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Discovery of Driver Genes in Colorectal HT29-derived Cancer Stem-Like Tumorspheres
Published on: July 22, 2020
c-Src antisense complexed with PAMAM denderimes decreases of c-Src expression and EGFR-dependent downstream genes in
Ali Reza Nourazarian1, Roghiyeh Pashaei-Asl, Yadollah Omidi
1Department of Biochemistry, Faculty of Medicine, Kerman University of Medical Sciences, Kerman, Iran.
Abstract:
c-Src is one member of non-receptor tyrosine kinase protein family that has over expression and activation in many human cancer cells. It has been shown that c-Src is implicated in various downstream signaling pathways associated with EGFR-dependent signaling such as MAPK and STAT5 pathways. Transactivation of EGFR by c-Src is more effective than EGFR ligands. To inhibit the c-Src expression, we used c-Src antisense oligonucleotide complexed with PAMAM Denderimes. The effect of c-Src antisense oligonucleotide on HT29 cell proliferation was determined by MTT assay. Then, the expression of c-Src, EGFR and the genes related to EGFR-depended signaling with P53 was applied by real time PCR. We used western blot analysis to elucidate the effect of antisense on the level of c-Src protein expression. The results showed, c-Src antisense complexed with PAMAM denderimers has an effective role in decrease of c-Src expression and EGFR-dependent downstream genes.
Insights
This study shows that c-Src antisense oligonucleotide complexed with PAMAM dendrimers effectively reduces c-Src expression and downstream EGFR signaling in cancer cells. This approach offers a potential strategy for cancer therapy by targeting key oncogenic pathways.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- c-Src, a non-receptor tyrosine kinase, is overexpressed and activated in numerous human cancers.
- c-Src plays a crucial role in EGFR-dependent signaling pathways, including MAPK and STAT5.
- EGFR transactivation by c-Src is more potent than by EGFR ligands, highlighting c-Src as a therapeutic target.
Purpose of the Study:
- To investigate the efficacy of c-Src antisense oligonucleotide complexed with PAMAM dendrimers in inhibiting c-Src expression and downstream signaling.
- To evaluate the impact of this complex on HT29 cancer cell proliferation.
Main Methods:
- Utilized MTT assay to assess HT29 cell proliferation.
- Employed real-time PCR to quantify the expression of c-Src, EGFR, P53, and related downstream genes.
- Applied western blot analysis to determine c-Src protein levels.
Main Results:
- c-Src antisense oligonucleotide complexed with PAMAM dendrimers significantly decreased c-Src expression at both mRNA and protein levels.
- The treatment led to a reduction in the expression of EGFR-dependent downstream signaling genes.
- HT29 cell proliferation was inhibited by the c-Src antisense complex.
Conclusions:
- c-Src antisense oligonucleotide complexed with PAMAM dendrimers demonstrates potent inhibitory effects on c-Src expression and associated oncogenic signaling pathways.
- This targeted approach holds promise for developing novel therapeutic strategies against cancers driven by c-Src and EGFR signaling.
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