Department： Breast Surgery
Medical School：Chinese Center for Disease Control and Prevention, China
Academic Rank：Professor
Metabolic reprogramming and epigenetic modifications in EMT and cancer metastasis
Lactylation and other modifications of protein in tumors
USCACA-NFCR Scholar Awards, US-Chinese Anti-Cancer Association
Member, American Association for Cancer Research
Basal-like breast cancer (BLBC) is associated with a poor clinical outcome due to few treatment options and poor therapeutic response. Notably, BLBC possess the activated epithelial-mesenchymal transition (EMT) program, which is required for tumor progression and metastasis. Thus there is a pressing need to characterize its aggressiveness and identify its therapeutic targets. We have identified that BLBC cells lose FBP1 expression due to transcription repression of Snail. Loss of FBP1 triggers a glycolytic reprogramming, which contributes to maintenance of CSCs property and EMT phenotype. In addition, we reported that AKR1B1 as a key modulator of tumor aggressiveness provides tumorigenic and metastatic advantages in BLBC through a positive regulatory feedback loop that activates the EMT program and enhances CSC-like properties. Interestingly, epalrestat, the only AKR1B1 inhibitor that has been approved for the targeted treatment of diabetic complications, exhibits apparent inhibitory effect on BLBC using cellular and mice models, suggesting that epalrestat has the potential to become a valuable targeted drug in clinical treatment of BLBC. Our study not only reveals a critical mechanism of how metabolic reprogramming contributes to EMT and metastasis, but also provides potential targets for the treatment of BLBC.
Huang P, Liao R, Chen X, Wu X, Li X, Wang Y, Cao Q, Dong C*. Nuclear translocation of PLSCR1 activates STAT1 signaling in basal-like breast cancer. Theranostics. 2020;10(10): 4644-4658.
Wang Y, Liao R, Chen X, Chen G, Dong C*. Twist-mediated PAR1 induction is required for breast cancer progression and metastasis by inhibiting Hippo pathway. Cell Death & Disease. 2020; 11: 520.
Wang Z, Dong C*. Gluconeogenesis in Cancer: Function and Regulation of PEPCK, FBPase, and G6Pase. Trends in Cancer. 2019; 5 (1): 30-45.
Chen X, Cao Q, Liao R, Wu, X, Xun S, Huang J, Dong C*. Loss of ABAT-mediated GABAergic system promotes basal-like breast cancer progression by activating Ca2+-NFAT1 axis. Theranostics. 2019; 9 (1): 34-47.
Cao Q, Chen X, Wu, X, Liao R, Huang P, Tan Y, Wang L, Ren G, Huang J and Dong C*. Inhibition of UGT8 Suppresses Basal-like Breast Cancer Progression by Attenuating Sulfatide-αVβ5 Axis. J Exp Med. 2018; 215 (6) 1679-1692.
Wu X, Li X, Fu Q, Cao Q, Chen X, Wang M, Yu J, Long J, Yao J, Liu H, Wang D, Liao R and Dong C*. AKR1B1 promotes basal-like breast cancer progression by a positive feedback loop that activates the EMT program. J Exp Med. 2017; 214 (4) 1065-1079.
Zhu X, Su D, Xuan S, Ma G, Dai Z, Liu T, Tang D, Mao W*, and Dong C*. Gene Therapy of Gastric Cancer Using LIGHT-Secreting Human Umbilical Cord Blood–Derived Mesenchymal Stem Cells. Gastric Cancer. 2013; 16(2):155-66.
Dong C, Yuan T, Wu Y, Wang Y, Fan T, Miriyala S, Lin Y, Yao J, Shi J, Kang T, Lorkiewicz P, Clair DS, Hung MC, Evers BM, and Zhou BP. Loss of FBP1 by Snail-mediated Repression Provides Metabolic Growth Advantages in Basal-like Breast Cancer. Cancer Cell, 23(3): 316-331, 2013. Commentary Coverage: Schieber, MS and Chandel, NS. ROS Links Glucose Metabolism to Breast Cancer Stem Cell and EMT Phenotype. Cancer Cell. 2013; 23(3): 265-267.
Dong C, Wu Y, Yao J, Wang Y, Yu Y, Rychahou PG, Evers BM, and Zhou BP. G9a interacts with Snail and is critical for Snail‐mediated E‐cadherin repression in human breast cancer. J Clin Invest. 2012; 122(4):1469-86.
Dong C, Wu Y, Wang Y, Wang C, Kang TB, Rychahou PG, Chi Y‐I, Evers BM, and Zhou BP. Interaction with Suv39H1 is Critical for Snail‐mediated E‐cadherin Repression in Breast Cancer. Oncogene. 2013; 14; 32(11):1351-62.
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