ArticleJournal of cancer research and clinical oncology2026
Effects of CDDO‑TFEA on non‑small cell lung cancer growth, apoptosis, and stemness via the MEK/ERK pathway.
Article in Journal of cancer research and clinical oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
purposeNon-small cell lung cancer (NSCLC) remains a leading cause of cancer-related mortality, and therapeutic resistance limits durable responses. We investigated the antitumor activity of CDDO-TFEA, a synthetic trifluoroethyl amide derivative of 2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid, in NSCLC models.
methodsA549 and H1299 cells were treated with CDDO-TFEA and evaluated using MTT assays, Annexin V/7-aminoactinomycin D flow cytometry, tumorsphere and tube-formation assays, immunoblotting, and A549 xenograft experiments.
resultsCDDO-TFEA decreased cell viability in a dose-dependent manner and induced apoptosis, as indicated by increased Annexin V positivity, PARP cleavage, cleaved caspase-3 expression, and TUNEL positivity. At 200 nM, CDDO-TFEA significantly suppressed tumorsphere formation in both cell lines and reduced CD133, octamer-binding transcription factor 4, SRY-box transcription factor 2, and vascular endothelial growth factor expression. Because only A549 cells formed tube-like networks, angiogenesis-related phenotypes were evaluated in A549 cells and were markedly inhibited by CDDO-TFEA. Mechanistically, CDDO-TFEA increased extracellular signal-regulated kinase phosphorylation, whereas MEK inhibition by U0126 or trametinib partially attenuated CDDO-TFEA-induced apoptosis and the suppression of tumorsphere formation, tube-like network formation, and stemness- and angiogenesis-related marker expression. In vivo, systemic CDDO-TFEA administration dose-dependently inhibited xenograft tumor growth.
conclusionCDDO-TFEA exerts antitumor activity in NSCLC by inducing apoptosis and suppressing stemness-associated and angiogenesis-related phenotypes, partly through mitogen-activated protein kinase kinase/extracellular signal-regulated kinase signaling. These findings support further preclinical development of CDDO-TFEA in NSCLC.
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