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Correction: RNA-binding protein RPS7 promotes hepatocellular carcinoma progression via LOXL2-dependent activation of ITGB1/FAK/SRC signaling

The Original Article was published on 08 February 2024

Correction: J Exp Clin Cancer Res 43, 45 (2024)

https://doi.org/10.1186/s13046-023-02929-1


Following publication of the original article [1], errors were spotted particularly in Fig. 6, specifically:

Fig. 6b – upper panels, incorrect representative image used for migration transwell assays of Huh7 cells transfected with EV

Fig. 6d – lower panels, incorrect representative image used for invasion transwell assays of MHCC97H cells transfected with siNTC

Authors missed the Production Editor’s email which resulted to not being able to check the modification status of Fig. 6. The correct figure is given below. The correction does not affect the overall result or conclusion of the article. The original article has been corrected.

Incorrect Fig. 6

Fig. 6
figure a

LOXL2 promotes focal adhesion (FA) formation, migration and invasion of HCC cells. A and B To evaluate the role of LOXL2 in HCC metastasis, two pcDNA3.1-LOXL2-3 × Flag mutant plasmids, catalytic activity deletion mutant of LOXL2 (LOXL2-Δ) and catalytically inactive point mutant of LOXL2 (LOXL2-Y689F), as well as wild type LOXL2 (LOXL2-WT) were respectively constructed and stably transfected into Huh7 cells. The effect of LOXL2 overexpression on cell–matrix adhesion ability (A) and migration and invasion (B) were analyzed. C The effect of LOXL2 silencing on cell–matrix adhesion ability in MHCC97H cells. D The effect of LOXL2 silencing on cell migration and invasion in MHCC97H cells. E–G. The effect of LOXL2 silencing (E), 20 μM CMMH (F), and LOXL2 overexpression (G) on FA formation in HCC cells were respectively detected by Immunofluorescence staining experiments. Representative data are from at least 3 independent experiments. Data are shown as mean ± SD. **, P < 0.01. ns, no significant

Correct Fig. 6

Fig. 6
figure 1

LOXL2 promotes focal adhesion (FA) formation, migration and invasion of HCC cells. A and B To evaluate the role of LOXL2 in HCC metastasis, two pcDNA3.1-LOXL2-3 × Flag mutant plasmids, catalytic activity deletion mutant of LOXL2 (LOXL2-Δ) and catalytically inactive point mutant of LOXL2 (LOXL2-Y689F), as well as wild type LOXL2 (LOXL2-WT) were respectively constructed and stably transfected into Huh7 cells. The effect of LOXL2 overexpression on cell–matrix adhesion ability (A) and migration and invasion (B) were analyzed. C The effect of LOXL2 silencing on cell–matrix adhesion ability in MHCC97H cells. D The effect of LOXL2 silencing on cell migration and invasion in MHCC97H cells. E–G. The effect of LOXL2 silencing (E), 20 μM CMMH (F), and LOXL2 overexpression (G) on FA formation in HCC cells were respectively detected by Immunofluorescence staining experiments. Representative data are from at least 3 independent experiments. Data are shown as mean ± SD. **, P < 0.01. ns, no significant

Reference

  1. Zhou YJ, Yang ML, He X, et al. RNA-binding protein RPS7 promotes hepatocellular carcinoma progression via LOXL2-dependent activation of ITGB1/FAK/SRC signaling. J Exp Clin Cancer Res. 2024;43:45. https://doi.org/10.1186/s13046-023-02929-1.

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Correspondence to Zhen-Zhen Zhang or Juan Chen.

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Zhou, YJ., Yang, ML., He, X. et al. Correction: RNA-binding protein RPS7 promotes hepatocellular carcinoma progression via LOXL2-dependent activation of ITGB1/FAK/SRC signaling. J Exp Clin Cancer Res 43, 80 (2024). https://doi.org/10.1186/s13046-024-02999-9

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  • DOI: https://doi.org/10.1186/s13046-024-02999-9