydrogen peroxide (H 2 O 2 ), intracellular Ca 2+ concentration ([Ca 2+ ] i ), and nicotinic acid adenine dinucleotide phosphate, whereas it is inhibited by the nucleotide adenosine monophosphate and by cellular acidification. [11][12][13][14] Because the TRPM2 channel responds to reactive oxygen species (ROS), it is involved in many oxidative stress-related pathological processes.…”

“…Increased ROS might behave as the TRPM2 channel to facilitate cancer therapy. 10,15 Recent studies have shown that 5-fluorouracil (5-FU) and cyclophosphamide may activate the TRPM2 channel in colon or breast cancer cells to enhance cell apoptosis. 15 However, the functional role of the TRPM2 channel in ESCC remains unknown.…”