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Correction: SPOCK1 as a potential cancer prognostic marker promotes the proliferation and metastasis of gallbladder cancer cells by activating the PI3K/AKT pathway

The Original Article was published on 27 January 2015

Correction: Mol Cancer 14, 12 (2015)

https://doi.org/10.1186/s12943-014-0276-y


Following publication of the original article [1], the author has requested the publication of an erratum to address the following issues stated below.

Recently, in planning and designing further studies of the roles of SPOCK1 in chemo-resistance of gallbladder cancer, based on the authors ‘ previous investigations including the above mentioned paper, they noticed an error in the Fig. 5 A&B. They found that in Fig. 5A, the pictures of NOZ cells in the shSPOCK1 group were placed incorrectly and in Fig. 5B, the pictures of SGC cells in the Mock group were placed incorrectly. There errors likely resulted from incorporation of the incorrect figure panels due to the high similarities of both file names and images from the repeated experiments in the original data folder. However, these errors in the images do not affect any statistical results and the relevant conclusions. They have carefully examined the original results and now the incorrect Fig. 5 and correct Fig. 5 are povided below.

Incorrect Fig. 5:

Fig. 5
figure 1

SPOCK1 promotes tumor invasion and metastasis in vitro by inducing EMT. A Wound closure was delayed in Lv-shSPOCK1-transduced cells compared with that in CTRL and Lv-shNC cells at 48 h in both GBC-SD and NOZ cells. Overexpression of SPOCK1 in SGC-996 cells had the opposite effects (*P < 0.05, **P < 0.01, and ***P < 0.001). B Matrigel invasion assay of CTRL, Lv-shNC, Lv-shSPOCK1, MOCK, and SPOCK1 transfectants cells. The number of invaded cells was calculated and is depicted in the bar chart. (*P < 0.05, **P < 0.01, and ***P < 0.001). C and D The protein expression of Snail, vimentin, N-cadherin and E-cadherin in the indicated cells was examined by western blotting. The protein expression of vementin and E-cadherin was examined by immunofluorescence analysis. The red signal represents staining for E-cadherin or vimentin. Nuclei were counterstained with DAPI

Correct Fig. 5:

Fig. 5
figure 2

SPOCK1 promotes tumor invasion and metastasis in vitro by inducing EMT. A Wound closure was delayed in Lv-shSPOCK1-transduced cells compared with that in CTRL and Lv-shNC cells at 48 h in both GBC-SD and NOZ cells. Overexpression of SPOCK1 in SGC-996 cells had the opposite effects (* P < 0.05, * *P < 0.01, and *** P < 0.001). B Matrigel invasion assay of CTRL, Lv-shNC, Lv-shSPOCK1, MOCK, and SPOCK1 transfectants cells. The number of invaded cells was calculated and is depicted in the bar chart. (* P < 0.05, ** P < 0.01, and ***P < 0.001). C and D The protein expression of Snail, vimentin, N-cadherin and E-cadherin in the indicated cells was examined by western blotting. The protein expression of vementin and E-cadherin was examined by immunofluorescence analysis. The red signal represents staining for E-cadherin or vimentin. Nuclei were counterstained with DAPI

Reference

  1. Shu YJ, Weng H, Ye YY, et al. SPOCK1 as a potential cancer prognostic marker promotes the proliferation and metastasis of gallbladder cancer cells by activating the PI3K/AKT pathway. Mol Cancer. 2015;14:12. https://doi.org/10.1186/s12943-014-0276-y.

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Correspondence to Zhi-Gang Jie or Ying-Bin Liu.

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Shu, YJ., Weng, H., Ye, YY. et al. Correction: SPOCK1 as a potential cancer prognostic marker promotes the proliferation and metastasis of gallbladder cancer cells by activating the PI3K/AKT pathway. Mol Cancer 24, 100 (2025). https://doi.org/10.1186/s12943-025-02313-x

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  • DOI: https://doi.org/10.1186/s12943-025-02313-x