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. 2020 Oct 22;44(6):2645–2655. doi: 10.3892/or.2020.7821

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Copyright: © Mu et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 2. — KTN1-AS1 knockdown attenuates the proliferation and invasive ability of glioma cells in vitro. (A) Upregulated level of KTN1-AS1 was measured in GBM tissues compared with adjacent normal brain tissues (n=35). GAPDH was used as a normalization control (P<0.001). The data were analyzed with Student's t-test. (B) KTN1-AS1 level in glioma cell lines was measured by RT-qPCR. (C) KTN1-AS1 level was transfected with siRNAs or pcDNA3.1 vector of KTN1-AS1 in T98G and U251 cells, and detected by RT-qPCR. (D) Glioma cell viability was analyzed using a CCK-8 assay. (E) Invasive ability was measured by Transwell assays. Magnification, ×100; scale bar, 50 µm. Data were presented as the means ± standard error of the mean of at least three independent experiments. *P<0.05, **P<0.01 and ***P<0.001. KTN1-AS1, Kinectin 1 Antisense RNA 1; GBM, glioblastoma; RT-qPCR, reverse transcription-quantitative PCR; NC, negative control; siRNA, small interfering RNA.