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Cancers
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  • Open Access

22 January 2025

Correction: Panneerselvam et al. Inflammatory Mediators and Gut Microbial Toxins Drive Colon Tumorigenesis by IL-23 Dependent Mechanism. Cancers 2021, 13, 5159

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1
Center for Cancer Prevention and Drug Development, The University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA
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Stephenson Cancer Center, The University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA
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Department of Medicine, The University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA
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Department of Surgery, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA
This article belongs to the Special Issue Tumor, Tumor-Associated Macrophages, and Therapy

Error in Figure

In the original publication [1], there was a mistake in Figures 5F and 6A as published. One of the images in Figure 4F was inadvertently duplicated in Figure 5F during our figure preparation process. A similar error was also noted between Figure 6A,D. The corrected Figure 5 and Figure 6 appear below. The authors state that the scientific conclusions are unaffected. This correction was approved by the Academic Editor. The original publication has also been updated.
Figure 5. IL-23 production by macrophages enhances colon tumor cell aggressiveness. (A) The level of IL-23 in the spent media of the co-culture system (Caco2/HCT116 + educated macrophages with AA/PGE2/LTA/LPS) was measured using ELISA. (B) The expression of IL-23R, IL-17A were analyzed in Caco2 and HCT116 cells co-cultured with educated macrophages compared to uneducated macrophages. Lane1-Vehicle control, Lane2-AA, Lane3- PGE2, Lane4- Vehicle control, Lane5- LTA, Lane6- LPS. β-actin was used as a protein loading control. (C) Co-culture of educated macrophages with tumor cells increased the self-renewal ability of cancer cells compared with uneducated macrophages co-culture system (Magnification 40×). (D,E) Quantification of organoids formed by tumor cells co-cultured with educated macrophages compared to uneducated macrophages. (F) Migration and invasion assay showed that tumor cells co-cultured with educated macrophages increased migration and invasion compared to uneducated macrophages (Magnification 10×). (G,H) Quantification of the number of migrated and invaded cells. All experiments were performed a minimum of three times. Bars denote standard deviation (SD). * p < 0.05, ** p < 0.01, and *** p < 0.001 were considered statistically significant.
Figure 6. Inhibition of IL-23 in DCs and macrophages reduced colon tumor cell self-renewal. (A,D) Effect of siRNA knockdown of IL-23 in educated DCs and macrophages on the self-renewal ability of co-cultured Caco2 and HCT116 cells compared to scramble siRNA and scramble siRNA + PGE2 stimulated immune cells (Magnification 40×). (B,C,E,F) Quantification of organoids formed per well by tumor cells co-cultured with siIL-23 treated and educated DCs and macrophages compared to scramble siRNA treated and uneducated macrophages. #-compared with siScramble; @-compared with siScramble + PGE2; $-compared with siIL-23. All experiments were performed a minimum of three times. Bars denote standard deviation (SD).

Reference

  1. Panneerselvam, J.; Madka, V.; Rai, R.; Morris, K.T.; Houchen, C.W.; Chandrakesan, P.; Rao, C.V. Inflammatory Mediators and Gut Microbial Toxins Drive Colon Tumorigenesis by IL-23 Dependent Mechanism. Cancers 2021, 13, 5159. [Google Scholar] [CrossRef] [PubMed]
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