Biochem Biophys Res Commun
Department of Surgery, Tokyo Medical University, Nishishinjuku, Shinjuku-ku, Tokyo 160-0023, Japan.
Published: April 2012
Lung cancer, predominantly non-small cell lung cancer (NSCLC), remains the leading cause of cancer-related deaths worldwide. Although epidermal growth factor receptor (EGFR) signaling is important and well studied with respect to NSCLC progression, little is known about how miRNAs mediate EGFR signaling to modulate tumorigenesis. To identify miRNAs that target EGFR, we performed a bioinformatics analysis and found that miR-542-5p down-regulates EGFR mRNA and protein expression in human lung cancer cells (H3255, A549, Hcc827). We observed increases in EGFR association with Ago2 in miR-542-5p-transfected cells. Interestingly, we observed an inverse correlation of miR-542-5p expression and EGFR protein levels in human lung cancer tissue samples, suggesting that miR-542-5p directly targets EGFR mRNA. Furthermore, we found that miR-542-5p inhibited the growth of human lung cancer cells. Our findings suggest that miR-542-5p may act as an important modulator of EGFR-mediated oncogenesis, with potential applications as a novel therapeutic target in lung cancer.
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http://dx.doi.org/10.1016/j.bbrc.2012.03.008 | DOI Listing |
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