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. 2024 Apr 30;28(1):184–197. doi: 10.1080/19768354.2024.2345644

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© 2024 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The terms on which this article has been published allow the posting of the Accepted Manuscript in a repository by the author(s) or with their consent.

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Figure 1. — Downregulation of oncogenic miR-29 and -140-5p causes TRAIL-induced Drug-tolerant (TDT) state. (A) A schematic diagram showing the strategy to generate TRAIL-revertant from the resistant cells. (B) Gene Ontology terms associated genes differentially expressed in TRAIL-resistant cell (H460R) compared with sensitive cell. Left panel is a principal component analysis showing clustering between sensitive and resistant quadruplicate. (C) Heatmap showing upregulated miR-29 target genes in H460R cell. (D) Heatmap of miR-29 target genes upregulated in TRAIL-resistant cells. Kaplan-Meier curve depicting the survival probability in the patients with LUAD associated with (E) miR-29 or (F) miR-140 expression. (G) The restored expression of miR-29 a/c and -140-5p in H460R in response to drug holiday. (H) Cell survival rate using CellTiter-Glo assay. Error bars indicate mean ±SD (n = 4) and the p-values were calculated by one-way ANOVA test (**p < 0.01). (I) Chamber invasion assay of H460R cell reconstituted by miR-29 and/or -140-5p. Error bars show mean ±SD (n = 6) and the p-values were calculated by two-tailed student t-test (* p < 0.05, **p < 0.01).