详情页 - 昆明医科大学第一附属医院知识库

当前位置：首页 > 详情页

The transcript NR 134251.1 of lncRNA APTR with an opposite function to all transcripts inhibits proliferation and induces apoptosis by regulating proliferation and apoptosis-related genes

74| 导出 | 链接全文 |

文献详情

资源类型：

WOS体系：

Pubmed体系：

收录情况： ◇ SCIE

作者：

机构： [1]School of Public Health, Kunming Medical University, Kunming, China [2]Pain Department, The First Affiliated Hospital of Kunming Medical University, Kunming, China

出处：

DOI：

ISSN：

关键词： Arsenic APTR Transcript Proliferation Apoptosis E2F1

摘要：

Arsenic (As) exposure has been a global public health concern for hundreds of millions worldwide. LncRNA APTR (Alu-mediated p21 transcriptional regulator) plays an essential role in tumor growth and development. However, its function in arsenic-induced toxicological responses is still unknown. In this study, we found that the expressions of all transcripts and the transcript NR 134251.1 of APTR were increased in a dose-dependent manner in 16HBE cells treated with sodium arsenite (NaAsO2). Silencing the transcript NR 134251.1 of APTR inhibited cell proliferation and induced apoptosis. However, silencing all transcripts of APTR had the opposite function to the transcript NR 134251.1. Then we examined the protein level of the proliferation and apoptosis-related genes after silencing the transcript NR 134251.1 of APTR. The results showed that silencing the transcript NR 134251.1 of APTR up-regulated the expression of transcription factor E2F1 and regulated its downstream genes involved in proliferation and apoptosis, including p53, phospho-p53-S392, phospho-p53-T55, p21, Cyclin D1, PUMA, Fas, Bim, BIK, Caspase-3, Caspase-7, and Cyt-c. In conclusion, arsenic induced APTR expression and the transcript NR 134251.1 of APTR have an opposite function to all transcripts, providing a theoretical basis for the prevention and treatment of arsenic exposure.

基金：

语种：

WOS：

PubmedID：

中科院(CAS)分区：

出版当年[2024]版：

无

最新[2023]版：

大类 | 4 区医学

小类 | 4 区毒理学

JCR分区：

出版当年[2023]版：

Q3 TOXICOLOGY

最新[2023]版：

Q3 TOXICOLOGY

影响因子： 2.7 最新[2023版] 3 最新五年平均 2.7 出版当年[2023版] 3 出版当年五年平均 2.8 出版前一年[2022版]

第一作者：

第一作者机构： [1]School of Public Health, Kunming Medical University, Kunming, China

通讯作者：

通讯机构： [1]School of Public Health, Kunming Medical University, Kunming, China [*1]School of Public Health, Kunming Medical University, Kunming 650500, China. [*2]School of Public Health, Kunming Medical University, Kunming 650500, China.

推荐引用方式(GB/T 7714)：

APA：

MLA：

相关文献

[1]Arsenic-induced downregulation of BRWD3 suppresses proliferation and induces apoptosis in lung adenocarcinoma cells through the p53 and p65 pathways [2]Hsa_circ_0062270 Promotes Tumorigenesis of Melanoma by Stabilizing the Linear Transcript Cell Division Cycle Protein 45 [3]Arsenic Trioxide Induces Apoptosis of Burkitt Lymphoma Cell Lines Through Multiple Apoptotic Pathways and Triggers Antiangiogenesis [4]三氧化二砷阻滞人Burkitt淋巴瘤细胞增殖和细胞周期作用及其相关机制 [5]Arsenic trioxide induces apoptosis of Burkitt lymphoma cell lines through multiple apoptotic pathways and triggers antiangiogenesis. [6]As2O3抑制人淋巴瘤Raji细胞增殖及VEGF表达 [7]细胞增殖和凋亡与结直肠癌的发生发展 [8]Effect of MT2A on apoptosis and proliferation in HL60 cells [9]Metabolites of arsenic and increased DNA damage of p53 gene in arsenic plant workers [10]Knockdown of mitochondrial threonyl-tRNA synthetase 2 inhibits lung adenocarcinoma cell proliferation and induces apoptosis.