Linc01588 deletion inhibits the malignant biological characteristics of hydroquinone-induced leukemic cells via miR-9-5p/SIRT1
Leukemia caused by environmental chemical pollutants has attracted great attention, the malignant leukemic transformation model of TK6 cells induced by hydroquinone (HQ) has been previously found in our team. However, the type of leukemia corresponding to this malignant transformed cell line model n...
| Main Authors: | , , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Elsevier
2024-05-01
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| Series: | Ecotoxicology and Environmental Safety |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S0147651324003713 |
| _version_ | 1827274356031488000 |
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| author | Yanquan Liu Minjuan Zeng Zhengzhen Li Caixiong Lin Jie Bao Weihua Ding Shimei Wang Qin Fan Qian Sun Hao Luo Jinqi Huang Shaopeng Chen Huanwen Tang |
| author_facet | Yanquan Liu Minjuan Zeng Zhengzhen Li Caixiong Lin Jie Bao Weihua Ding Shimei Wang Qin Fan Qian Sun Hao Luo Jinqi Huang Shaopeng Chen Huanwen Tang |
| author_sort | Yanquan Liu |
| collection | DOAJ |
| description | Leukemia caused by environmental chemical pollutants has attracted great attention, the malignant leukemic transformation model of TK6 cells induced by hydroquinone (HQ) has been previously found in our team. However, the type of leukemia corresponding to this malignant transformed cell line model needs further study and interpretation. Furthermore, the molecular mechanism of malignant proliferation of leukemic cells induced by HQ remains unclear. This study is the first to reveal the expression of aberrant genes in leukemic cells of HQ-induced malignant transformation, which may correspond to chronic lymphocytic leukemia (CLL). The expression of Linc01588, a long non-coding RNA (lncRNA), was significantly up-regulated in CLL patients and leukemic cell line model which previously described. After gain-of-function assays and loss-of-function assays, feeble cell viability, severe apoptotic phenotype and the increased secretion of TNF-α were easily observed in malignant leukemic TK6 cells with Linc01588 deletion after HQ intervention. The tumors derived from malignant TK6 cells with Linc01588 deletion inoculated subcutaneously in nude mice were smaller than controls. In CLL and its cell line model, the expression of Linc01588 and miR-9–5p, miR-9–5p and SIRT1 were negative correlation respectively in CLL and cell line model, while the expression of Linc01588 and SIRT1 were positive correlation. The dual-luciferase reporter assay showed that Linc01588 & miR-9–5p, miR-9–5p & SIRT1 could bind directly, respectively. Furthermore, knockdown of miR-9–5p successfully rescued the severe apoptotic phenotype and the increased secretion of TNF-α caused by the Linc01588 deletion, the deletion of Linc01588 in human CLL cell line MEC-2 could also inhibit malignant biological characteristics, and the phenotype caused by the deletion of Linc01588 could also be rescued after overexpression of SIRT1. Moreover, the regulation of SIRT1 expression in HQ19 cells by Linc01588 and miR-9–5 P may be related to the Akt/NF-κB pathway. In brief, Linc01588 deletion inhibits the malignant biological characteristics of HQ-induced leukemic cells via miR-9–5p/SIRT1, and it is a novel and hopeful clue for the clinical targeted therapy of CLL. |
| first_indexed | 2024-04-24T12:46:46Z |
| format | Article |
| id | doaj.art-6458e24b3a434bffa65106d7bad52aac |
| institution | Directory Open Access Journal |
| issn | 0147-6513 |
| language | English |
| last_indexed | 2025-03-22T06:23:42Z |
| publishDate | 2024-05-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Ecotoxicology and Environmental Safety |
| spelling | doaj.art-6458e24b3a434bffa65106d7bad52aac2024-04-26T04:58:04ZengElsevierEcotoxicology and Environmental Safety0147-65132024-05-01276116295Linc01588 deletion inhibits the malignant biological characteristics of hydroquinone-induced leukemic cells via miR-9-5p/SIRT1Yanquan Liu0Minjuan Zeng1Zhengzhen Li2Caixiong Lin3Jie Bao4Weihua Ding5Shimei Wang6Qin Fan7Qian Sun8Hao Luo9Jinqi Huang10Shaopeng Chen11Huanwen Tang12Department of Hematology, The First Dongguan Affiliated Hospital of Guangdong Medical University, Dongguan 523808, China; School of Public Health, Guangdong Medical University, Dongguan 523808, China; Dongguan Key Laboratory of Environmental Medicine, Dongguan 523808, ChinaSchool of Basic Medicine, Guangdong Medical University, Dongguan Key Laboratory for Development and Application of Experimental Animal Resources in Biomedical Industry, Dongguan 523808, ChinaSchool of Public Health, Guangdong Medical University, Dongguan 523808, China; Dongguan Key Laboratory of Environmental Medicine, Dongguan 523808, ChinaSchool of Public Health, Guangdong Medical University, Dongguan 523808, China; Dongguan Key Laboratory of Environmental Medicine, Dongguan 523808, ChinaDepartment of Clinical Laboratory, The Affiliated Hospital of Guangdong Medical University, Zhanjiang 524002, ChinaCentral People’s Hospital of Zhanjiang, Zhanjiang 524033, ChinaSchool of Public Health, Guangdong Medical University, Dongguan 523808, China; Dongguan Key Laboratory of Environmental Medicine, Dongguan 523808, ChinaSchool of Public Health, Guangdong Medical University, Dongguan 523808, China; Dongguan Key Laboratory of Environmental Medicine, Dongguan 523808, ChinaSchool of Public Health, Guangdong Medical University, Dongguan 523808, China; Dongguan Key Laboratory of Environmental Medicine, Dongguan 523808, ChinaSchool of Public Health, Guangdong Medical University, Dongguan 523808, China; Dongguan Key Laboratory of Environmental Medicine, Dongguan 523808, ChinaDepartment of Hematology, Guangzhou First People’s Hospital, South China University of Technology, Guangzhou 510180, ChinaZhanjiang Blood Center, Zhanjiang 524002, China; Corresponding author.Department of Hematology, The First Dongguan Affiliated Hospital of Guangdong Medical University, Dongguan 523808, China; School of Public Health, Guangdong Medical University, Dongguan 523808, China; Dongguan Key Laboratory of Environmental Medicine, Dongguan 523808, China; Correspondence to: School of Public Health, Guangdong Medical University, Dongguan Key Laboratory of Environmental Medicine, Dongguan 523808, China.Leukemia caused by environmental chemical pollutants has attracted great attention, the malignant leukemic transformation model of TK6 cells induced by hydroquinone (HQ) has been previously found in our team. However, the type of leukemia corresponding to this malignant transformed cell line model needs further study and interpretation. Furthermore, the molecular mechanism of malignant proliferation of leukemic cells induced by HQ remains unclear. This study is the first to reveal the expression of aberrant genes in leukemic cells of HQ-induced malignant transformation, which may correspond to chronic lymphocytic leukemia (CLL). The expression of Linc01588, a long non-coding RNA (lncRNA), was significantly up-regulated in CLL patients and leukemic cell line model which previously described. After gain-of-function assays and loss-of-function assays, feeble cell viability, severe apoptotic phenotype and the increased secretion of TNF-α were easily observed in malignant leukemic TK6 cells with Linc01588 deletion after HQ intervention. The tumors derived from malignant TK6 cells with Linc01588 deletion inoculated subcutaneously in nude mice were smaller than controls. In CLL and its cell line model, the expression of Linc01588 and miR-9–5p, miR-9–5p and SIRT1 were negative correlation respectively in CLL and cell line model, while the expression of Linc01588 and SIRT1 were positive correlation. The dual-luciferase reporter assay showed that Linc01588 & miR-9–5p, miR-9–5p & SIRT1 could bind directly, respectively. Furthermore, knockdown of miR-9–5p successfully rescued the severe apoptotic phenotype and the increased secretion of TNF-α caused by the Linc01588 deletion, the deletion of Linc01588 in human CLL cell line MEC-2 could also inhibit malignant biological characteristics, and the phenotype caused by the deletion of Linc01588 could also be rescued after overexpression of SIRT1. Moreover, the regulation of SIRT1 expression in HQ19 cells by Linc01588 and miR-9–5 P may be related to the Akt/NF-κB pathway. In brief, Linc01588 deletion inhibits the malignant biological characteristics of HQ-induced leukemic cells via miR-9–5p/SIRT1, and it is a novel and hopeful clue for the clinical targeted therapy of CLL.http://www.sciencedirect.com/science/article/pii/S0147651324003713LeukemiaHydroquinoneLinc01588miR-9-5p/SIRT1 axisMalignant biological characteristics |
| spellingShingle | Yanquan Liu Minjuan Zeng Zhengzhen Li Caixiong Lin Jie Bao Weihua Ding Shimei Wang Qin Fan Qian Sun Hao Luo Jinqi Huang Shaopeng Chen Huanwen Tang Linc01588 deletion inhibits the malignant biological characteristics of hydroquinone-induced leukemic cells via miR-9-5p/SIRT1 Ecotoxicology and Environmental Safety Leukemia Hydroquinone Linc01588 miR-9-5p/SIRT1 axis Malignant biological characteristics |
| title | Linc01588 deletion inhibits the malignant biological characteristics of hydroquinone-induced leukemic cells via miR-9-5p/SIRT1 |
| title_full | Linc01588 deletion inhibits the malignant biological characteristics of hydroquinone-induced leukemic cells via miR-9-5p/SIRT1 |
| title_fullStr | Linc01588 deletion inhibits the malignant biological characteristics of hydroquinone-induced leukemic cells via miR-9-5p/SIRT1 |
| title_full_unstemmed | Linc01588 deletion inhibits the malignant biological characteristics of hydroquinone-induced leukemic cells via miR-9-5p/SIRT1 |
| title_short | Linc01588 deletion inhibits the malignant biological characteristics of hydroquinone-induced leukemic cells via miR-9-5p/SIRT1 |
| title_sort | linc01588 deletion inhibits the malignant biological characteristics of hydroquinone induced leukemic cells via mir 9 5p sirt1 |
| topic | Leukemia Hydroquinone Linc01588 miR-9-5p/SIRT1 axis Malignant biological characteristics |
| url | http://www.sciencedirect.com/science/article/pii/S0147651324003713 |
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