ArticleOncoscience2026
Dual targeting of oncogenic microtubules and mitochondria in PDAC.
Article in Oncoscience, 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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7 authors.
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Abstract
Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest cancers. Microtubule inhibition is a promising therapeutic target as microtubule dynamics play a critical role in growth of metastases due to over expression of several β-tubulin subtypes compared to normal cells. Previous studies have shown that decreased expression of βIII- and βIVb-tubulin is associated with decreased PDAC cell growth. Bromodomain and Extra-Terminal domain (BET) proteins are transcription factors that regulate mitochondria proteins. In this study, we hypothesize that SB-216 and Veru-111 (related novel compounds) inhibit cell growth via suppression of oncogenic βIII- and βIVb-tubulin subtypes and mitochondria function via suppression of BRD4, the most active BET protein. PDAC cell growth was analyzed with the IncuCyte Live-Cell Analysis system. mRNA expression of βIII- and βIVb-tubulin was evaluated with quantitative real time PCR. Western blot analysis was performed for βIII, βIVb-tubulin, and BRD4 protein expression and expression of autophagy and mitophagy markers LC3B and p62/SQSTM1. Mitochondrial function/respiration was measured using a Seahorse XF-24 Flux Analyzer. Cell growth was greatly inhibited across all doses in multiple PDAC cell lines (
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