Long noncoding RNA BCAR4 promotes glioma cell proliferation via EGFR/PI3K/AKT signaling pathway. Issue 12 (7th June 2019)
- Record Type:
- Journal Article
- Title:
- Long noncoding RNA BCAR4 promotes glioma cell proliferation via EGFR/PI3K/AKT signaling pathway. Issue 12 (7th June 2019)
- Main Title:
- Long noncoding RNA BCAR4 promotes glioma cell proliferation via EGFR/PI3K/AKT signaling pathway
- Authors:
- Wei, Lian
Yi, Zhao
Guo, Kongyan
Long, Xu - Abstract:
- Abstract: Long noncoding RNA Breast Cancer Antiestrogen Resistance 4 (BCAR4) has been identified to be oncogenic in several cancers. In our study, we demonstrated that BCAR4 expression was significantly upregulated in glioma tissues compared with paired nontumor tissues. In addition, higher BCAR4 level was associated with poor overall survival in patients with glioma. Besides, we also discovered that knockdown of BCAR4 inhibited cell proliferation, whereas BCAR4 overexpression promoted this process. Intriguingly, we proved a cellular transformation of normal human astrocyte cells (NHAs) in response to enforced expression of BCAR4. In addition, we revealed that BCAR4 affected cell proliferation in glioma cells by promoting cell cycle progression and inhibiting cell apoptosis. Mechanistically, we uncovered that BCAR4 activated PI3K/AKT signaling pathway in glioma through upregulating EGFR and interacting with it. Moreover, activating PI3K/AKT pathway could reverse the repressive effects caused by BCAR4 silence on the biological behaviors of glioma cells, whereas inhibition of this pathway rescued the impact of BACR4 upregulation in NHAs. These findings disclosed that BCAR4 contributes to glioma progression by enhancing cell growth via activating EGFR/PI3K/AKT pathway, providing potent evidence that BCAR4 could be an effective new target for treatment and prognosis of glioma patients. Abstract : BCAR4 contributes to glioma cell proliferation through accelerating cell cycleAbstract: Long noncoding RNA Breast Cancer Antiestrogen Resistance 4 (BCAR4) has been identified to be oncogenic in several cancers. In our study, we demonstrated that BCAR4 expression was significantly upregulated in glioma tissues compared with paired nontumor tissues. In addition, higher BCAR4 level was associated with poor overall survival in patients with glioma. Besides, we also discovered that knockdown of BCAR4 inhibited cell proliferation, whereas BCAR4 overexpression promoted this process. Intriguingly, we proved a cellular transformation of normal human astrocyte cells (NHAs) in response to enforced expression of BCAR4. In addition, we revealed that BCAR4 affected cell proliferation in glioma cells by promoting cell cycle progression and inhibiting cell apoptosis. Mechanistically, we uncovered that BCAR4 activated PI3K/AKT signaling pathway in glioma through upregulating EGFR and interacting with it. Moreover, activating PI3K/AKT pathway could reverse the repressive effects caused by BCAR4 silence on the biological behaviors of glioma cells, whereas inhibition of this pathway rescued the impact of BACR4 upregulation in NHAs. These findings disclosed that BCAR4 contributes to glioma progression by enhancing cell growth via activating EGFR/PI3K/AKT pathway, providing potent evidence that BCAR4 could be an effective new target for treatment and prognosis of glioma patients. Abstract : BCAR4 contributes to glioma cell proliferation through accelerating cell cycle progression and repressing cell apoptosis. BCAR4 activates PI3K/AKT signaling through upregulating and interacting with EGFR. BCAR4 promotes glioma cell growth through targeting the EGFR/PI3K/AKT pathway. … (more)
- Is Part Of:
- Journal of cellular physiology. Volume 234:Issue 12(2019:Dec.)
- Journal:
- Journal of cellular physiology
- Issue:
- Volume 234:Issue 12(2019:Dec.)
- Issue Display:
- Volume 234, Issue 12 (2019)
- Year:
- 2019
- Volume:
- 234
- Issue:
- 12
- Issue Sort Value:
- 2019-0234-0012-0000
- Page Start:
- 23608
- Page End:
- 23617
- Publication Date:
- 2019-06-07
- Subjects:
- BCAR4 -- EGFR -- glioma -- PI3K/AKT pathway -- proliferation
Physiology -- Periodicals
Cell physiology -- Periodicals
571.6 - Journal URLs:
- http://onlinelibrary.wiley.com/journal/10.1002/(ISSN)1097-4652 ↗
http://onlinelibrary.wiley.com/ ↗ - DOI:
- 10.1002/jcp.28929 ↗
- Languages:
- English
- ISSNs:
- 0021-9541
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 4955.020000
British Library DSC - BLDSS-3PM
British Library HMNTS - ELD Digital store - Ingest File:
- 23655.xml