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High expression of RAB38 promotes malignant progression of pancreatic cancer
Ras-Related Protein Rab-38 (RAB38), which belongs to the RAB family, is involved in the biogenesis of lysosome-related organelles and defense against certain microbial infections. However, the clinical significance and potential function of RAB38 in pancreatic adenocarcinoma remain unclear. In the p...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6323198/ https://www.ncbi.nlm.nih.gov/pubmed/30569114 http://dx.doi.org/10.3892/mmr.2018.9732 |
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author | Li, Bao-Yu He, Li-Jie Zhang, Xiang-Lian Liu, Hui Liu, Bin |
author_facet | Li, Bao-Yu He, Li-Jie Zhang, Xiang-Lian Liu, Hui Liu, Bin |
author_sort | Li, Bao-Yu |
collection | PubMed |
description | Ras-Related Protein Rab-38 (RAB38), which belongs to the RAB family, is involved in the biogenesis of lysosome-related organelles and defense against certain microbial infections. However, the clinical significance and potential function of RAB38 in pancreatic adenocarcinoma remain unclear. In the present study, an immunohistochemical assay was performed to analyze the expression of RAB38 in pancreatic adenocarcinoma tumor specimens from 82 patients, and the clinicopathological characteristics and survival rate of these patients were further examined. To validate the role of RAB38 in tumors, the effect of RAB38 on tumor cell proliferation, migration and invasion was assessed by establishing RAB38 knockdown cell lines. Reverse transcription-quantitative polymerase chain reaction and western blotting were used to examine the expression levels of proteins associated with the cancer cell behavior. In addition, the inhibitory effect of RAB38 silencing on pancreatic cancer was examined in mice. The immunohistochemistry results revealed that RAB38 was upregulated and positively correlated with the grade of progression in pancreatic adenocarcinoma patients. Further investigation indicated that RAB38 downregulation significantly suppressed the proliferation, migration and invasive capacity of pancreatic cancer cells, as well as decreased the expression levels of Ki67, proliferating cell nuclear antigen, and matrix metalloproteinases 2 and 9. RAB38 silencing also inhibited the development of pancreatic cancer in vivo. Taken together, a high level of RAB38 was significantly associated with the malignant phenotypes of pancreatic cancer, suggesting that RAB38 may serve as a novel biomarker and a potential therapeutic target for pancreatic cancer. |
format | Online Article Text |
id | pubmed-6323198 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-63231982019-01-15 High expression of RAB38 promotes malignant progression of pancreatic cancer Li, Bao-Yu He, Li-Jie Zhang, Xiang-Lian Liu, Hui Liu, Bin Mol Med Rep Articles Ras-Related Protein Rab-38 (RAB38), which belongs to the RAB family, is involved in the biogenesis of lysosome-related organelles and defense against certain microbial infections. However, the clinical significance and potential function of RAB38 in pancreatic adenocarcinoma remain unclear. In the present study, an immunohistochemical assay was performed to analyze the expression of RAB38 in pancreatic adenocarcinoma tumor specimens from 82 patients, and the clinicopathological characteristics and survival rate of these patients were further examined. To validate the role of RAB38 in tumors, the effect of RAB38 on tumor cell proliferation, migration and invasion was assessed by establishing RAB38 knockdown cell lines. Reverse transcription-quantitative polymerase chain reaction and western blotting were used to examine the expression levels of proteins associated with the cancer cell behavior. In addition, the inhibitory effect of RAB38 silencing on pancreatic cancer was examined in mice. The immunohistochemistry results revealed that RAB38 was upregulated and positively correlated with the grade of progression in pancreatic adenocarcinoma patients. Further investigation indicated that RAB38 downregulation significantly suppressed the proliferation, migration and invasive capacity of pancreatic cancer cells, as well as decreased the expression levels of Ki67, proliferating cell nuclear antigen, and matrix metalloproteinases 2 and 9. RAB38 silencing also inhibited the development of pancreatic cancer in vivo. Taken together, a high level of RAB38 was significantly associated with the malignant phenotypes of pancreatic cancer, suggesting that RAB38 may serve as a novel biomarker and a potential therapeutic target for pancreatic cancer. D.A. Spandidos 2019-02 2018-12-10 /pmc/articles/PMC6323198/ /pubmed/30569114 http://dx.doi.org/10.3892/mmr.2018.9732 Text en Copyright: © Li et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Li, Bao-Yu He, Li-Jie Zhang, Xiang-Lian Liu, Hui Liu, Bin High expression of RAB38 promotes malignant progression of pancreatic cancer |
title | High expression of RAB38 promotes malignant progression of pancreatic cancer |
title_full | High expression of RAB38 promotes malignant progression of pancreatic cancer |
title_fullStr | High expression of RAB38 promotes malignant progression of pancreatic cancer |
title_full_unstemmed | High expression of RAB38 promotes malignant progression of pancreatic cancer |
title_short | High expression of RAB38 promotes malignant progression of pancreatic cancer |
title_sort | high expression of rab38 promotes malignant progression of pancreatic cancer |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6323198/ https://www.ncbi.nlm.nih.gov/pubmed/30569114 http://dx.doi.org/10.3892/mmr.2018.9732 |
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