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MACC1 regulates the AKT/STAT3 signaling pathway to induce migration, invasion, cancer stemness, and suppress apoptosis in cervical cancer cells

Cervical cancer (CC) ranks as the second most frequent tumor in women, and CC stem cells have been vital in the tumorigenesis of CC. Recently, the metastasis- associated in colon cancer 1 (MACC1) gene was proven to be a promising biomarker of CC. However, the role and mechanism of MACC1 in CC remain...

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Autores principales: Mei, Jie, Zhu, ChengYa, Pan, LiuLiu, Li, Mian
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8805864/
https://www.ncbi.nlm.nih.gov/pubmed/34939526
http://dx.doi.org/10.1080/21655979.2021.2006567
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author Mei, Jie
Zhu, ChengYa
Pan, LiuLiu
Li, Mian
author_facet Mei, Jie
Zhu, ChengYa
Pan, LiuLiu
Li, Mian
author_sort Mei, Jie
collection PubMed
description Cervical cancer (CC) ranks as the second most frequent tumor in women, and CC stem cells have been vital in the tumorigenesis of CC. Recently, the metastasis- associated in colon cancer 1 (MACC1) gene was proven to be a promising biomarker of CC. However, the role and mechanism of MACC1 in CC remain undetermined. Expressions of MACC1 were estimated by qRT-PCR, immunohistochemistry, and Western blot assays in cervical cancer tissues and cells. Three siRNAs were generated to knockdown expressions of MACC1 in CC cells. After knockdown of MACC1 or/and Colivelin treatment, cell migration, invasion, apoptosis, and stemness were evaluated through a series of functional experiments including Transwell, flow cytometry, Hoechst staining, and sphere-formation assays. MACC1 was found to express more highly in CC tissues in comparison with corresponding non-tumor tissues at both mRNA and protein levels. Functionally, the knocking- down of MACC1 significantly repressed migration and invasion, and induced apoptosis of CC cells. Also, knockdown of MACC1 was discovered to suppress sphere-formation of CC cells and downregulate OCT4 and Nanog. It was proved that knockdown of MACC1 had a significant blocking effect on the AKT/STAT3 pathway. In addition, we verified that treatment with the STAT3 activator (Colivelin) had significant reversal effects on the malignant behaviors of CC cells and CC stemness. Our study concluded that MACC1 might be a novel regulator of CC by regulating the AKT/STAT3 pathway to change the migration, invasion, apoptosis, and cancer stemness of CC cells.
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spelling pubmed-88058642022-02-02 MACC1 regulates the AKT/STAT3 signaling pathway to induce migration, invasion, cancer stemness, and suppress apoptosis in cervical cancer cells Mei, Jie Zhu, ChengYa Pan, LiuLiu Li, Mian Bioengineered Research Paper Cervical cancer (CC) ranks as the second most frequent tumor in women, and CC stem cells have been vital in the tumorigenesis of CC. Recently, the metastasis- associated in colon cancer 1 (MACC1) gene was proven to be a promising biomarker of CC. However, the role and mechanism of MACC1 in CC remain undetermined. Expressions of MACC1 were estimated by qRT-PCR, immunohistochemistry, and Western blot assays in cervical cancer tissues and cells. Three siRNAs were generated to knockdown expressions of MACC1 in CC cells. After knockdown of MACC1 or/and Colivelin treatment, cell migration, invasion, apoptosis, and stemness were evaluated through a series of functional experiments including Transwell, flow cytometry, Hoechst staining, and sphere-formation assays. MACC1 was found to express more highly in CC tissues in comparison with corresponding non-tumor tissues at both mRNA and protein levels. Functionally, the knocking- down of MACC1 significantly repressed migration and invasion, and induced apoptosis of CC cells. Also, knockdown of MACC1 was discovered to suppress sphere-formation of CC cells and downregulate OCT4 and Nanog. It was proved that knockdown of MACC1 had a significant blocking effect on the AKT/STAT3 pathway. In addition, we verified that treatment with the STAT3 activator (Colivelin) had significant reversal effects on the malignant behaviors of CC cells and CC stemness. Our study concluded that MACC1 might be a novel regulator of CC by regulating the AKT/STAT3 pathway to change the migration, invasion, apoptosis, and cancer stemness of CC cells. Taylor & Francis 2021-12-23 /pmc/articles/PMC8805864/ /pubmed/34939526 http://dx.doi.org/10.1080/21655979.2021.2006567 Text en © 2021 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
Mei, Jie
Zhu, ChengYa
Pan, LiuLiu
Li, Mian
MACC1 regulates the AKT/STAT3 signaling pathway to induce migration, invasion, cancer stemness, and suppress apoptosis in cervical cancer cells
title MACC1 regulates the AKT/STAT3 signaling pathway to induce migration, invasion, cancer stemness, and suppress apoptosis in cervical cancer cells
title_full MACC1 regulates the AKT/STAT3 signaling pathway to induce migration, invasion, cancer stemness, and suppress apoptosis in cervical cancer cells
title_fullStr MACC1 regulates the AKT/STAT3 signaling pathway to induce migration, invasion, cancer stemness, and suppress apoptosis in cervical cancer cells
title_full_unstemmed MACC1 regulates the AKT/STAT3 signaling pathway to induce migration, invasion, cancer stemness, and suppress apoptosis in cervical cancer cells
title_short MACC1 regulates the AKT/STAT3 signaling pathway to induce migration, invasion, cancer stemness, and suppress apoptosis in cervical cancer cells
title_sort macc1 regulates the akt/stat3 signaling pathway to induce migration, invasion, cancer stemness, and suppress apoptosis in cervical cancer cells
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8805864/
https://www.ncbi.nlm.nih.gov/pubmed/34939526
http://dx.doi.org/10.1080/21655979.2021.2006567
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