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Expression of Tim4 in Glioma and its Regulatory Role in LN-18 Glioma Cells
BACKGROUND: Tim4 is a transmembrane protein known as T cell immunoglobulin and mucin domain containing protein-4. We speculated that Tim4 might be associated with glioma. This study aimed to investigate the expression level of Tim4 in gliomas and the regulatory role of Tim4 on the growth and apoptos...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
International Scientific Literature, Inc.
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4710195/ https://www.ncbi.nlm.nih.gov/pubmed/26741116 http://dx.doi.org/10.12659/MSM.894963 |
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author | Li, Weiguo Li, Xingang Xu, Shujun Ma, Xiangyu Zhang, Qiujie |
author_facet | Li, Weiguo Li, Xingang Xu, Shujun Ma, Xiangyu Zhang, Qiujie |
author_sort | Li, Weiguo |
collection | PubMed |
description | BACKGROUND: Tim4 is a transmembrane protein known as T cell immunoglobulin and mucin domain containing protein-4. We speculated that Tim4 might be associated with glioma. This study aimed to investigate the expression level of Tim4 in gliomas and the regulatory role of Tim4 on the growth and apoptosis of LN-18 glioma cells. MATERIAL/METHODS: Tumor tissues and adjacent normal tissues were collected from patients with glioma. The expression level of Tim4 mRNA and protein was determined by RT-PCR and Western blot analyses, respectively to evaluate their association with glioma. Tim4 was overexpressed or silenced by siRNA interference in cultured human glioma cells LN-18. The growth and apoptosis of LN-18 cells was detected by MTT assay and flow cytometry. The colony-forming ability of LN-18 cells was assessed by the colony formation assay. The collection of human tissues was approved by the Research Ethics Committee at the Harbin Medical University Cancer Hospital and performed in strict accordance with international standards. All patients were required to sign the informed consent. RESULTS: The expression level of Tim4 mRNA and protein in tumor tissues was significantly higher compared with adjacent normal tissues. Antisense miRNA targeting Tim4 inhibited the growth of LN-18 cells, induced their apoptosis, and reduced their clonogenic capacity. In contrast, overexpression of Tim4 promoted the growth of LN-18 cells, inhibited their apoptosis, and enhanced their clonogenic potential. CONCLUSIONS: The expression level of Tim-4 is closely associated with glioma. Decreased expression of Tim4 inhibited the growth and colony-forming ability of LN-18 cells and induced their apoptosis, whereas increased expression of Tim4 stimulated the growth and clonogenic potential of LN-18 cells and suppressed their apoptosis. |
format | Online Article Text |
id | pubmed-4710195 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | International Scientific Literature, Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-47101952016-01-14 Expression of Tim4 in Glioma and its Regulatory Role in LN-18 Glioma Cells Li, Weiguo Li, Xingang Xu, Shujun Ma, Xiangyu Zhang, Qiujie Med Sci Monit Clinical Research BACKGROUND: Tim4 is a transmembrane protein known as T cell immunoglobulin and mucin domain containing protein-4. We speculated that Tim4 might be associated with glioma. This study aimed to investigate the expression level of Tim4 in gliomas and the regulatory role of Tim4 on the growth and apoptosis of LN-18 glioma cells. MATERIAL/METHODS: Tumor tissues and adjacent normal tissues were collected from patients with glioma. The expression level of Tim4 mRNA and protein was determined by RT-PCR and Western blot analyses, respectively to evaluate their association with glioma. Tim4 was overexpressed or silenced by siRNA interference in cultured human glioma cells LN-18. The growth and apoptosis of LN-18 cells was detected by MTT assay and flow cytometry. The colony-forming ability of LN-18 cells was assessed by the colony formation assay. The collection of human tissues was approved by the Research Ethics Committee at the Harbin Medical University Cancer Hospital and performed in strict accordance with international standards. All patients were required to sign the informed consent. RESULTS: The expression level of Tim4 mRNA and protein in tumor tissues was significantly higher compared with adjacent normal tissues. Antisense miRNA targeting Tim4 inhibited the growth of LN-18 cells, induced their apoptosis, and reduced their clonogenic capacity. In contrast, overexpression of Tim4 promoted the growth of LN-18 cells, inhibited their apoptosis, and enhanced their clonogenic potential. CONCLUSIONS: The expression level of Tim-4 is closely associated with glioma. Decreased expression of Tim4 inhibited the growth and colony-forming ability of LN-18 cells and induced their apoptosis, whereas increased expression of Tim4 stimulated the growth and clonogenic potential of LN-18 cells and suppressed their apoptosis. International Scientific Literature, Inc. 2016-01-07 /pmc/articles/PMC4710195/ /pubmed/26741116 http://dx.doi.org/10.12659/MSM.894963 Text en © Med Sci Monit, 2016 This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License |
spellingShingle | Clinical Research Li, Weiguo Li, Xingang Xu, Shujun Ma, Xiangyu Zhang, Qiujie Expression of Tim4 in Glioma and its Regulatory Role in LN-18 Glioma Cells |
title | Expression of Tim4 in Glioma and its Regulatory Role in LN-18 Glioma Cells |
title_full | Expression of Tim4 in Glioma and its Regulatory Role in LN-18 Glioma Cells |
title_fullStr | Expression of Tim4 in Glioma and its Regulatory Role in LN-18 Glioma Cells |
title_full_unstemmed | Expression of Tim4 in Glioma and its Regulatory Role in LN-18 Glioma Cells |
title_short | Expression of Tim4 in Glioma and its Regulatory Role in LN-18 Glioma Cells |
title_sort | expression of tim4 in glioma and its regulatory role in ln-18 glioma cells |
topic | Clinical Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4710195/ https://www.ncbi.nlm.nih.gov/pubmed/26741116 http://dx.doi.org/10.12659/MSM.894963 |
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