Younes Aftabi - Tuberculosis and Lung Disease Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
Habib Zarredar - Tuberculosis and Lung Disease Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
Mohammadreza Sheikhi - Department of Molecular and Cell Biology, Faculty of Basic Sciences, University of Tehran, Tehran, Iran
Zahra Khoshkam - Department of Molecular and Cell Biology, Faculty of Basic Sciences, University of Mazandaran, Babolsar, Mazandaran, Iran
Abasalt Hosseinzadeh Colagar - Department of Molecular and Cell Biology, Faculty of Basic Sciences, University of Tehran, Tehran, Iran

Aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor and its induction may result insuppressing of cell proliferation in colorectal cancer (CRC). Cucurbitacin D (CucD), E (CucE) and I (CucI) are plantderived metabolites that inhibit cancer cells. This study aimed to evaluate the possible potency of the cucurbitacinsfor activation of AHR expression in CRC cell lines SW-480 and HT-29. The MTT assay was used to find the IC50value of the metabolites in the cell lines. Afterwards, the cells were incubated with the IC50 concentrations of thecucurbitacins and AHR-mRNA expression assessed using RT-PCR. The IC50 values of CucD, CucE, and CucI were4.5, 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 weremore resistant against cucurbitacins in comparison with HT-29 cells and all three cucurbitacins led to more AHRmRNAexpression in HT-29 cells. CucE had the lowest effect on AHR-mRNA expression in the cell lines and CucIwas a common metabolite for both HT-29 and SW-480 cells, which showed the lowest IC50 value (the highesttoxicity) and the highest effect on AHR-mRNA expression. CucI may have a potential AHR-induction role and itcould be applicable as an AHR-expression inducer in CRC studies.

Aryl hydrocarbon receptor, Colon cancer, Cucurbitacin, HT-29, SW-480