Apolipoprotein M promotes proliferation and invasion in non-small cell lung cancers via upregulating S1PR1 and activating the ERK1/2 and PI3K/AKT signaling pathways
(2018) In Biochemical and Biophysical Research Communications 501(2). p.520-526- Abstract
Apolipoprotein M (ApoM) is a sphingosine 1-phosphate (S1P) carrier involved in the regulation of S1P. Signaling pathways involving sphingosine kinases (SphKs) and S1P-S1P receptors (S1PRs) play important roles in the oncogenesis of multiple cancers including non-small cell lung cancer (NSCLC). In the present study we have clarified the potential roles of ApoM on the oncogenesis process of NSCLC cells. We detected the ApoM expression in NSCLC tissues and further analyzed its clinical significance. Moreover, we determined effects of ApoM overexpression on tumor cellular behaviours of NSCLC in vitro and in vivo. Our results demonstrated that ApoM protein mass were clearly higher in the NSCLC tissues than in non-NSCLS tissues.... (More)
Apolipoprotein M (ApoM) is a sphingosine 1-phosphate (S1P) carrier involved in the regulation of S1P. Signaling pathways involving sphingosine kinases (SphKs) and S1P-S1P receptors (S1PRs) play important roles in the oncogenesis of multiple cancers including non-small cell lung cancer (NSCLC). In the present study we have clarified the potential roles of ApoM on the oncogenesis process of NSCLC cells. We detected the ApoM expression in NSCLC tissues and further analyzed its clinical significance. Moreover, we determined effects of ApoM overexpression on tumor cellular behaviours of NSCLC in vitro and in vivo. Our results demonstrated that ApoM protein mass were clearly higher in the NSCLC tissues than in non-NSCLS tissues. Overexpression of ApoM could promote NSCLC cell proliferation and invasion in vitro and tumor growth in vivo, which might be via upregulating S1PR1 and activating the ERK1/2 and PI3K/AKT signaling pathways. It is concluded that up-regulation of ApoM in NSCLC might be associated with the tumor induced inflammation and tumor microenvironment as well as promoting oncogenesis of NSCLC. Further study needs to elucidate the underlying mechanisms.
(Less)
- author
- Zhu, Yifei ; Luo, Guanghua ; Jiang, Bo ; Yu, Miaomei ; Feng, Yuehua ; Wang, Min ; Xu, Ning LU and Zhang, Xiaoying
- organization
- publishing date
- 2018-06-22
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Apolipoprotein M, ERK1/2 signal pathway, Non-small cell lung cancer, PI3K/AKT signal pathway, Sphingosine 1-phosphate receptors
- in
- Biochemical and Biophysical Research Communications
- volume
- 501
- issue
- 2
- pages
- 7 pages
- publisher
- Elsevier
- external identifiers
-
- scopus:85047049171
- pmid:29750961
- ISSN
- 0006-291X
- DOI
- 10.1016/j.bbrc.2018.05.029
- language
- English
- LU publication?
- yes
- id
- 42b9a44b-9a57-4582-a3e3-7fc9395c73c3
- date added to LUP
- 2018-05-29 14:31:41
- date last changed
- 2024-03-01 19:50:59
@article{42b9a44b-9a57-4582-a3e3-7fc9395c73c3,
abstract = {{<p>Apolipoprotein M (ApoM) is a sphingosine 1-phosphate (S1P) carrier involved in the regulation of S1P. Signaling pathways involving sphingosine kinases (SphKs) and S1P-S1P receptors (S1PRs) play important roles in the oncogenesis of multiple cancers including non-small cell lung cancer (NSCLC). In the present study we have clarified the potential roles of ApoM on the oncogenesis process of NSCLC cells. We detected the ApoM expression in NSCLC tissues and further analyzed its clinical significance. Moreover, we determined effects of ApoM overexpression on tumor cellular behaviours of NSCLC in vitro and in vivo. Our results demonstrated that ApoM protein mass were clearly higher in the NSCLC tissues than in non-NSCLS tissues. Overexpression of ApoM could promote NSCLC cell proliferation and invasion in vitro and tumor growth in vivo, which might be via upregulating S1PR1 and activating the ERK1/2 and PI3K/AKT signaling pathways. It is concluded that up-regulation of ApoM in NSCLC might be associated with the tumor induced inflammation and tumor microenvironment as well as promoting oncogenesis of NSCLC. Further study needs to elucidate the underlying mechanisms.</p>}},
author = {{Zhu, Yifei and Luo, Guanghua and Jiang, Bo and Yu, Miaomei and Feng, Yuehua and Wang, Min and Xu, Ning and Zhang, Xiaoying}},
issn = {{0006-291X}},
keywords = {{Apolipoprotein M; ERK1/2 signal pathway; Non-small cell lung cancer; PI3K/AKT signal pathway; Sphingosine 1-phosphate receptors}},
language = {{eng}},
month = {{06}},
number = {{2}},
pages = {{520--526}},
publisher = {{Elsevier}},
series = {{Biochemical and Biophysical Research Communications}},
title = {{Apolipoprotein M promotes proliferation and invasion in non-small cell lung cancers via upregulating S1PR1 and activating the ERK1/2 and PI3K/AKT signaling pathways}},
url = {{http://dx.doi.org/10.1016/j.bbrc.2018.05.029}},
doi = {{10.1016/j.bbrc.2018.05.029}},
volume = {{501}},
year = {{2018}},
}