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Inducible and Reversible Dominant-negative (DN) Protein Inhibition
Published on: January 7, 2019
Downregulating activated epidermal growth factor receptor has no effect on RBM5 expression
Twinkle J Masilamani1, Nina D Rintala-Maki, Ke Wang
1Tumor Biology Group, Regional Cancer Program of the Sudbury Regional Hospital, Sudbury, Ontario, Canada P3E 5J1.
Chinese Medical Journal
|August 14, 2012
Summary
Epidermal Growth Factor Receptor (EGFR) activation does not directly regulate the tumor suppressor gene RBM5 in lung adenocarcinomas. Further research is needed to understand RBM5 regulation in lung cancer.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Genetics
Background:
- The tumor suppressor gene RBM5 is regulated differently across lung cancer subtypes.
- RBM5 expression is reduced in non-small cell lung carcinomas (NSCLC) and deleted in small cell lung cancers.
- In lung adenocarcinomas, smoking is linked to KRAS mutations, while non-smokers show EGFR mutations, suggesting a link to RBM5 inhibition.
Purpose of the Study:
- To investigate the hypothesis that activating mutations in EGFR indirectly inhibit RBM5 in lung adenocarcinomas.
- To determine if EGFR activation and RBM5 expression are negatively correlated in lung adenocarcinoma.
Main Methods:
- EGFR expression was inhibited in the NCI-H1975 lung adenocarcinoma cell line using small interfering RNA.
- RBM5 expression was quantified at both RNA and protein levels using real-time quantitative PCR and Western blotting.
Main Results:
- Inhibition of EGFR expression did not result in any significant change in RBM5 expression.
- RBM5 expression remained unchanged at both the RNA and protein levels despite EGFR manipulation.
Conclusions:
- EGFR does not appear to directly regulate RBM5 expression in non-smoker associated lung adenocarcinomas.
- Alternative mechanisms likely control RBM5 expression or function in lung cancers that retain the RBM5 gene.
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