Interleukin-27 disrupts the crosstalk of apoptotic activities between 4T1 breast cancer cells and M2 macrophages

Introduction: Cytokine immunotherapy such as Interleukin-27 (IL-27) has been foreseen as a promising alternative anti-cancer treatment. Thus, this study aimed to investigate whether IL-27 gene therapy regulates crosstalk between breast cancer cells and macrophages in the sense of pro-apoptotic activ...

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Main Authors: Mohd Yusof, Nurliyana, Mohamed Noor Fuadi, Natasha Nurafiqah, Hamid, Muhajir, Mohammed Alitheen, Noorjahan Banu, Mohd Hanafi, Nursyuhaida, Nik Abd Rahman, Nik Mohd Afizan
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Published: Universiti Putra Malaysia Press 2022
Online Access:http://psasir.upm.edu.my/id/eprint/101959/
https://medic.upm.edu.my/jurnal_kami/volume_18_2022/mjmhs_vol18_no_6_november_2022-70224
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spelling my.upm.eprints.1019592024-03-15T03:59:04Z http://psasir.upm.edu.my/id/eprint/101959/ Interleukin-27 disrupts the crosstalk of apoptotic activities between 4T1 breast cancer cells and M2 macrophages Mohd Yusof, Nurliyana Mohamed Noor Fuadi, Natasha Nurafiqah Hamid, Muhajir Mohammed Alitheen, Noorjahan Banu Mohd Hanafi, Nursyuhaida Nik Abd Rahman, Nik Mohd Afizan Introduction: Cytokine immunotherapy such as Interleukin-27 (IL-27) has been foreseen as a promising alternative anti-cancer treatment. Thus, this study aimed to investigate whether IL-27 gene therapy regulates crosstalk between breast cancer cells and macrophages in the sense of pro-apoptotic activities. Methods: This study has led to the development of recombinant pcDNA3.4-IL27. The recombinant pcDNA3.4-IL27 was transfected into 4T1 murine mammary carcinoma cells alone and co-culture of 4T1 with M2 macrophages. The successful expression of IL-27 in the cells were determine through the immunofluorescence staining and detection of CD206, M2 macrophages marker. Apoptotic effects of pcDNA3.4-IL27 were assessed through MTT assay, Annexin V flow cytometer analysis, and AO/PI dual staining. Results: Our findings shows that pcDNA3.4-IL27 has the ability to induce apoptosis in both of the cell group and performs better in the co-culture of 4T1 with M2 macrophages compared to 4T1 cells alone. PcDNA3.4-IL27 induced apoptosis through the altered cell morphology and reduction in the number of viable cells. Conclusion: These data demonstrate that pcDNA3.4-IL27 has the ability to induce apoptosis in both 4T1 cell alone and co-cultured 4T1 with M2 macrophages. Thus, could serve as a potential anti cancer candidate against breast cancer. Universiti Putra Malaysia Press 2022-11 Article PeerReviewed Mohd Yusof, Nurliyana and Mohamed Noor Fuadi, Natasha Nurafiqah and Hamid, Muhajir and Mohammed Alitheen, Noorjahan Banu and Mohd Hanafi, Nursyuhaida and Nik Abd Rahman, Nik Mohd Afizan (2022) Interleukin-27 disrupts the crosstalk of apoptotic activities between 4T1 breast cancer cells and M2 macrophages. Malaysian Journal of Medicine and Health Sciences, 18 (6). 125 - 133. ISSN 2636-9346 https://medic.upm.edu.my/jurnal_kami/volume_18_2022/mjmhs_vol18_no_6_november_2022-70224 10.47836/mjmhs18.6.18
institution Universiti Putra Malaysia
building UPM Library
collection Institutional Repository
continent Asia
country Malaysia
content_provider Universiti Putra Malaysia
content_source UPM Institutional Repository
url_provider http://psasir.upm.edu.my/
description Introduction: Cytokine immunotherapy such as Interleukin-27 (IL-27) has been foreseen as a promising alternative anti-cancer treatment. Thus, this study aimed to investigate whether IL-27 gene therapy regulates crosstalk between breast cancer cells and macrophages in the sense of pro-apoptotic activities. Methods: This study has led to the development of recombinant pcDNA3.4-IL27. The recombinant pcDNA3.4-IL27 was transfected into 4T1 murine mammary carcinoma cells alone and co-culture of 4T1 with M2 macrophages. The successful expression of IL-27 in the cells were determine through the immunofluorescence staining and detection of CD206, M2 macrophages marker. Apoptotic effects of pcDNA3.4-IL27 were assessed through MTT assay, Annexin V flow cytometer analysis, and AO/PI dual staining. Results: Our findings shows that pcDNA3.4-IL27 has the ability to induce apoptosis in both of the cell group and performs better in the co-culture of 4T1 with M2 macrophages compared to 4T1 cells alone. PcDNA3.4-IL27 induced apoptosis through the altered cell morphology and reduction in the number of viable cells. Conclusion: These data demonstrate that pcDNA3.4-IL27 has the ability to induce apoptosis in both 4T1 cell alone and co-cultured 4T1 with M2 macrophages. Thus, could serve as a potential anti cancer candidate against breast cancer.
format Article
author Mohd Yusof, Nurliyana
Mohamed Noor Fuadi, Natasha Nurafiqah
Hamid, Muhajir
Mohammed Alitheen, Noorjahan Banu
Mohd Hanafi, Nursyuhaida
Nik Abd Rahman, Nik Mohd Afizan
spellingShingle Mohd Yusof, Nurliyana
Mohamed Noor Fuadi, Natasha Nurafiqah
Hamid, Muhajir
Mohammed Alitheen, Noorjahan Banu
Mohd Hanafi, Nursyuhaida
Nik Abd Rahman, Nik Mohd Afizan
Interleukin-27 disrupts the crosstalk of apoptotic activities between 4T1 breast cancer cells and M2 macrophages
author_facet Mohd Yusof, Nurliyana
Mohamed Noor Fuadi, Natasha Nurafiqah
Hamid, Muhajir
Mohammed Alitheen, Noorjahan Banu
Mohd Hanafi, Nursyuhaida
Nik Abd Rahman, Nik Mohd Afizan
author_sort Mohd Yusof, Nurliyana
title Interleukin-27 disrupts the crosstalk of apoptotic activities between 4T1 breast cancer cells and M2 macrophages
title_short Interleukin-27 disrupts the crosstalk of apoptotic activities between 4T1 breast cancer cells and M2 macrophages
title_full Interleukin-27 disrupts the crosstalk of apoptotic activities between 4T1 breast cancer cells and M2 macrophages
title_fullStr Interleukin-27 disrupts the crosstalk of apoptotic activities between 4T1 breast cancer cells and M2 macrophages
title_full_unstemmed Interleukin-27 disrupts the crosstalk of apoptotic activities between 4T1 breast cancer cells and M2 macrophages
title_sort interleukin-27 disrupts the crosstalk of apoptotic activities between 4t1 breast cancer cells and m2 macrophages
publisher Universiti Putra Malaysia Press
publishDate 2022
url http://psasir.upm.edu.my/id/eprint/101959/
https://medic.upm.edu.my/jurnal_kami/volume_18_2022/mjmhs_vol18_no_6_november_2022-70224
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