@article { author = {Aftabi, Younes and Zarredar, Habib and Sheikhi, Mohammadreza and Khoshkam, Zahra and Hosseinzadeh Colagar, Abasalt}, title = {Induction of AHR Gene Expression in Colorectal Cancer Cell Lines by Cucurbitacin D, E, and I}, journal = {Journal of Cell and Molecular Research}, volume = {10}, number = {2}, pages = {67-75}, year = {2019}, publisher = {Ferdowsi University of Mashhad}, issn = {2008-9147}, eissn = {2717-3364}, doi = {10.22067/jcmr.v10i2.74806}, abstract = {     Aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor and its induction may result in suppressing of cell proliferation in colorectal cancer (CRC). Cucurbitacin D (CucD), E (CucE) and I (CucI) are plant derived metabolites that inhibit cancer cells. This study aimed to evaluate the possible potency of the cucurbitacins for activation of AHR expression in CRC cell lines SW-480 and HT-29. The MTT assay was used to find the LC50 value of the metabolites in the cell lines. Afterward, the cells incubated with the LC50 concentrations and AHR-mRNA expression assessed using RT-PCR. The LC50 values of CucD, CucE, and CucI were 4.5, 6.8, and 3.8 μM in HT-29 cell line and 35, 19, 17.5 μM in SW-480 cells respectively. The SW-480 cells were more resistant against Cucs in comparison with HT-29 cells and all three Cucs cause to more AHR-mRNA expression in HT-29 cells. CucE had the lowest effect on AHR-mRNA expression in the cell lines and CucI was a common metabolite for both HT-29 and SW-480 cells, which showed the lowest LC50 value (the highest toxicity) and the highest effect on AHR-mRNA expression. CucI may have a potential to be used as an activator of AHR expression in CRC studies.}, keywords = {Aryl hydrocarbon receptor,Colon cancer,Cucurbitacin,HT-29,SW-480}, url = {https://jcmr.um.ac.ir/article_29516.html}, eprint = {https://jcmr.um.ac.ir/article_29516_e06ad1773f35704adab1b9e8d4865167.pdf} }