Fig. 4: Upregulation of KRT7-AS enhances cisplatin-induced DNA damage and increases lung cancer cell sensibility to the drug. | Cell Death & Disease

Fig. 4: Upregulation of KRT7-AS enhances cisplatin-induced DNA damage and increases lung cancer cell sensibility to the drug.

From: The long non-coding RNA keratin-7 antisense acts as a new tumor suppressor to inhibit tumorigenesis and enhance apoptosis in lung and breast cancers

Fig. 4: Upregulation of KRT7-AS enhances cisplatin-induced DNA damage and increases lung cancer cell sensibility to the drug.The alternative text for this image may have been generated using AI.

Cell Titer-Glo luminescent (CTG) assay showed that KRT7-AS overexpression enhanced the sensibility of SPC-A-1 (A) and H1299 (C) lung cancer cells to the anti-cancer drug cisplatin. Flow cytometry analysis showed that KRT7-AS overexpression significantly enhanced cisplatin-induced apoptosis of SPC-A-1 (B, E) and H1299 (D, E) lung cancer cells. CTG and flow cytometry analysis showed that in KRT7-AS- silenced A549 lung cancer cells, reduction of KRT7-AS levels diminished cisplatin-induced apoptosis (F, G, H). The effect of KRT7-AS on the DNA damage marker γ-H2AX in KRT7-AS-overexpressed SPC-A-1 and KRT7-AS-silenced A549 cells in the presence of cisplatin was accessed by IF staining (I, J) and Western blotting (K, L). Time course study showed that KRT7-AS-induced elevation of γ-H2AX levels in SPC-A-1 (M, P), H1299 (N, Q), and A549 (O, R) lung cancer cells was in a time-dependent manner (M-R). Data are shown as mean ± SD of three independent replicates. **P < 0.01, ***P < 0.001.

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