ICT1 Promotes Osteosarcoma Cell Proliferation and Inhibits Apoptosis via STAT3/BCL-2 Pathway

Osteosarcoma (OS) is a familiar malignant bone tumor that occurs mainly in adolescents. Immature colon carcinoma transcript-1 (ICT1) is an important member of the large mitoribosomal subunit in mitochondrial ribosomes, which has been shown to be closely related to tumorigenesis. Its expression and f...

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Autores principales: Pan, Xiaohui, Tan, Jingxue, Weng, Xiaokun, Du, Rui, Jiang, Yuqing, Weng, Yiping, Zhou, Dong, Shen, Yifei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2021
Materias:
Research Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7853870/
https://www.ncbi.nlm.nih.gov/pubmed/33585660
http://dx.doi.org/10.1155/2021/8971728
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author Pan, Xiaohui
Tan, Jingxue
Weng, Xiaokun
Du, Rui
Jiang, Yuqing
Weng, Yiping
Zhou, Dong
Shen, Yifei
author_facet Pan, Xiaohui
Tan, Jingxue
Weng, Xiaokun
Du, Rui
Jiang, Yuqing
Weng, Yiping
Zhou, Dong
Shen, Yifei
author_sort Pan, Xiaohui
collection PubMed
description Osteosarcoma (OS) is a familiar malignant bone tumor that occurs mainly in adolescents. Immature colon carcinoma transcript-1 (ICT1) is an important member of the large mitoribosomal subunit in mitochondrial ribosomes, which has been shown to be closely related to tumorigenesis. Its expression and function in OS, however, remained unclear. Here, we showed that ICT1 was significantly upregulated in OS and promoted the growth of OS cells. Mechanistically, ICT1 acted as an oncogene in OS and promoted proliferation and inhibited apoptosis of OS cells through the STAT3/BCL-2 axis. These results reveal a novel insight into the role of the ICT1/STAT3/BCL-2 axis in OS and therefore may represent a novel molecular target for novel treatments.
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spelling pubmed-78538702021-02-11 ICT1 Promotes Osteosarcoma Cell Proliferation and Inhibits Apoptosis via STAT3/BCL-2 Pathway Pan, Xiaohui Tan, Jingxue Weng, Xiaokun Du, Rui Jiang, Yuqing Weng, Yiping Zhou, Dong Shen, Yifei Biomed Res Int Research Article Osteosarcoma (OS) is a familiar malignant bone tumor that occurs mainly in adolescents. Immature colon carcinoma transcript-1 (ICT1) is an important member of the large mitoribosomal subunit in mitochondrial ribosomes, which has been shown to be closely related to tumorigenesis. Its expression and function in OS, however, remained unclear. Here, we showed that ICT1 was significantly upregulated in OS and promoted the growth of OS cells. Mechanistically, ICT1 acted as an oncogene in OS and promoted proliferation and inhibited apoptosis of OS cells through the STAT3/BCL-2 axis. These results reveal a novel insight into the role of the ICT1/STAT3/BCL-2 axis in OS and therefore may represent a novel molecular target for novel treatments. Hindawi 2021-01-22 /pmc/articles/PMC7853870/ /pubmed/33585660 http://dx.doi.org/10.1155/2021/8971728 Text en Copyright © 2021 Xiaohui Pan et al. https://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Pan, Xiaohui
Tan, Jingxue
Weng, Xiaokun
Du, Rui
Jiang, Yuqing
Weng, Yiping
Zhou, Dong
Shen, Yifei
ICT1 Promotes Osteosarcoma Cell Proliferation and Inhibits Apoptosis via STAT3/BCL-2 Pathway
title ICT1 Promotes Osteosarcoma Cell Proliferation and Inhibits Apoptosis via STAT3/BCL-2 Pathway
title_full ICT1 Promotes Osteosarcoma Cell Proliferation and Inhibits Apoptosis via STAT3/BCL-2 Pathway
title_fullStr ICT1 Promotes Osteosarcoma Cell Proliferation and Inhibits Apoptosis via STAT3/BCL-2 Pathway
title_full_unstemmed ICT1 Promotes Osteosarcoma Cell Proliferation and Inhibits Apoptosis via STAT3/BCL-2 Pathway
title_short ICT1 Promotes Osteosarcoma Cell Proliferation and Inhibits Apoptosis via STAT3/BCL-2 Pathway
title_sort ict1 promotes osteosarcoma cell proliferation and inhibits apoptosis via stat3/bcl-2 pathway
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7853870/
https://www.ncbi.nlm.nih.gov/pubmed/33585660
http://dx.doi.org/10.1155/2021/8971728
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