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Correction: MALAT1/ mir-1-3p mediated BRF2 expression promotes HCC progression via inhibiting the LKB1/AMPK signaling pathway

The Original Article was published on 31 August 2023

Correction to: Cancer Cell International (2023) 23:188

https://doi.org/10.1186/s12935-023-03034-1.

In this article [1], the wrong figure appeared as Fig. 7, the figure should have appeared as shown below.

Fig. 7
figure 7

Overexpression of BRF2 abrogated MALAT1 knockdown. (a, b) The transfection efficiency of OE-BRF2 in Huh7 and Hep3B cells was detected by qRT-PCR. (c, d) After silencing MALAT1 and overexpression BRF2, cell viability of Huh7 and Hep3B cells was detected by CCK-8 assay on days 0, 1, 2, 3, 4 and 5. (e, f) Transwell assay was used to detect migration and invasion of HCC cells after MALAT1 down-regulation and overexpression of BRF2. (g) The apoptosis rate of HCC cells after MALAT1 down-regulation and overexpression of BRF2 was detected by flow cytometry. (h) Western blot analysis was performed to detect the expression levels of apoptosis-related proteins and LKB1/AMPK in HCC cells after MALAT1 down-regulation and overexpression of BRF2. **P < 0.01, ***P < 0.001

References

  1. Li GZ, Meng GX, Pan GQ, Zhang X, Yan LJ, Li RZ, Ding ZN, Tan SY, Wang DX, Tian BW, Yan YC. MALAT1/mir-1-3p mediated BRF2 expression promotes HCC progression via inhibiting the LKB1/AMPK signaling pathway. Cancer Cell Int. 2023;23(1):188.

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Correspondence to Jian-Guo Hong or Tao Li.

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Li, GZ., Meng, GX., Pan, GQ. et al. Correction: MALAT1/ mir-1-3p mediated BRF2 expression promotes HCC progression via inhibiting the LKB1/AMPK signaling pathway. Cancer Cell Int 24, 260 (2024). https://doi.org/10.1186/s12935-024-03399-x

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  • DOI: https://doi.org/10.1186/s12935-024-03399-x