Correction to: LncRNA MYLK-AS1 facilitates tumor progression and angiogenesis by targeting miR-424-5p/E2F7 axis and acti
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(2020) 39:277
CORRECTION
Open Access
Correction to: LncRNA MYLK-AS1 facilitates tumor progression and angiogenesis by targeting miR-424-5p/E2F7 axis and activating VEGFR-2 signaling pathway in hepatocellular carcinoma Fei Teng1,2†, Ju-Xiang Zhang3†, Qi-Meng Chang1,2, Xu-Bo Wu1,2, Wei-Guo Tang1,2, Jian-Fa Wang1,2, Jin-Feng Feng1,2, Zi-Ping Zhang1,2* and Zhi-Qiu Hu1,2* Correction to: J Exp Clin Cancer Res 39, 235 (2020) https://doi.org/10.1186/s13046-020-01739-z Following publication of the article [1], the authors identified errors in Figure 1g,1i,1j,1k, Figure 5e,f, and Figure 6d,e. In addition, figure captions for Figure 2, Figure 4, Figure 5, Figure 6, Figure 7, and Additional file 2: Figure S1 should be corrected. The corrected figures and captions can be found below. The corrections do not change the results or the conclusions of this article. The original article has been updated. Fig. 2 MYLK-AS1 and E2F7 overexpression is positively correlated with HCC progression and poor prognosis. A-C Relative expression of MYLK-AS1, miR424-5p and E2F7 detected by qRT-PCR in 156 paired HCC cancer tissues and matched normal liver tissues. Results are presented as the relative expression (compare to internal control, the 2-△△CT method) in tumor tissues and peritumoral tissues. D MYLK-AS1 expression in peritumoral tissues and HCC tissues by ISH. E Relative MYLK-AS1 expression by qRT-PCR in 156 HCC tissues. The original article can be found online at https://doi.org/10.1186/s13046020-01739-z. * Correspondence: [email protected]; [email protected] † Fei Teng and Ju-Xiang Zhang contributed equally to this work. 1 Department of Hepatobiliary and Pancreatic Surgery, Minhang Hospital, Fudan University, Shanghai 201199, People’s Republic of China Full list of author information is available at the end of the article
Relative MYLK-AS1 expression presented as the relative expression (compare to internal control, the 2-△△CT method) in tumor tissues and the matched normal tissues. HCC patients were divided into high (n = 78) and low (n = 78) group according to the median value (0.50). F-G Relative MYLK-AS1 expression in HCC with different size and stage. Results were presented as the relative expression (compare to internal control, the 2-△△CT method) in tumor tissues and normal tissues. H-I Kaplan-Meier plots of the OS and PFS of HCC patients with high (n = 78) and low (n = 78) MYLK-AS1 expression. Data are presented as mean ± SD. *P < 0.05, **P < 0.01, and ***P < 0.001. J ROC analysis of the performance of MYLKAS1 expression of 1-year OS in all patients. K Kaplan-Meier plots of the PFS of HCC patients after postoperative adjuvant TACE therapy with high (n = 36) and low (n = 36) MYLK-AS1 expression. Data are presented as mean ± SD. *P < 0.05, **P < 0.01, and ***P < 0.001. Fig. 4 MYLK-AS1 up-regulates E2F7 expression by competitively binding miR-424-5p in HCC. A-B Binding ability of MYLK-AS1, miR-424-5p, and E2F7 to anti-Ago2 in Hep-G2 and MHCC-97H (anti-igG was used as control) by RIP assay. C HEK-293FT cells co-transfected wit
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