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CLPTM1L Is a Novel Putative Oncogene Promoting Tumorigenesis in Oral Squamous Cell Carcinoma
This study aimed to explore the function of CLPTM1L in oral squamous cell carcinoma and mechanism of tumorigenesis. The expression of CLPTM1L was detected by immunohistochemistry. The localization in cells was detected by immunofluorescence. Cell invasion, proliferation, and migration were detected...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
SAGE Publications
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8485279/ https://www.ncbi.nlm.nih.gov/pubmed/34586883 http://dx.doi.org/10.1177/09636897211045970 |
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author | Hou, Yunwen Xue, Feifei Fu, Yu Feng, Guanying Wang, Ruixia Yuan, Hua |
author_facet | Hou, Yunwen Xue, Feifei Fu, Yu Feng, Guanying Wang, Ruixia Yuan, Hua |
author_sort | Hou, Yunwen |
collection | PubMed |
description | This study aimed to explore the function of CLPTM1L in oral squamous cell carcinoma and mechanism of tumorigenesis. The expression of CLPTM1L was detected by immunohistochemistry. The localization in cells was detected by immunofluorescence. Cell invasion, proliferation, and migration were detected by transwell, CCK-8 and scratch-wound test. The possible characteristics of CLPTM1L were analysed in TCGA, GO, KEGG and String databases. IHC revealed that the expression of CLPTM1L in 92 cases of OSCC tissues was significantly higher (P < 0.01) than 29 cases of normal oral epithelium tissues. The expression of CLPTM1L was significantly higher in oral squamous cell carcinoma in TCGA database. CLPTM1L expression was not significantly correlated with the patients’ clinical parameters. High expression of CLPTM1L was associated with worse prognosis. Cox regression analysis demonstrated that the CLPTM1L expression was the significant risk factor. CLPTM1L was mainly localized in the perinuclear cytoplasm. The vitro studies revealed that the knockdown of CLPTM1L suppressed invasion, proliferation and migration. CLPTM1L related genes were enriched in protein processing in the endoplasmic reticulum, protein folding, endoplasmic reticulum formation, N-glycan biosynthesis, and protein hydroxylation. Highly expressed CLPTM1L may contribute to a poor prognosis and increase invasion, proliferation and migration of oral squamous cell carcinoma. CLPTM1L may play an important role in tumorgenesis and would be a valuable target gene for the treatment of oral squamous cell carcinoma. |
format | Online Article Text |
id | pubmed-8485279 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | SAGE Publications |
record_format | MEDLINE/PubMed |
spelling | pubmed-84852792021-10-02 CLPTM1L Is a Novel Putative Oncogene Promoting Tumorigenesis in Oral Squamous Cell Carcinoma Hou, Yunwen Xue, Feifei Fu, Yu Feng, Guanying Wang, Ruixia Yuan, Hua Cell Transplant Original Article This study aimed to explore the function of CLPTM1L in oral squamous cell carcinoma and mechanism of tumorigenesis. The expression of CLPTM1L was detected by immunohistochemistry. The localization in cells was detected by immunofluorescence. Cell invasion, proliferation, and migration were detected by transwell, CCK-8 and scratch-wound test. The possible characteristics of CLPTM1L were analysed in TCGA, GO, KEGG and String databases. IHC revealed that the expression of CLPTM1L in 92 cases of OSCC tissues was significantly higher (P < 0.01) than 29 cases of normal oral epithelium tissues. The expression of CLPTM1L was significantly higher in oral squamous cell carcinoma in TCGA database. CLPTM1L expression was not significantly correlated with the patients’ clinical parameters. High expression of CLPTM1L was associated with worse prognosis. Cox regression analysis demonstrated that the CLPTM1L expression was the significant risk factor. CLPTM1L was mainly localized in the perinuclear cytoplasm. The vitro studies revealed that the knockdown of CLPTM1L suppressed invasion, proliferation and migration. CLPTM1L related genes were enriched in protein processing in the endoplasmic reticulum, protein folding, endoplasmic reticulum formation, N-glycan biosynthesis, and protein hydroxylation. Highly expressed CLPTM1L may contribute to a poor prognosis and increase invasion, proliferation and migration of oral squamous cell carcinoma. CLPTM1L may play an important role in tumorgenesis and would be a valuable target gene for the treatment of oral squamous cell carcinoma. SAGE Publications 2021-09-29 /pmc/articles/PMC8485279/ /pubmed/34586883 http://dx.doi.org/10.1177/09636897211045970 Text en © The Author(s) 2021 https://creativecommons.org/licenses/by-nc/4.0/This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage). |
spellingShingle | Original Article Hou, Yunwen Xue, Feifei Fu, Yu Feng, Guanying Wang, Ruixia Yuan, Hua CLPTM1L Is a Novel Putative Oncogene Promoting Tumorigenesis in Oral Squamous Cell Carcinoma |
title | CLPTM1L Is a Novel Putative Oncogene Promoting Tumorigenesis in Oral Squamous Cell Carcinoma |
title_full | CLPTM1L Is a Novel Putative Oncogene Promoting Tumorigenesis in Oral Squamous Cell Carcinoma |
title_fullStr | CLPTM1L Is a Novel Putative Oncogene Promoting Tumorigenesis in Oral Squamous Cell Carcinoma |
title_full_unstemmed | CLPTM1L Is a Novel Putative Oncogene Promoting Tumorigenesis in Oral Squamous Cell Carcinoma |
title_short | CLPTM1L Is a Novel Putative Oncogene Promoting Tumorigenesis in Oral Squamous Cell Carcinoma |
title_sort | clptm1l is a novel putative oncogene promoting tumorigenesis in oral squamous cell carcinoma |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8485279/ https://www.ncbi.nlm.nih.gov/pubmed/34586883 http://dx.doi.org/10.1177/09636897211045970 |
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