Amir Sabbaghian
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Amir Sabbaghian has a total of 11 co-authors. Here are the top co-authors by number of shared publications:
- E. Shyong Tai
Saw Swee Hock School of Public Health, National University of Singapore, Singapore, Singapore
1 shared publication - Fei Xie
Department of Breast Disease Center, Peking University People’s Hospital, Beijing 100044, China
1 shared publication - Hexian Lin
School of Medicine, Zhejiang University-University of Edinburgh Institute, Zhejiang University, Hangzhou 314400, China
1 shared publication - Lih-Wen Deng
Integrative Sciences and Engineering Programme, NUS Graduate School, National University of Singapore, Singapore, Singapore
1 shared publication - Shin-Ae Kang
Department of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117596, Singapore
1 shared publication - Shu Wang
Breast Center, Peking University People’s Hospital, Beijing 100044, China
1 shared publication
Latest Publications
- Open Access
WBP2 Attenuates Metformin Response in HER2-Positive Breast Cancer Cells by Repressing AMPK Activation and Inducing a Lower AMP:ATP Ratio State Through Enhanced ATP Production
Metformin is an antidiabetic drug that has been tested widely as an anti-cancer agent. However, data from clinical trials have been mixed. Evidence for metformin’s efficacy in HER2+ breast cancer exists. Hence, we evaluated whether WBP2, a HER2-coamplified gene, can regulate the response of HER2+ breast cancer to metformin. Identification of biomarkers for predicting metformin response has implications in repurposing metformin for precision oncology. The effect of WBP2 on breast cancer response to metformin was studied using in vitro and mouse models. The mechanism of WBP2 on metformin-induced AMPK activation was elucidated, and its co-expression with p-AMPK was examined in clinical specimens using IHC. RNA-seq analyses were performed to elucidate WBP2’s mechanism in energy metabolism. WBP2 inhibited the metformin response of HER2+ breast cancer in vitro and in vivo. These effects were concomitant with WBP2-mediated repression of metformin-induced AMPK activation and mTOR inhibition in HER2+ breast cancer cells, a lower AMP:ATP ratio state, and enhanced glycolytic capacity and mitochondria respiration. Analysis of HER2-positive breast cancer samples supports the negative correlation between WBP2 expression and activated AMPK observed in vitro. RNA-seq analysis revealed the potential mechanism of WBP2 in regulating ATP production processes and preferential effect of WBP2 on metformin response in HER2+ breast cancer. This study reported a novel role of WBP2 in cancer metabolism and energetics that contributes new insights into the molecular etiology of cancer. WBP2 may be a biomarker for patient stratification, paving the way towards repurposing metformin for precision oncology.
Open AccessWBP2 Attenuates Metformin Response in HER2-Positive Breast Cancer Cells by Repressing AMPK Activation and Inducing a Lower AMP:ATP Ratio State Through Enhanced ATP Production
Metformin is an antidiabetic drug that has been tested widely as an anti-cancer agent. However, data from clinical trials have been mixed. Evidence for metformin’s efficacy in HER2+ breast cancer exists. Hence, we evaluated whether WBP2, a HER2-coamplified gene, can regulate the response of HER2+ breast cancer to metformin. Identification of biomarkers for predicting metformin response has implications in repurposing metformin for precision oncology. The effect of WBP2 on breast cancer response to metformin was studied using in vitro and mouse models. The mechanism of WBP2 on metformin-induced AMPK activation was elucidated, and its co-expression with p-AMPK was examined in clinical specimens using IHC. RNA-seq analyses were performed to elucidate WBP2’s mechanism in energy metabolism. WBP2 inhibited the metformin response of HER2+ breast cancer in vitro and in vivo. These effects were concomitant with WBP2-mediated repression of metformin-induced AMPK activation and mTOR inhibition in HER2+ breast cancer cells, a lower AMP:ATP ratio state, and enhanced glycolytic capacity and mitochondria respiration. Analysis of HER2-positive breast cancer samples supports the negative correlation between WBP2 expression and activated AMPK observed in vitro. RNA-seq analysis revealed the potential mechanism of WBP2 in regulating ATP production processes and preferential effect of WBP2 on metformin response in HER2+ breast cancer. This study reported a novel role of WBP2 in cancer metabolism and energetics that contributes new insights into the molecular etiology of cancer. WBP2 may be a biomarker for patient stratification, paving the way towards repurposing metformin for precision oncology.