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Mast Cell Targeted Chimeric Toxin Can Be Developed as an Adjunctive Therapy in Colon Cancer Treatment

Wang, Shan, Li, Linmei, Shi, Renren, Liu, Xueting, Zhang, Junyan, Zou, Zehong, Hao, Zhuofang, Tao, Ailin·2016·Toxins
DOI 10.3390/toxins8030071PMC PMC4810216
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Abstract

The association of colitis with colorectal cancer has become increasingly clear with mast cells being identified as important inflammatory cells in the process. In view of the relationship between mast cells and cancer, we studied the effect and mechanisms of mast cells in the development of colon cancer. Functional and mechanistic insights were gained from ex vivo and in vivo studies of cell interactions between mast cells and CT26 cells. Further evidence was reversely obtained in studies of mast cell targeted Fcε-PE40 chimeric toxin. Experiments revealed mast cells could induce colon tumor cell proliferation and invasion. Cancer progression was found to be related to the density of mast cells in colonic submucosa. The activation of MAPK, Rho-GTPase, and STAT pathways in colon cancer cells was triggered by mast cells during cell-to-cell interaction. Lastly, using an Fcε-PE40 chimeric toxin we constructed, we confirmed the promoting effect of mast cells in development of colon cancer. Mast cells are a promoting factor of colon cancer and thus also a potential therapeutic target. The Fcε-PE40 chimeric toxin targeting mast cells could effectively prevent colon cancer in vitro and in vivo. Consequently, these data may demonstrate a novel immunotherapeutic approach for the treatment of tumors.

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Figure 1 Mast cell infiltration relates with colon cancer development. (A) Immunohistochemistry-stained pictures of CD117 and tryptase show mast cells infiltration in different colonic tumor tissues. Magnification, ×400. Scale bar, 100 μm. (B) Mast cell counts carried out on tryptase Immunohistochemistry-stained colonic tumor sections in per 400× field. Tumor tissues are characterized by colonic adenoma, well differentiated adenocarcinoma, and poor differentiated adenocarcinoma. (C) Mast cell counts carried out on tryptase immunohistochemistry-stained colonic tumor sections. Tumor tissues are characterized by non-metastatic colon cancer and metastatic colon cancer. Arrows indicate mast cells.
Figure 1 Mast cell infiltration relates with colon cancer development. (A) Immunohistochemistry-stained pictures of CD117 and tryptase show mast cells infiltration in different colonic tumor tissues. Magnification, ×400. Scale bar, 100 μm. (B) Mast cell counts carried out on tryptase Immunohistochemistry-stained colonic tumor sections in per 400× field. Tumor tissues are characterized by colonic adenoma, well differentiated adenocarcinoma, and poor differentiated adenocarcinoma. (C) Mast cell counts carried out on tryptase immunohistochemistry-stained colonic tumor sections. Tumor tissues are characterized by non-metastatic colon cancer and metastatic colon cancer. Arrows indicate mast cells.CC BY · PubMed Central
Figure 2 Piecemeal degranulation of mast cells can promote colon cancer cell proliferation and migration. (A) Toluidine blue staining of bone marrow-derived mast cells induced for 4 weeks and 6 weeks. Arrows indicate mature mast cells enriching with granules. Magnification, ×1000, Scale bar, 20 μm. (B) Histogram of bone marrow-derived mast cells (BMMCs) induced for 4 weeks and 6 weeks. Mast cells were identified by flow cytometry as CD117+ cells which were 13.9% at 4 weeks and 76.7% at 6 weeks. (C) Histamine release analysis shows bone marrow-derived mast cell “piecemeal degranulation” without stimulation and Calcium Ionophore (CaIO) makes bone marrow-derived mast cells degranulation with a dose-dependent way. (D) Quantification of CT26 cells proliferation cultured with or without BMMCs after 48 h by MTS. (E,F) The wound healing assay showed different cell migration in CT26 cells and CT26 cells co-cultured with BMMCs. (E) Representative images were taken at different time points. (F) Quantification of CT26 cells migration by measuring the wound width. The amount of motility was expressed as a percent of migration at the time point 0. ** p < 0.01; and *** p < 0.001.
Figure 2 Piecemeal degranulation of mast cells can promote colon cancer cell proliferation and migration. (A) Toluidine blue staining of bone marrow-derived mast cells induced for 4 weeks and 6 weeks. Arrows indicate mature mast cells enriching with granules. Magnification, ×1000, Scale bar, 20 μm. (B) Histogram of bone marrow-derived mast cells (BMMCs) induced for 4 weeks and 6 weeks. Mast cells were identified by flow cytometry as CD117+ cells which were 13.9% at 4 weeks and 76.7% at 6 weeks. (C) Histamine release analysis shows bone marrow-derived mast cell “piecemeal degranulation” without stimulation and Calcium Ionophore (CaIO) makes bone marrow-derived mast cells degranulation with a dose-dependent way. (D) Quantification of CT26 cells proliferation cultured with or without BMMCs after 48 h by MTS. (E,F) The wound healing assay showed different cell migration in CT26 cells and CT26 cells co-cultured with BMMCs. (E) Representative images were taken at different time points. (F) Quantification of CT26 cells migration by measuring the wound width. The amount of motility was expressed as a percent of migration at the time point 0. ** p < 0.01; and *** p < 0.001.CC BY · PubMed Central
Figure 3 Mast cells up-regulate the expression of RhoA and VEGFc in colon cancer cells. (A) Western blotting analysis of the expression levels of RhoA in CT26 cells with different stimulation conditions. (B,C) RT-PCR analysis detected the VEGF-A/B/C and TGF-β expression in CT26 cells with or without BMMCs co-cultured.
Figure 3 Mast cells up-regulate the expression of RhoA and VEGFc in colon cancer cells. (A) Western blotting analysis of the expression levels of RhoA in CT26 cells with different stimulation conditions. (B,C) RT-PCR analysis detected the VEGF-A/B/C and TGF-β expression in CT26 cells with or without BMMCs co-cultured.CC BY · PubMed Central
Figure 4 MAPK/Rho-GTPase/STATs pathways participate in the regulation mechanism of mast cells function to colon cancer cells. (A) CT26 cells were co-cultured with BMMCs for different time. Suspended BMMCs were then washed out and CT26 cells were further processed to cell lysates for western blotting analysis. Western blotting analysis detected the phosphorylation of signaling proteins in CT26 cells after BMMCs stimulation, including ERK 1/2, P38 MAPK, JNK/SAPK, and Rac1. (B) Western blotting analysis detected the phosphorylation of STATs pathway signaling protein in CT26 cells after BMMCs stimulation, including STAT3, STAT5 and STAT6. (C) Relative quantization of the pathways activation included Figure 4A,B during BMMCs stimulation. The band intensity was quantized by the Quantity One.
Figure 4 MAPK/Rho-GTPase/STATs pathways participate in the regulation mechanism of mast cells function to colon cancer cells. (A) CT26 cells were co-cultured with BMMCs for different time. Suspended BMMCs were then washed out and CT26 cells were further processed to cell lysates for western blotting analysis. Western blotting analysis detected the phosphorylation of signaling proteins in CT26 cells after BMMCs stimulation, including ERK 1/2, P38 MAPK, JNK/SAPK, and Rac1. (B) Western blotting analysis detected the phosphorylation of STATs pathway signaling protein in CT26 cells after BMMCs stimulation, including STAT3, STAT5 and STAT6. (C) Relative quantization of the pathways activation included Figure 4A,B during BMMCs stimulation. The band intensity was quantized by the Quantity One.CC BY · PubMed Central
Figure 5 Mast cell targeted Fcε-PE40 chimeric toxin induce mast cells apoptosis without degranulation. (A) The purity and concentration of recombinant protein Fcε-PE40 chimeric toxin were measured by 12% SDS-PAGE (arrow indicating). (B) The protein Fcε (17 KD) and Fcε-PE40 chimeric toxin (55 KD) were verified by western blotting with Pseudomonas Exotoxin A antibody (a) and mouse IgE antibody (b). (C) Images show the growth of CT26 cells and BMMCs with or without Fcε-PE40 chimeric toxin (1 μg/mL) after 24 h. Magnification, ×100. Scale bar, 100 μm. (D) Cell death dose dependent curves after CT26 cells and BMMCs co-cultured with Fcε-PE40 for 24 h were assessed by MTS assay. (E) Mast cells’ degranulation after treated by Fcε-PE40 for 24 h was assessed by histamine release analysis. (F) Expression level of cleaved caspase3 in CT26 cells and BMMCs co-cultured with Fcε-PE40 for 24 h was detected by western blotting.
Figure 5 Mast cell targeted Fcε-PE40 chimeric toxin induce mast cells apoptosis without degranulation. (A) The purity and concentration of recombinant protein Fcε-PE40 chimeric toxin were measured by 12% SDS-PAGE (arrow indicating). (B) The protein Fcε (17 KD) and Fcε-PE40 chimeric toxin (55 KD) were verified by western blotting with Pseudomonas Exotoxin A antibody (a) and mouse IgE antibody (b). (C) Images show the growth of CT26 cells and BMMCs with or without Fcε-PE40 chimeric toxin (1 μg/mL) after 24 h. Magnification, ×100. Scale bar, 100 μm. (D) Cell death dose dependent curves after CT26 cells and BMMCs co-cultured with Fcε-PE40 for 24 h were assessed by MTS assay. (E) Mast cells’ degranulation after treated by Fcε-PE40 for 24 h was assessed by histamine release analysis. (F) Expression level of cleaved caspase3 in CT26 cells and BMMCs co-cultured with Fcε-PE40 for 24 h was detected by western blotting.CC BY · PubMed Central
Figure 6 Mast cells targeted Fcε-PE40 chimeric toxin can assist colon cancer control in vivo. (A) Tumor growth in mice implanted with CT26 cells and CT26 cells together with BMMCs. Tumor growth is measured by the weight of solid tumor mass. (B) Solid tumor masses obtained from mice implanted with CT26 cells and CT26 cells together with BMMCs. (C) H & E staining and Immunohistochemistry of tryptase sections of tumor mass implanted with CT26 cells and CT26 cells together with BMMCs. Arrows indicate mast cells rich in tryptase in tumor tissues. Scale bar, 50 μm. (D) Determination of the tumor growth. Tumor weight was calculated 4 weeks after injection. (E) Representative image for tumor growth is shown. BAL B/C mice were subcutaneously injected with 2.0 × 106 CT26 cells. Fcε-PE40 chimeric toxin was injected after 2 weeks. * p < 0.05; ** p < 0.01.
Figure 6 Mast cells targeted Fcε-PE40 chimeric toxin can assist colon cancer control in vivo. (A) Tumor growth in mice implanted with CT26 cells and CT26 cells together with BMMCs. Tumor growth is measured by the weight of solid tumor mass. (B) Solid tumor masses obtained from mice implanted with CT26 cells and CT26 cells together with BMMCs. (C) H & E staining and Immunohistochemistry of tryptase sections of tumor mass implanted with CT26 cells and CT26 cells together with BMMCs. Arrows indicate mast cells rich in tryptase in tumor tissues. Scale bar, 50 μm. (D) Determination of the tumor growth. Tumor weight was calculated 4 weeks after injection. (E) Representative image for tumor growth is shown. BAL B/C mice were subcutaneously injected with 2.0 × 106 CT26 cells. Fcε-PE40 chimeric toxin was injected after 2 weeks. * p < 0.05; ** p < 0.01.CC BY · PubMed Central

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Metadata

Authors
Wang, S., Li, L., Shi, R., Liu, X., Zhang, J., Zou, Z., Hao, Z., & Tao, A.
Affiliations
  • The Second Affiliated Hospital of Guangzhou Medical University, Guangdong Provincial Key Laboratory of Allergy &amp; Clinical Immunology, The State Key Clinical Specialty in Allergy, The State Key Laboratory of Respiratory Disease; Guangzhou 510260, China
  • The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou 510260, China
Venue
Toxins
Publisher
MDPI AG
Published
2016-03-11
Volume
8
Issue
3
Pages
71
ISSN
2072-6651
DOI
10.3390/toxins8030071
PMC
PMC4810216
Cited by
17
References
2
Language
en
Licence
creativecommons.org/licenses/by/4.0/ (vor)
Funders
  • the National Natural Science Foundation of China (81373128, 81402025)
  • Guangdong provincal public welfare research and capacity building special fundation (2014A020212363)

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CoChat. (2026). Citation check: Mast Cell Targeted Chimeric Toxin Can Be Developed as an Adjunctive Therapy in Colon Cancer Treatment. https://app.cochat.ai/papers/10.3390/toxins8030071
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Wang, S., Li, L., Shi, R., Liu, X., Zhang, J., Zou, Z., Hao, Z., & Tao, A. (2016). Mast Cell Targeted Chimeric Toxin Can Be Developed as an Adjunctive Therapy in Colon Cancer Treatment. Toxins. https://doi.org/10.3390/toxins8030071