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The interferon regulatory factor 6 promotes cisplatin sensitivity in colorectal cancer
Colorectal cancer (CRC) is one of the most common malignancies and causes of cancer-related mortality worldwide. Cell proliferation and tumor metastasis as well as chemoresistance are correlated with poor survival of CRC. The interferon regulatory factor 6 (IRF6) is functioned as a tumor suppressor...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Taylor & Francis
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9161955/ https://www.ncbi.nlm.nih.gov/pubmed/35443865 http://dx.doi.org/10.1080/21655979.2022.2062103 |
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author | Tan, Lin Qu, Weiming Wu, Dajun Liu, Minji Ai, Qiongjia Hu, Hongsai Wang, Qian Chen, Weishun Zhou, Hongbing |
author_facet | Tan, Lin Qu, Weiming Wu, Dajun Liu, Minji Ai, Qiongjia Hu, Hongsai Wang, Qian Chen, Weishun Zhou, Hongbing |
author_sort | Tan, Lin |
collection | PubMed |
description | Colorectal cancer (CRC) is one of the most common malignancies and causes of cancer-related mortality worldwide. Cell proliferation and tumor metastasis as well as chemoresistance are correlated with poor survival of CRC. The interferon regulatory factor 6 (IRF6) is functioned as a tumor suppressor gene in several cancers and is associated with risk of CRC. We explored the role of IRF6 in CRC in the present study. The protein expressions of IRF6 in human CRC tissues, normal para-carcinoma tissue and liver metastases from CRC were measured. Cell proliferation, chemotherapeutic sensitivity, cell apoptosis, migration and invasion including the related markers along with IRF6 expression were explored. Our results indicated that IRF6 expression in CRC and liver metastasis were lower than normal tissues, which were correlated positively with E-cadherin and negatively with Ki67 expression in CRC tissue. IRF6 promoted CRC cell sensitivity to cisplatin to suppress cell proliferation, migration and invasion as well as aggravate cell apoptosis. Our study suggested that IRF6 may enhance chemotherapeutic sensitivity of cisplatin mediated by affecting cell proliferation, migration and invasion along with apoptosis through regulating E-cadherin and Ki67, while the identified molecular mechanisms remain to be further explored. |
format | Online Article Text |
id | pubmed-9161955 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Taylor & Francis |
record_format | MEDLINE/PubMed |
spelling | pubmed-91619552022-06-03 The interferon regulatory factor 6 promotes cisplatin sensitivity in colorectal cancer Tan, Lin Qu, Weiming Wu, Dajun Liu, Minji Ai, Qiongjia Hu, Hongsai Wang, Qian Chen, Weishun Zhou, Hongbing Bioengineered Research Paper Colorectal cancer (CRC) is one of the most common malignancies and causes of cancer-related mortality worldwide. Cell proliferation and tumor metastasis as well as chemoresistance are correlated with poor survival of CRC. The interferon regulatory factor 6 (IRF6) is functioned as a tumor suppressor gene in several cancers and is associated with risk of CRC. We explored the role of IRF6 in CRC in the present study. The protein expressions of IRF6 in human CRC tissues, normal para-carcinoma tissue and liver metastases from CRC were measured. Cell proliferation, chemotherapeutic sensitivity, cell apoptosis, migration and invasion including the related markers along with IRF6 expression were explored. Our results indicated that IRF6 expression in CRC and liver metastasis were lower than normal tissues, which were correlated positively with E-cadherin and negatively with Ki67 expression in CRC tissue. IRF6 promoted CRC cell sensitivity to cisplatin to suppress cell proliferation, migration and invasion as well as aggravate cell apoptosis. Our study suggested that IRF6 may enhance chemotherapeutic sensitivity of cisplatin mediated by affecting cell proliferation, migration and invasion along with apoptosis through regulating E-cadherin and Ki67, while the identified molecular mechanisms remain to be further explored. Taylor & Francis 2022-04-20 /pmc/articles/PMC9161955/ /pubmed/35443865 http://dx.doi.org/10.1080/21655979.2022.2062103 Text en © 2022 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Paper Tan, Lin Qu, Weiming Wu, Dajun Liu, Minji Ai, Qiongjia Hu, Hongsai Wang, Qian Chen, Weishun Zhou, Hongbing The interferon regulatory factor 6 promotes cisplatin sensitivity in colorectal cancer |
title | The interferon regulatory factor 6 promotes cisplatin sensitivity in colorectal cancer |
title_full | The interferon regulatory factor 6 promotes cisplatin sensitivity in colorectal cancer |
title_fullStr | The interferon regulatory factor 6 promotes cisplatin sensitivity in colorectal cancer |
title_full_unstemmed | The interferon regulatory factor 6 promotes cisplatin sensitivity in colorectal cancer |
title_short | The interferon regulatory factor 6 promotes cisplatin sensitivity in colorectal cancer |
title_sort | interferon regulatory factor 6 promotes cisplatin sensitivity in colorectal cancer |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9161955/ https://www.ncbi.nlm.nih.gov/pubmed/35443865 http://dx.doi.org/10.1080/21655979.2022.2062103 |
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