Cargando…
Oncogene APOL1 promotes proliferation and inhibits apoptosis via activating NOTCH1 signaling pathway in pancreatic cancer
APOL1 encodes a secreted high-density lipoprotein, which has been considered as an aberrantly expressed gene in multiple cancers. Nevertheless, the role of APOL1 in the regulatory mechanisms of pancreatic cancer remains unknown and should be explored. We identified APOL1 was abnormally elevated in h...
Autores principales: | , , , , , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2021
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8329288/ https://www.ncbi.nlm.nih.gov/pubmed/34341330 http://dx.doi.org/10.1038/s41419-021-03985-1 |
_version_ | 1783732466026020864 |
---|---|
author | Lin, Jiewei Xu, Zhiwei Xie, Junjie Deng, Xiaxing Jiang, Lingxi Chen, Hao Peng, Chenghong Li, Hongwei Zhang, Jiaqiang Shen, Baiyong |
author_facet | Lin, Jiewei Xu, Zhiwei Xie, Junjie Deng, Xiaxing Jiang, Lingxi Chen, Hao Peng, Chenghong Li, Hongwei Zhang, Jiaqiang Shen, Baiyong |
author_sort | Lin, Jiewei |
collection | PubMed |
description | APOL1 encodes a secreted high-density lipoprotein, which has been considered as an aberrantly expressed gene in multiple cancers. Nevertheless, the role of APOL1 in the regulatory mechanisms of pancreatic cancer remains unknown and should be explored. We identified APOL1 was abnormally elevated in human pancreatic cancer tissues compared with that in adjacent tissues and was associated with poor prognosis. The effects of APOL1 in PC cell proliferation, cell cycle, and apoptosis was verified via functional in vitro and in vivo experiments. The results showed that knockdown of APOL1 significantly inhibited the proliferation and promoted apoptosis of pancreatic cancer. In addition, we identified APOL1 could be a regulator of NOTCH1 signaling pathway using bioinformatics tools, qRT-PCR, dual-luciferase reporter assay, and western blotting. In summary, APOL1 could function as an oncogene to promote proliferation and inhibit apoptosis through activating NOTCH1 signaling pathway expression in pancreatic cancer; therefore, it may act as a novel therapeutic target for pancreatic cancer. |
format | Online Article Text |
id | pubmed-8329288 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-83292882021-08-03 Oncogene APOL1 promotes proliferation and inhibits apoptosis via activating NOTCH1 signaling pathway in pancreatic cancer Lin, Jiewei Xu, Zhiwei Xie, Junjie Deng, Xiaxing Jiang, Lingxi Chen, Hao Peng, Chenghong Li, Hongwei Zhang, Jiaqiang Shen, Baiyong Cell Death Dis Article APOL1 encodes a secreted high-density lipoprotein, which has been considered as an aberrantly expressed gene in multiple cancers. Nevertheless, the role of APOL1 in the regulatory mechanisms of pancreatic cancer remains unknown and should be explored. We identified APOL1 was abnormally elevated in human pancreatic cancer tissues compared with that in adjacent tissues and was associated with poor prognosis. The effects of APOL1 in PC cell proliferation, cell cycle, and apoptosis was verified via functional in vitro and in vivo experiments. The results showed that knockdown of APOL1 significantly inhibited the proliferation and promoted apoptosis of pancreatic cancer. In addition, we identified APOL1 could be a regulator of NOTCH1 signaling pathway using bioinformatics tools, qRT-PCR, dual-luciferase reporter assay, and western blotting. In summary, APOL1 could function as an oncogene to promote proliferation and inhibit apoptosis through activating NOTCH1 signaling pathway expression in pancreatic cancer; therefore, it may act as a novel therapeutic target for pancreatic cancer. Nature Publishing Group UK 2021-08-02 /pmc/articles/PMC8329288/ /pubmed/34341330 http://dx.doi.org/10.1038/s41419-021-03985-1 Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Article Lin, Jiewei Xu, Zhiwei Xie, Junjie Deng, Xiaxing Jiang, Lingxi Chen, Hao Peng, Chenghong Li, Hongwei Zhang, Jiaqiang Shen, Baiyong Oncogene APOL1 promotes proliferation and inhibits apoptosis via activating NOTCH1 signaling pathway in pancreatic cancer |
title | Oncogene APOL1 promotes proliferation and inhibits apoptosis via activating NOTCH1 signaling pathway in pancreatic cancer |
title_full | Oncogene APOL1 promotes proliferation and inhibits apoptosis via activating NOTCH1 signaling pathway in pancreatic cancer |
title_fullStr | Oncogene APOL1 promotes proliferation and inhibits apoptosis via activating NOTCH1 signaling pathway in pancreatic cancer |
title_full_unstemmed | Oncogene APOL1 promotes proliferation and inhibits apoptosis via activating NOTCH1 signaling pathway in pancreatic cancer |
title_short | Oncogene APOL1 promotes proliferation and inhibits apoptosis via activating NOTCH1 signaling pathway in pancreatic cancer |
title_sort | oncogene apol1 promotes proliferation and inhibits apoptosis via activating notch1 signaling pathway in pancreatic cancer |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8329288/ https://www.ncbi.nlm.nih.gov/pubmed/34341330 http://dx.doi.org/10.1038/s41419-021-03985-1 |
work_keys_str_mv | AT linjiewei oncogeneapol1promotesproliferationandinhibitsapoptosisviaactivatingnotch1signalingpathwayinpancreaticcancer AT xuzhiwei oncogeneapol1promotesproliferationandinhibitsapoptosisviaactivatingnotch1signalingpathwayinpancreaticcancer AT xiejunjie oncogeneapol1promotesproliferationandinhibitsapoptosisviaactivatingnotch1signalingpathwayinpancreaticcancer AT dengxiaxing oncogeneapol1promotesproliferationandinhibitsapoptosisviaactivatingnotch1signalingpathwayinpancreaticcancer AT jianglingxi oncogeneapol1promotesproliferationandinhibitsapoptosisviaactivatingnotch1signalingpathwayinpancreaticcancer AT chenhao oncogeneapol1promotesproliferationandinhibitsapoptosisviaactivatingnotch1signalingpathwayinpancreaticcancer AT pengchenghong oncogeneapol1promotesproliferationandinhibitsapoptosisviaactivatingnotch1signalingpathwayinpancreaticcancer AT lihongwei oncogeneapol1promotesproliferationandinhibitsapoptosisviaactivatingnotch1signalingpathwayinpancreaticcancer AT zhangjiaqiang oncogeneapol1promotesproliferationandinhibitsapoptosisviaactivatingnotch1signalingpathwayinpancreaticcancer AT shenbaiyong oncogeneapol1promotesproliferationandinhibitsapoptosisviaactivatingnotch1signalingpathwayinpancreaticcancer |