Sayyed Emad Aldin Tayyebi; Mahyar Heydarpour; Hesam Dehghani
Abstract
Colorectal cancer is one of the most common cancers and is one of the leading causes of cancer-related deaths worldwide. The underlying biological mechanisms for the development of colorectal cancer are largely unidentified. Several genes have been identified that are most likely involved in the pathogenesis ...
Read More
Colorectal cancer is one of the most common cancers and is one of the leading causes of cancer-related deaths worldwide. The underlying biological mechanisms for the development of colorectal cancer are largely unidentified. Several genes have been identified that are most likely involved in the pathogenesis of colorectal cancer disease. However, some other genes might have less evident functions. One gene family with prominent functional roles in the normal colon is mucin. Multiple studies have demonstrated the involvement of mucins in the pathogenesis of human malignancies. Therefore, due to the lack of an inclusive investigation for mucins' expression, mechanism of action, and their involvement in the underlying biology, diagnosis, and prognosis of colon adenocarcinoma, we sought to unearth their potential involvement and their related regulatory networks in this disease. In this investigation, through a stepwise manner, a plethora of databases and algorithmic tools were applied. Due to a significant upregulation at both mRNA and protein levels and following a thorough evaluation of diagnostic and prognostic values in colon adenocarcinoma, MUC13 was determined to be the most relevant regulatory mucin in colon carcinoma. Altogether, these findings indicate a putative ncRNA-mRNA network, including hsa-mir-136-5p, hsa-mir-27a-3p, NEAT1, and XIST to be involved in regulating MUC13 in colon cancer. This stepwise investigation implies that MUC13 may have a crucial role in the underlying molecular mechanisms for the initiation or progression of colon cancer. In addition, it provides insights into molecular mechanisms and possible regulatory non-coding RNA networks that might be responsible for regulating MUC13 expression.
Younes Aftabi; Habib Zarredar; Mohammadreza Sheikhi; Zahra Khoshkam; Abasalt Hosseinzadeh Colagar
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 ...
Read More
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.
