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investigating the expression level of ccat2 and bim genes in colorectal cancer patients
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نویسنده
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jenagh fateme ,rangin alireza
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منبع
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journal of genetic resources - 2025 - دوره : 11 - شماره : 1 - صفحه:31 -40
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چکیده
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Colon cancer ranks as the second most common cancer among women and the third among men globally. research has demonstrated that reduced expression of the bcl-2-like protein 11 (bim) gene in various cancers, including colon cancer, lowers cancer cell apoptosis, thereby enhancing their survival. another crucial molecular factor in cancer is non-coding rnas, which influence protein-coding genes such as oncogenes and tumor suppressor genes. colon cancer-associated transcript 2 (ccat2), a long non-coding rna, is known to play a regulatory role in several cancers, affecting gene expression. this study aimed to measure and compare the expression levels of bim and ccat2 genes in colon cancer tissues and healthy tissues. total rna was extracted from paraffin-embedded tissue samples using the trizol method. specific primers for the bim and ccat2 genes, along with the glyceraldehyde-3-phosphate dehydrogenase (gapdh) reference gene, were designed using oligo 7 software. following cdna synthesis, rt-pcr was conducted to assess gene expression levels relative to the gapdh control gene. data analysis, performed using graphpad prism and excel2020 with one way anova and one-sided t-test, revealed a 10-fold decrease in bim gene expression in cancerous tissues compared to healthy tissues (p < 0.01). in contrast, ccat2 gene expression was 325 times higher in cancerous tissues (p < 0.0001). the present study revealed that the expression of the ccat2 gene was significantly elevated in colon cancer patients compared to healthy individuals. this increase may be mediated through various signaling pathways, including bop1, mtor, and wnt. additionally, interactions with other regulatory factors, such as mirnas, can contribute to tumor cell proliferation, inhibition of apoptosis, and metastasis in patients. the reduced bim expression could result from genetic and epigenetic mutations disrupting the akt and erk pathways, thereby promoting tumor growth.
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کلیدواژه
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apoptosis ,bim ,ccat2 ,lncrna ,non-coding rna
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آدرس
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islamic azad university, ilam branch, department of biology, iran, islamic azad university, ilam branch, department of biology, iran
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پست الکترونیکی
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alireza1121sar@gmail.com
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Authors
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