高级检索
当前位置: 首页 > 详情页

Arsenic-induced downregulation of BRWD3 suppresses proliferation and induces apoptosis in lung adenocarcinoma cells through the p53 and p65 pathways

文献详情

资源类型:
WOS体系:

收录情况: ◇ SCIE

机构: [1]Kunming Med Univ, Dept Clin Lab, Affiliated Hosp 1, 295 Xichang Rd, Kunming, Yunnan, Peoples R China [2]Yunnan Key Lab Lab Med, Kunming, Peoples R China [3]Yunnan Prov Clin Res Ctr Lab Med, Kunming, Peoples R China [4]Kunming Med Univ, Sch Publ Hlth, 1168 Chunrongxi Rd, Kunming, Yunnan, Peoples R China
出处:
ISSN:

关键词: Arsenic bromodomain and WD-repeat domain-containing protein 3 proliferation apoptosis p53 pathway NF-kappa B/p65 signaling

摘要:
Bromodomain and WD-repeat domain-containing protein 3 (BRWD3) exhibits high expression in lung adenocarcinoma (LUAD) tissues and cells; however, its function in arsenic-induced toxicological responses remains unclear. This study aimed to investigate BRWD3 expression in response to arsenic-induced conditions and its impact on the proliferation and apoptosis of LUAD cell line SPC-A1 upon BRWD3 knockdown. The results revealed a decrease in BRWD3 expression in SPC-A1 cells treated with sodium arsenite (NaAsO2), but not sodium arsenite's metabolites. BRWD3 knockdown suppressed cell proliferation and induced apoptosis in SPC-A1 cells. Western blot analysis revealed that BRWD3 knockdown resulted in the upregulation of p53, phospho-p53-Ser392, and its downstream factors including MDM2, Bak, and Bax. Additionally, we observed the downregulation of p65, phospho-p65-Ser276, phospho-p65-Ser536, and its downstream factors, including I kappa B alpha, BIRC3, XIAP and CIAP1. Moreover, polymerase chain reaction analysis showed that BRWD3 knockdown also resulted in the downregulation of proliferation-related genes and upregulation of apoptosis-related genes. In conclusion, BRWD3 mediated proliferation and apoptosis via the p53 and p65 pathways in response to arsenic exposure, suggesting potential implications for LUAD treatment through BRWD3 downregulation by arsenic.

基金:

基金编号: 81660388 202101AT070223 D-2018024 2023535D08 YNWR-QNBJ-2019-159 2023zdpy05 CXTD202201

语种:
WOS:
PubmedID:
中科院(CAS)分区:
出版当年[2025]版:
最新[2023]版:
大类 | 4 区 医学
小类 | 4 区 毒理学
JCR分区:
出版当年[2024]版:
最新[2023]版:
Q3 TOXICOLOGY

影响因子: 最新[2023版] 最新五年平均 出版当年[2024版] 出版当年五年平均 出版前一年[2023版]

第一作者:
第一作者机构: [1]Kunming Med Univ, Dept Clin Lab, Affiliated Hosp 1, 295 Xichang Rd, Kunming, Yunnan, Peoples R China [2]Yunnan Key Lab Lab Med, Kunming, Peoples R China [3]Yunnan Prov Clin Res Ctr Lab Med, Kunming, Peoples R China
通讯作者:
通讯机构: [1]Kunming Med Univ, Dept Clin Lab, Affiliated Hosp 1, 295 Xichang Rd, Kunming, Yunnan, Peoples R China [2]Yunnan Key Lab Lab Med, Kunming, Peoples R China [3]Yunnan Prov Clin Res Ctr Lab Med, Kunming, Peoples R China
推荐引用方式(GB/T 7714):
APA:
MLA:

资源点击量:57189 今日访问量:0 总访问量:1788 更新日期:2025-01-01 建议使用谷歌、火狐浏览器 常见问题

版权所有©2020 昆明医科大学第一附属医院 技术支持:重庆聚合科技有限公司 地址:云南省昆明市西昌路295号(650032)