Literature DB >> 35793028

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Year:  2022        PMID: 35793028      PMCID: PMC9258694          DOI: 10.1111/jcmm.17423

Source DB:  PubMed          Journal:  J Cell Mol Med        ISSN: 1582-1838            Impact factor:   5.295


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In Song Chen et al, there was an error in the figure panel labelling in Figure 7B(ii) and an image assembly error in Figure 8D(ii). The correct legends and figures are shown below. The authors confirm that all results and conclusions of this article remain unchanged.
FIGURE 7

Inhibition of MELK by OTSSP167 results in potent anti‐tumour effects in bladder cancer in vivo. (A) The OTSSP167 injection anti‐tumour experiment performed with a mouse xenograft model is shown. (B, C) The measurement of tumour growth activity and mouse bodyweight as well as analysis of the dissected tumours. (D, E) Haematoxylin and eosin staining of the tumour tissues, livers and kidneys of mice from each group. (F–I) Immunofluorescence analysis of Ki‐67, MELK, p‐ATM and p53 in each group of mouse tumour tissues, *p < 0.05; **p < 0.01; ***p < 0.001

FIGURE 8

OTSSP167 restored the up‐regulation effect of the MELK plasmid. (A) The expression of MELK was up‐regulated at transcription level with MELK plasmid; it was down‐regulated by OTSSP167. OTSSP167 could restore the up‐regulation effect caused by transfection with the MELK plasmid. (B–D) Cellular functional studies, MTT (B), clonogenic forming (C) and migration (D) assays confirmed the restoration function of OTSSP167. E, OTSSP167 restored the cell cycle effect caused by transfection with the MELK plasmid. (F) OTSSP167 restored the inhibition effect of the ATM/CHK2/p53 pathway, which was caused transfection with the MELK plasmid, *p < 0.05; **p < 0.01; ***p < 0.001

Inhibition of MELK by OTSSP167 results in potent anti‐tumour effects in bladder cancer in vivo. (A) The OTSSP167 injection anti‐tumour experiment performed with a mouse xenograft model is shown. (B, C) The measurement of tumour growth activity and mouse bodyweight as well as analysis of the dissected tumours. (D, E) Haematoxylin and eosin staining of the tumour tissues, livers and kidneys of mice from each group. (F–I) Immunofluorescence analysis of Ki‐67, MELK, p‐ATM and p53 in each group of mouse tumour tissues, *p < 0.05; **p < 0.01; ***p < 0.001 OTSSP167 restored the up‐regulation effect of the MELK plasmid. (A) The expression of MELK was up‐regulated at transcription level with MELK plasmid; it was down‐regulated by OTSSP167. OTSSP167 could restore the up‐regulation effect caused by transfection with the MELK plasmid. (B–D) Cellular functional studies, MTT (B), clonogenic forming (C) and migration (D) assays confirmed the restoration function of OTSSP167. E, OTSSP167 restored the cell cycle effect caused by transfection with the MELK plasmid. (F) OTSSP167 restored the inhibition effect of the ATM/CHK2/p53 pathway, which was caused transfection with the MELK plasmid, *p < 0.05; **p < 0.01; ***p < 0.001
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1.  Inhibition of MELK produces potential anti-tumour effects in bladder cancer by inducing G1/S cell cycle arrest via the ATM/CHK2/p53 pathway.

Authors:  Song Chen; Qiang Zhou; Zicheng Guo; Yejinpeng Wang; Lu Wang; Xuefeng Liu; Mengxin Lu; Lingao Ju; Yu Xiao; Xinghuan Wang
Journal:  J Cell Mol Med       Date:  2019-12-10       Impact factor: 5.310

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