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. 2022 Mar 28;28:366–386. doi: 10.1016/j.omtn.2022.03.020

Figure 7.

Figure 7

Overexpression of GMDS-AS1 and LINC01128 augments the magnitude of CDDP/PEM-caused G2/M arrest and lipid peroxidation by inhibiting miR-6077, and inhibiting miR-6077 results in chemosensitivity to CDDP/PEM in LUAD cells

(A–D) Cell-cycle analyses (A), lipid peroxidation (B), glutathione levels (C), and protein levels of CDKN1A/KEAP1 and their downstream molecules (D) in GMDS-AS1/LINC01128-overexpressing H358 cells transfected with miR-NC1, miR-NC2, and miR-6077 upon treatment with PBS or CDDP (20 μM)/PEM (2 μM) for 48 h. (E and F) Relative expression levels of miR-6077 (E) and CDKN1A and KEAP1 (F) in H1299 and H1299-CDDP/PEM-resistant cells. (G) Western blotting assay showing the protein levels of CDKN1A and KEAP1 in H1299-CDDP/PEM-resistant cells transfected with miR-NC1, miR-NC2 inhibitor, and miR-6077 inhibitor upon CDDP (20 μM)/PEM (2 μM) treatment for 48 h. (H) Single-cell sequencing data displaying the sample origin (top) and expression levels of CDKN1A (middle) and KEAP1 (bottom) of tumor cells derived from patients receiving or not receiving neoadjuvant CDDP/PEM treatment. (I–L) Dose-toxicity curves (I), cell-cycle analyses (J), lipid peroxidation levels (K), and relative glutathione levels (L) in H1299-CDDP/PEM-resistant cells transfected with miR-NC1, miR-NC2, and miR-6077 upon PBS or CDDP (20 μM)/PEM (2 μM) treatment for 48 h; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001; ns, not significant.