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Correction: CircSMARCC1 facilitates tumor progression by disrupting the crosstalk between prostate cancer cells and tumor-associated macrophages via miR-1322/CCL20/CCR6 signaling

The Original Article was published on 01 September 2022

Correction: Mol Cancer 21, 173 (2022)

https://doi.org/10.1186/s12943-022-01630-9

Following publication of the original article [1], the authors requested to update the figures as stated below.

  • We request to replace the misused image in C4-2 cells (sh-circ group) in Fig. 3H with the correct image which produced in May 26, 2021 when we conducted the experiment.

  • We request to replace the misused images in C4-2 cells in Fig. 4J with the correct images which produced in June 2, 2021 when we conducted the experiment.

  • We request to replace the misused image in the C4-2-sh-nc-CM group in Fig. 7F with the correct image which produced in April 14, 2021 when we conducted the experiment.

  • We request to replace the misused image in the THP-1-Mø-CM group in Fig. 7H with the correct image which produced in June 3, 2021 when we conducted the experiment.

Fig. 3
figure 1

CircSMARCC1 promotes proliferation, migration and invasion of PCa cells. A three siRNAs (si-#01,02,03) targeting circSMARCC1 were constructed to silence its expression and confirmed by qRT-PCR. B The relative expression of circSMARCC1 and SMARCC1 in PCa cells transfected with circSMARCC1 overexpressing or knockdown lentivirus by qRT-PCR. C-E Assessment of cell proliferation capacity by colony formation, EdU assay (scale bar, 100 μm) and CCK-8 assay. F Western blot analysis evaluated expression of cell cycle-associated proteins and EMT biomarkers following overexpression or knockdown of circSMARCC1. G Flow cytometric analysis of changes in the cell cycle profile of PCa cells stably transfected with circSMARCC1. H, I Transwell assays and wound healing assays assessed the migration and invasion abilities of PCa cells stably transfected with circSMARCC1 (Scalebar, 50 μm). The data are presented as the mean ± SD, **p < 0.01, ***p < 0.001, ****p < 0.0001

Fig. 4
figure 2

CircSMARCC1 acts as a sponge for miR-1322 and miR-1322 reverses the oncogenic effects of circSMARCC1 on proliferation, invasion and migration in PCa cells. A Schematic diagram of circSMARCC1 luciferase reporter vectors carrying wild-type (Wt) or mutant (Mut) miR-1322 binding sites. B Luciferase reporter assay to analyze the effects of 9 candidate miRNAs on the luciferase activity of circSMARCC1. C The RNA pull-down assay performed in DU145 cells using circSMARCC1 and negative control probes. D The relative expression of miR-1322 in PCa cells after transfection of circSMARCC1 was detected by qRT-PCR. E The relative luciferase activities measured in 293 T cells co-transfected with circSMARCC1-Wt or circSMARCC1-Mut and miR-1322 mimics or miR-nc by luciferase reporter assay. F The co-localization of circSMARCC1 and miR-1322 observed using RNA-FISH in DU145 cells (scale bar, 5 μm). The nuclei were stained with DAPI. G-I The viability of PCa cells in miR-1322 rescue experiments was analyzed by colony formation assay, EdU assay (scale bar, 100 μm) and CCK8 assay, respectively. J, K The migration and invasion capacity of PCa cells in the miR-1322 rescue experiment was analyzed by transwell assays (scale bar, 50 μm) and wound healing (scale bar, 100 μm) assays. The data are presented as the mean ± SD, *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001

Fig. 7
figure 3

circSMARCC1 promotes M2 macrophage polarization and recruitment via the CCL20-CCR6 axis. A IHC detected the infiltration of CD68+/ CD163+/ CD206+ macrophages in human PCa tissue and Para-cancerous tissues (scale bar, 100 μm and 20 μm). B IHC detected the infiltration of CD68+/ CD163+/ CD206+ macrophages in mouse xenograft tumors (scale bar, 100 μm and 20 μm). C, D The expression of M1 phenotype (TNF-a, CD80 and CD86) and M2 phenotype (IL-10, ARG-1 and CD163) markers were detected by qRT-PCR in THP-1 cells, THP-1-Mø and THP-1-M2 cells. E The proportion of CD68 and CD163 positive cells detected by flow cytometry. F The CM prepared from lv-circSMARCC1 or vector and sh-circSMARCC1 or sh-nc tumor cells was used to evaluate the migration ability of macrophages through transwell experiments (scale bar, 50 μm). G The migration ability of TAM was detected by transwell assay using CCL20 recombinant protein and CCR6 neutralizing antibody (scale bar, 50 μm). H The CM prepared from THP-1-Mø or THP-1-M2 cells for PCa cells migration experiments (scale bar, 50 μm). I, J qRT-PCR tested the expression of M2 phenotypes marker (IL-10, ARG-1, CD68 and CD163) when co-cultured with DU145-lv-circSMARCC1 cells or vector cells or using CCL20 recombinant protein, with IL-4 and IL-3 polarization as the reference. K The expression of CD68, CD163 and CCR6 in THP-1 cells, THP-1-Mø cells stimulated by CCL20 recombinant protein, and THP-1-Mø cells (with and without co-culture) were detected by Western blotting. L The expression of CD68, CD163 and CCR6 in THP-1-Mø cells and THP-1-M2 cells (with and without anti-CCR6) were detected by Western blotting. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

Reference

  1. Xie T, Fu Dj, Li Zm, et al. CircSMARCC1 facilitates tumor progression by disrupting the crosstalk between prostate cancer cells and tumor-associated macrophages via miR-1322/CCL20/CCR6 signaling. Mol Cancer. 2022; 21: 173. https://doi.org/10.1186/s12943-022-01630-9.

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Correspondence to Jiacheng Wu, Ning-Han Feng or Shan-Chao Zhao.

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Xie, T., Fu, Dj., Li, Zm. et al. Correction: CircSMARCC1 facilitates tumor progression by disrupting the crosstalk between prostate cancer cells and tumor-associated macrophages via miR-1322/CCL20/CCR6 signaling. Mol Cancer 22, 173 (2023). https://doi.org/10.1186/s12943-023-01881-0

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