Correction to: The role of deoxycholic acid in macrophage polarization and remodeling of the tumor microenvironment during colorectal adenoma-carcinoma transition

Correction to: Cancer & Metabolism (2025) 13:47

https://doi.org/10.1186/s40170-025-00416-z

In this article Fig. 3I, Fig. 4D, and Fig. S2F appeared incorrectly and have now been corrected in the original publication. For completeness and transparency, the old incorrect versions are displayed below.

Fig. 3.

DCA promotes the polarization of macrophages toward the M2 phenotype. (A) Schematic diagram of the establishment of the THP-1 macrophage system and the DCA intervention process. (B) The levels of TNF-α, IL-1β, IL-10, and TGF-β in the cell supernatant of each type of macrophage treated with DCA for 48 h were measured via ELISA kits. (C-D) Immunofluorescence staining images of CD206, CD86, CD68 and DAPI in different types of macrophages treated with DCA for 48 h. (E) Statistics of the relative fluorescence intensity of CD206 in different types of macrophages after DCA treatment for 48 h. (F) The protein expression of CD206 and CD86 in each type of macrophage treated with DCA for 48 h was determined by flow cytometry. (G) RT-qPCR was used to detect the gene expression of IL-6, IL-1β, ARG1, and MRC1 in each type of macrophage after DCA treatment for 48 h. (H) Schematic diagram of the isolation and purification of colon tumor-associated macrophages. (I) Immunofluorescence images of CD206, CD68 and DAPI staining in TAMs treated with DCA for 48 h. (J) Statistics of the fluorescence intensity of CD206 expression. P values were indicated as follows: * p<0.001

Fig. 4.

DCA-mediated M2 macrophages facilitated the EMT of colorectal tumor cells. (A) Schematic of macrophages and DCA-mediated polarized macrophages cocultured with tumors for 72 h. (B) Tumor invasion of HCT116 and LOVO cells with M0 macrophages and DCA-stimulated macrophages. (C) Statistical plots of the migration experiments of M0 macrophages and DCA-stimulated macrophages with HCT116 and LOVO cells (n=3). (D) Immunofluorescence staining of EMT-related markers in Med-, THP-1-, M0-, and DCA-stimulated macrophages cocultured with HCT116 cells for 72 hours. (E) Western blot analysis of the expression of Vimentin and N-cadherin and the expression of E-cadherin in macrophage-pretreated HCT116 colorectal cancer cells. (F) Statistical analysis of protein expression in HCT116 colorectal cancer cells. (G) Western blot analysis of the expression of Vimentin and N-cadherin and the expression of E-cadherin in macrophage-pretreated LOVO colorectal cancer cells (n=3). (H) Statistical analysis of protein expression in LOVO colorectal cancer cells. P values were indicated as follows: * p<0.001

Incorrect Figure 3

Correct Figure 3

Fig. 3.

DCA promotes the polarization of macrophages toward the M2 phenotype. (A) Schematic diagram of the establishment of the THP-1 macrophage system and the DCA intervention process. (B) The levels of TNF-α, IL-1β, IL-10, and TGF-β in the cell supernatant of each type of macrophage treated with DCA for 48 h were measured via ELISA kits. (C-D) Immunofluorescence staining images of CD206, CD86, CD68 and DAPI in different types of macrophages treated with DCA for 48 h. (E) Statistics of the relative fluorescence intensity of CD206 in different types of macrophages after DCA treatment for 48 h. (F) The protein expression of CD206 and CD86 in each type of macrophage treated with DCA for 48 h was determined by flow cytometry. (G) RT‒qPCR was used to detect the gene expression of IL-6, IL-1β, ARG1, and MRC1 in each type of macrophage after DCA treatment for 48 h. (H) Schematic diagram of the isolation and purification of colon tumor-associated macrophages. (I) Immunofluorescence images of CD206, CD68 and DAPI staining in TAMs treated with DCA for 48 h. (J) Statistics of the fluorescence intensity of CD206 expression. P values were indicated as follows: * p<0.001

Incorrect Figure 4

Correct Figure 4

Fig. 4.

DCA-mediated M2 macrophages facilitated the EMT of colorectal tumor cells. (A) Schematic of macrophages and DCA-mediated polarized macrophages cocultured with tumors for 72 h. (B) Tumor invasion of HCT116 and LOVO cells with M0 macrophages and DCA-stimulated macrophages. (C) Statistical plots of the migration experiments of M0 macrophages and DCA-stimulated macrophages with HCT116 and LOVO cells (n=3). (D) Immunofluorescence staining of EMT-related markers in Med-, THP-1-, M0-, and DCA-stimulated macrophages cocultured with HCT116 cells for 72 hours. (E) Western blot analysis of the expression of Vimentin and N-cadherin and the expression of E-cadherin in macrophage-pretreated HCT116 colorectal cancer cells. (F) Statistical analysis of protein expression in HCT116 colorectal cancer cells. (G) Western blot analysis of the expression of Vimentin and N-cadherin and the expression of E-cadherin in macrophage-pretreated LOVO colorectal cancer cells (n=3). (H) Statistical analysis of protein expression in LOVO colorectal cancer cells. P values were indicated as follows: * p<0.001

Incorrect Figure S2

Fig S2.

DCA promotes macrophages to polarize to M2 phenotype. (A) The levels of IL-6, IL-1β, ARG1, and MRC1 in the cell supernatant of each type of macrophages treated with DCA for 48 hours. (B) Immunofluorescence staining images of CD206, CD86, CD68 and DAPI in different types of macrophages treated with DCA for 48 hours. (C) Statistics of the fluorescence intensity of CD206 and CD86 in different types of macrophages after DCA treatment for 48 hours. (D) The protein expression of TNF-α, IL-1β, IL-10, and TGF-β of macrophages treated with DCA for 48 hours were measured by ELISA kits. (E) Schematic diagram of the establishment of macrophages derived from PBMC and DCA intervention process. (F) Immunofluorescence staining images of CD206, CD86, CD68 and DAPI in different types of macrophages treated with DCA for 48 hours. (G) The protein expression of TNF-α, IL-1β, IL-10, and TGF-β of macrophages treated with DCA for 48 hours were measured by ELISA kits

Correct Figure S2

Fig S2.

DCA promotes macrophages to polarize to M2 phenotype. (A) The levels of IL-6, IL-1β, ARG1, and MRC1 in the cell supernatant of each type of macrophages treated with DCA for 48 hours. (B) Immunofluorescence staining images of CD206, CD86, CD68 and DAPI in different types of macrophages treated with DCA for 48 hours. (C) Statistics of the fluorescence intensity of CD206 and CD86 in different types of macrophages after DCA treatment for 48 hours. (D) The protein expression of TNF-α, IL-1β, IL-10, and TGF-β of macrophages treated with DCA for 48 hours were measured by ELISA kits. (E) Schematic diagram of the establishment of macrophages derived from PBMC and DCA intervention process. (F) Immunofluorescence staining images of CD206, CD86, CD68 and DAPI in different types of macrophages treated with DCA for 48 hours. (G) The protein expression of TNF-α, IL-1β, IL-10, and TGF-β of macrophages treated with DCA for 48 hours were measured by ELISA kits

The original article has been corrected.