AIB1 induces epithelial‐mesenchymal transition in gastric cancer via the PI3K/AKT signaling. Issue 9 (6th November 2019)
- Record Type:
- Journal Article
- Title:
- AIB1 induces epithelial‐mesenchymal transition in gastric cancer via the PI3K/AKT signaling. Issue 9 (6th November 2019)
- Main Title:
- AIB1 induces epithelial‐mesenchymal transition in gastric cancer via the PI3K/AKT signaling
- Authors:
- Diao, Lei
Li, Yang
Mei, Qiao
Han, Wei
Hu, Jing - Abstract:
- Abstract: Amplified in breast cancer 1 (AIB1) is overexpression in various cancers and promotes tumor cell proliferation, survival, and invasiveness. However, the role of AIB1 in the regulation of gastric cancer (GC) cell epithelial‐mesenchymal transition (EMT) is still largely unclear. In the present study, immunohistochemistry showed that AIB1 was upregulated in our cohort of patients with GC and correlated with poor survival. Knockdown of AIB1 reduced the invasive ability of GC cells, downregulated the expression of epithelial cell marker E‐cadherin, and upregulated mesenchymal cell marker vimentin. AIB1 overexpression elicited the opposite effect. PI‐103, the inhibitor of the PI3K/AKT signaling, partially reversed AIB1 overexpression mediated a decrease in E‐cadherin and an increase in vimentin. The present data demonstrated that AIB1 augmented the EMT via activation of PI3K/AKT signaling. In conclusion, our results suggested a novel role of AIB1 in GC invasion and EMT and raised the possibility of using this molecule as an indicator for GC treatment. Abstract : Gastric cancer (GC) is the fifth most frequently diagnosed cancer and the third leading cause of cancer death worldwide. The aim of this study was to investigate the role of amplified in breast cancer 1 (AIB1) in the regulation GC cell epithelial‐mesenchymal transition (EMT). The results suggested a novel role of AIB1 in GC invasion and EMT and raised the possibility of using this molecule as an indicator for GCAbstract: Amplified in breast cancer 1 (AIB1) is overexpression in various cancers and promotes tumor cell proliferation, survival, and invasiveness. However, the role of AIB1 in the regulation of gastric cancer (GC) cell epithelial‐mesenchymal transition (EMT) is still largely unclear. In the present study, immunohistochemistry showed that AIB1 was upregulated in our cohort of patients with GC and correlated with poor survival. Knockdown of AIB1 reduced the invasive ability of GC cells, downregulated the expression of epithelial cell marker E‐cadherin, and upregulated mesenchymal cell marker vimentin. AIB1 overexpression elicited the opposite effect. PI‐103, the inhibitor of the PI3K/AKT signaling, partially reversed AIB1 overexpression mediated a decrease in E‐cadherin and an increase in vimentin. The present data demonstrated that AIB1 augmented the EMT via activation of PI3K/AKT signaling. In conclusion, our results suggested a novel role of AIB1 in GC invasion and EMT and raised the possibility of using this molecule as an indicator for GC treatment. Abstract : Gastric cancer (GC) is the fifth most frequently diagnosed cancer and the third leading cause of cancer death worldwide. The aim of this study was to investigate the role of amplified in breast cancer 1 (AIB1) in the regulation GC cell epithelial‐mesenchymal transition (EMT). The results suggested a novel role of AIB1 in GC invasion and EMT and raised the possibility of using this molecule as an indicator for GC treatment. … (more)
- Is Part Of:
- Journal of cellular biochemistry. Volume 122:Issue 9(2021)
- Journal:
- Journal of cellular biochemistry
- Issue:
- Volume 122:Issue 9(2021)
- Issue Display:
- Volume 122, Issue 9 (2021)
- Year:
- 2021
- Volume:
- 122
- Issue:
- 9
- Issue Sort Value:
- 2021-0122-0009-0000
- Page Start:
- 926
- Page End:
- 933
- Publication Date:
- 2019-11-06
- Subjects:
- AIB1 -- epithelial‐mesenchymal transition -- gastric cancer -- PI3K/AKT signaling
Cytochemistry -- Periodicals
572 - Journal URLs:
- http://onlinelibrary.wiley.com/journal/10.1002/(ISSN)1097-4644 ↗
http://onlinelibrary.wiley.com/ ↗ - DOI:
- 10.1002/jcb.29530 ↗
- Languages:
- English
- ISSNs:
- 0730-2312
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 4955.010000
British Library DSC - BLDSS-3PM
British Library HMNTS - ELD Digital store - Ingest File:
- 23839.xml