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. 2020 Nov 27;13:12253–12254. doi: 10.2147/OTT.S292577

IL-6/STAT3 Signaling Contributes to Sorafenib Resistance in Hepatocellular Carcinoma Through Targeting Cancer Stem Cells [Corrigendum]

PMCID: PMC7708306  PMID: 33273830

Li Y, Chen G, Han Z, Cheng H, Qiao L, Li Y. Onco Targets Ther. 2020;13:9721–9730.

The authors have advised due to an error at the time of figure assembly, Figure 4 on page 9728 is incorrect. The correct Figure 4 is shown below.

Figure 4.

Figure 4

Establishment of subcutaneous xenografts in nude mice using resistant LCSCs, which block the IL-6/STAT3 signaling pathway. (A) Tumor images of all subcutaneous xenografts in nude mice. Each indicated treatment group included 5 mouse tumors. (B) Growth curves of xenograft tumors from day 1 to day 11 in various treatment groups. (C, D) Analysis of IL-6R and STAT3 protein expression in xenograft tumors to confirm that the IL-6/STAT3 signaling pathway was blocked. (E, F) The LCSC markers (EpCAM and CD44), stemness markers (Oct3/4 and β-catenin) and angiogenic factors (VEGF and VEGFR) were assessed by WB (Sor-Block-IL-6): subcutaneous xenograft tumors in nude mice were established using resistant LCSCs, which blocked IL-6 signaling, treated with sorafenib, 100 mg/kg/d; sor: subcutaneous xenograft tumors in nude mice were established using resistant LCSCs, in which IL-6 signaling is NOT blocked, and sorafenib as the treatment, 100 mg/kg/d; PBS: subcutaneous xenograft tumors were established in nude mice using resistant LCSCs, in which IL-6 signaling is blocked, and PBS as the treatment (ns P>0.05, *P<0.05, **P<0.01, ***P<0.005).

Figure 4.

Figure 4

Continued.

The authors apologize for this error and advise it does not affect the results of the paper.


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