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Circular RNA circTTBK2 facilitates non-small cell lung cancer malignancy through the miR-873-5p/TEAD1/DERL1 axis. Supplementary figures

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posted on 2022-08-02, 08:34 authored by Guang-Ping Meng, Ting-Ting Dong, Cheng-Hao Sun, Hai Bin He, Yue Yao, Qiang Zhang, Jin-Ying Wei

  

Figure S1. The subcellular localization of circTTBK2 in NSCLC cells. Nuclear-cytoplasmic fractionation assay was performed, and the data indicated that circTTBK2 was mainly localized in the cytoplasm of H1755 and A549 cells.

Figure S2. DERL1 promotes NSCLC cell proliferation, migration and invasion. (A and B) Levels of DERL1 by qRT-PCR and western blot analysis. (C) Cell viability by CCK-8 assay. (D) Transwell assay to determine the change of cell migration and invasion number. Data were expressed as the mean ± SD of n = 3 experiments. *, P < 0.05, **, P < 0.01, ***, P < 0.001.

Figure S3. Schematic graph of circTTBK2 in NSCLC progression. In summary, circTTBK2 was found to function as an oncogene to facilitate malignant progression of NSCLC cells by sponging miR-873-5p, and miR-873-5p exerted its anti-tumor role via directly binding to TEAD1. TEAD1 triggered the transcription activity of DERL1 through binding to its promoter region. These supported the circTTBK2/miR-873-5p/TEAD1/DERL1 regulatory network contributing to NSCLC tumorigenesis.

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