فهرست نشریات علمی دسترسی آزاد ایران

Background: Colorectal cancer (CRC) remains a major cause of cancer deaths worldwide, emphasizing the need for new treatments. Although vitamin D is known to impact cell growth and apoptosis, its precise mechanisms in affecting CRC and regulating apoptosis-related genes are not fully understood. This study investigated the possible cytotoxicity of vitamin D on human colon adenocarcinoma HT-29 cells and examined changes in BAX and BCL-2 gene expression.Methods: HT29 cells were cultured and exposed to vitamin D at concentrations ranging from 50 to 3750 µg/ml for 24 hours, with untreated cells as controls. Cell viability was assessed using an MTT assay, followed by RNA extraction. The RNA was reverse-transcribed into cDNA, allowing quantitative measurement of BAX and BCL-2 transcripts through real-time PCR, with data normalized to GAPDH. Statistical analysis of cell viability was performed using one-way ANOVA and Dunnett's post-hoc tests, while differences in gene expression were examined with t-tests.Results: Vitamin D decreased HT-29 cell viability in a dose-dependent and nonlinear way (p < 0.0001), with the highest inhibition seen at concentrations between 250-500 µg/ml. However, there was no significant difference in BAX expression (p = 0.1431) or BCL-2 expression (p = 0.5943). Conclusions: These data indicate that Vitamin D can cause cytotoxicity in HT-29 cells without altering the transcriptional targets BAX/BCL-2, and may also induce cell death through other pathways such as inhibited proliferation. Overall, this suggests that Vitamin D has potential association as a complementary therapy for CRC and warrants further mechanistic research, including studies with in vivo CRC models.