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shRNA‑mediated knockdown of KNTC1 inhibits non-small-cell lung cancer through regulating PSMB8
In view of the important roles played by Kinetochore proteins in mitosis, we believed that they may contribute to the development and progression of human cancers, which has been reported recently elsewhere. Kinetochore-associated 1 (KNTC1) participates in the segregation of sister chromatids during...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9357013/ https://www.ncbi.nlm.nih.gov/pubmed/35933405 http://dx.doi.org/10.1038/s41419-022-05140-w |
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author | Liu, Ruijun Liu, Ruili Guo, Zhiyi Ren, Jianghao Huang, Jia Luo, Qingquan Tan, Qiang |
author_facet | Liu, Ruijun Liu, Ruili Guo, Zhiyi Ren, Jianghao Huang, Jia Luo, Qingquan Tan, Qiang |
author_sort | Liu, Ruijun |
collection | PubMed |
description | In view of the important roles played by Kinetochore proteins in mitosis, we believed that they may contribute to the development and progression of human cancers, which has been reported recently elsewhere. Kinetochore-associated 1 (KNTC1) participates in the segregation of sister chromatids during mitosis, the effects of which on non-small-cell lung cancer (NSCLC) remain unclear. Here, we sought to identify the biological significance of KNTC1 in NSCLC. KNTC1 protein expression in NSCLC tissues was investigated by immunohistochemistry. Lentivirus delivered short hairpin RNA (shRNA) was utilized to establish KNTC1 silence NSCLC cell lines. The effects of KNTC1 depletion on NSCLC cell proliferation, migration, apoptosis, and tumor formation were analyzed by MTT assay, wound-healing assay, transwell assay, flow cytometry assay, and in nude mouse models in vivo. After KNTC1 reduction, NSCLC cell viability, proliferation, migration, and invasion were restrained. A xenograft tumor model was also provided to demonstrate the inhibited tumorigenesis in NSCLC. In addition, the downstream mechanism analysis indicated that KNTC1 depletion was positively associated with PSMB8. The findings of the present study suggested that KNTC1 may have a pivotal role in mediating NSCLC progression and may act as a novel therapeutic target for NSCLC. |
format | Online Article Text |
id | pubmed-9357013 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-93570132022-08-08 shRNA‑mediated knockdown of KNTC1 inhibits non-small-cell lung cancer through regulating PSMB8 Liu, Ruijun Liu, Ruili Guo, Zhiyi Ren, Jianghao Huang, Jia Luo, Qingquan Tan, Qiang Cell Death Dis Article In view of the important roles played by Kinetochore proteins in mitosis, we believed that they may contribute to the development and progression of human cancers, which has been reported recently elsewhere. Kinetochore-associated 1 (KNTC1) participates in the segregation of sister chromatids during mitosis, the effects of which on non-small-cell lung cancer (NSCLC) remain unclear. Here, we sought to identify the biological significance of KNTC1 in NSCLC. KNTC1 protein expression in NSCLC tissues was investigated by immunohistochemistry. Lentivirus delivered short hairpin RNA (shRNA) was utilized to establish KNTC1 silence NSCLC cell lines. The effects of KNTC1 depletion on NSCLC cell proliferation, migration, apoptosis, and tumor formation were analyzed by MTT assay, wound-healing assay, transwell assay, flow cytometry assay, and in nude mouse models in vivo. After KNTC1 reduction, NSCLC cell viability, proliferation, migration, and invasion were restrained. A xenograft tumor model was also provided to demonstrate the inhibited tumorigenesis in NSCLC. In addition, the downstream mechanism analysis indicated that KNTC1 depletion was positively associated with PSMB8. The findings of the present study suggested that KNTC1 may have a pivotal role in mediating NSCLC progression and may act as a novel therapeutic target for NSCLC. Nature Publishing Group UK 2022-08-06 /pmc/articles/PMC9357013/ /pubmed/35933405 http://dx.doi.org/10.1038/s41419-022-05140-w Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Article Liu, Ruijun Liu, Ruili Guo, Zhiyi Ren, Jianghao Huang, Jia Luo, Qingquan Tan, Qiang shRNA‑mediated knockdown of KNTC1 inhibits non-small-cell lung cancer through regulating PSMB8 |
title | shRNA‑mediated knockdown of KNTC1 inhibits non-small-cell lung cancer through regulating PSMB8 |
title_full | shRNA‑mediated knockdown of KNTC1 inhibits non-small-cell lung cancer through regulating PSMB8 |
title_fullStr | shRNA‑mediated knockdown of KNTC1 inhibits non-small-cell lung cancer through regulating PSMB8 |
title_full_unstemmed | shRNA‑mediated knockdown of KNTC1 inhibits non-small-cell lung cancer through regulating PSMB8 |
title_short | shRNA‑mediated knockdown of KNTC1 inhibits non-small-cell lung cancer through regulating PSMB8 |
title_sort | shrna‑mediated knockdown of kntc1 inhibits non-small-cell lung cancer through regulating psmb8 |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9357013/ https://www.ncbi.nlm.nih.gov/pubmed/35933405 http://dx.doi.org/10.1038/s41419-022-05140-w |
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