Mechanism of TRIM24 to Regulate Resistance of Gefitinib in NSCLC cells
Background and objective Epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) resistance significantly limits its use in clinical practice. Study found that TRIM24 was overexpressed in non-small cell lung cancer (NSCLC) tissues and regulate cell growth, cell cycle and apoptosis in l...
| Main Authors: | , , , , |
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| Format: | Article |
| Language: | zho |
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Chinese Anti-Cancer Association; Chinese Antituberculosis Association
2016-01-01
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| Series: | Chinese Journal of Lung Cancer |
| Subjects: | |
| Online Access: | http://dx.doi.org/10.3779/j.issn.1009-3419.2016.01.03 |
| _version_ | 1828815167428755456 |
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| author | Haiying LI Qingling WANG Haijun BAO Heng ZHANG Ying ZHUANG |
| author_facet | Haiying LI Qingling WANG Haijun BAO Heng ZHANG Ying ZHUANG |
| author_sort | Haiying LI |
| collection | DOAJ |
| description | Background and objective Epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) resistance significantly limits its use in clinical practice. Study found that TRIM24 was overexpressed in non-small cell lung cancer (NSCLC) tissues and regulate cell growth, cell cycle and apoptosis in lung cell lines. The aim of this study is to explore the mechanism of TRIM24 to regulate resistance of Gefitinib in NSCLC cells. Methods MTT and apoptosis were used to detect the change of cell grow and cell apoptosis with down-expression TRIM24 and ShTRIM24 with presence of Gefitinib. Meanwhile, Western blot was used to detect the expression of protein related to apoptosis and AKT signal path. Results TRIM24 interference could improve the effect of gefitinib on cell growth inhibition and upregulate the cell apoptosis in A549 cell. Down-regulated of endogenous TRIM24 and ShTRIM24 with Gifitinib could also reduce the protein related apoptosis, such as p-BAD and Bcl-2, and the protein PIK3CA related AKT signal path in A549 cell. Conclusion TRIM24 could regulate required resistance to Gefitinib via Akt pathway in NSCLC. |
| first_indexed | 2024-12-12T10:38:20Z |
| format | Article |
| id | doaj.art-75af5e83705845f98e1b4963dbe8271d |
| institution | Directory Open Access Journal |
| issn | 1009-3419 1999-6187 |
| language | zho |
| last_indexed | 2024-12-12T10:38:20Z |
| publishDate | 2016-01-01 |
| publisher | Chinese Anti-Cancer Association; Chinese Antituberculosis Association |
| record_format | Article |
| series | Chinese Journal of Lung Cancer |
| spelling | doaj.art-75af5e83705845f98e1b4963dbe8271d2022-12-22T00:27:07ZzhoChinese Anti-Cancer Association; Chinese Antituberculosis AssociationChinese Journal of Lung Cancer1009-34191999-61872016-01-01191242910.3779/j.issn.1009-3419.2016.01.03Mechanism of TRIM24 to Regulate Resistance of Gefitinib in NSCLC cellsHaiying LI0Qingling WANG1Haijun BAO2Heng ZHANG3Ying ZHUANG4Department of Pathology, College of Basic Medical Science, Xuzhou Medical College, Xuzhou 221000, ChinaDepartment of Pathology, College of Basic Medical Science, Xuzhou Medical College, Xuzhou 221000, ChinaDepartment of Pathology, College of Basic Medical Science, Xuzhou Medical College, Xuzhou 221000, ChinaDepartment of Pathology, College of Basic Medical Science, Xuzhou Medical College, Xuzhou 221000, ChinaDepartment of Pathology, College of Basic Medical Science, Xuzhou Medical College, Xuzhou 221000, ChinaBackground and objective Epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) resistance significantly limits its use in clinical practice. Study found that TRIM24 was overexpressed in non-small cell lung cancer (NSCLC) tissues and regulate cell growth, cell cycle and apoptosis in lung cell lines. The aim of this study is to explore the mechanism of TRIM24 to regulate resistance of Gefitinib in NSCLC cells. Methods MTT and apoptosis were used to detect the change of cell grow and cell apoptosis with down-expression TRIM24 and ShTRIM24 with presence of Gefitinib. Meanwhile, Western blot was used to detect the expression of protein related to apoptosis and AKT signal path. Results TRIM24 interference could improve the effect of gefitinib on cell growth inhibition and upregulate the cell apoptosis in A549 cell. Down-regulated of endogenous TRIM24 and ShTRIM24 with Gifitinib could also reduce the protein related apoptosis, such as p-BAD and Bcl-2, and the protein PIK3CA related AKT signal path in A549 cell. Conclusion TRIM24 could regulate required resistance to Gefitinib via Akt pathway in NSCLC.http://dx.doi.org/10.3779/j.issn.1009-3419.2016.01.03Lung neoplasmsGefitinibEpidermal growth factor receptor tyrosine kinase inhibitor |
| spellingShingle | Haiying LI Qingling WANG Haijun BAO Heng ZHANG Ying ZHUANG Mechanism of TRIM24 to Regulate Resistance of Gefitinib in NSCLC cells Chinese Journal of Lung Cancer Lung neoplasms Gefitinib Epidermal growth factor receptor tyrosine kinase inhibitor |
| title | Mechanism of TRIM24 to Regulate Resistance of Gefitinib in NSCLC cells |
| title_full | Mechanism of TRIM24 to Regulate Resistance of Gefitinib in NSCLC cells |
| title_fullStr | Mechanism of TRIM24 to Regulate Resistance of Gefitinib in NSCLC cells |
| title_full_unstemmed | Mechanism of TRIM24 to Regulate Resistance of Gefitinib in NSCLC cells |
| title_short | Mechanism of TRIM24 to Regulate Resistance of Gefitinib in NSCLC cells |
| title_sort | mechanism of trim24 to regulate resistance of gefitinib in nsclc cells |
| topic | Lung neoplasms Gefitinib Epidermal growth factor receptor tyrosine kinase inhibitor |
| url | http://dx.doi.org/10.3779/j.issn.1009-3419.2016.01.03 |
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