Photo of Bin Zheng,  PhD

Bin Zheng, PhD

Massachusetts General Hospital

Massachusetts General Hospital
Phone: (617) 724-9958

Bin Zheng, PhD

Massachusetts General Hospital


  • Assistant Professor, Dermatology, Harvard Medical School
  • Assistant Biologist, Dermatology, Massachusetts General Hospital


Research Abstract

The focus of our laboratory research is on metabolic signaling in melanoma. We are interested in understanding how rewired metabolism in cancer cells is coordinated with other hallmarks of cancer to influence cancer initiation, promotion and progression. Approximately half of all melanomas harbor an activating mutation in BRAF (BRAFV600E) that drives cancer growth due to the constitutive activation of the downstream MEK/ERK pathway. The “addiction” of melanomas harboring this BRAF mutation has stimulated the development of BRAF inhibitors (BRAFi), such as Vemurafenib and Dabrafenib. These BRAFi have shown great clinical benefits in malignant melanoma with BRAFV600E mutations in the initial phase of treatment. However, the vast majority of the responsive melanoma patients treated with BRAF inhibitors develop resistance during the course of treatment and relapsed. In addition to the BRAF-targeted therapy, another recent major groundbreaking approach in melanoma treatment is to target the immune checkpoints that exploit melanoma’s intrinsically high immunogenicity. Biological drugs that target CTLA-4, PD-1 or PD-L1 have shown significant clinical benefits in melanoma patients with a high degree of durable responses, but only in a subset of patients. Therefore, improving the response rates of immunotherapies and overcoming BRAFi resistance represent two of the greatest challenges facing this field. The overarching goal of our research is to address this by gaining a better understanding of metabolic programming in melanoma and to translate these basic research findings into better strategies for melanoma prevention, diagnosis and treatment. In particular, we currently focus on the following areas of research:

1) BRAF-dependent metabolic wiring and rewiring;

2) Metabolic heterogeneity in cancer;

3) Metabolic regulation of tumor immunity;

4) Roles of AMPK at the interface of metabolism and Cancer;

5) Reviving Phenformin for Cancer Therapy.



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  • Trousil S, Zheng B. Addicted to AA (Acetoacetate): A Point of Convergence between Metabolism and BRAF Signaling. Mol Cell 2015; 59:333-4. PubMed
  • Zheng B, Fisher DE. Metabolic vulnerability in melanoma: a ME2 (me too) story. J Invest Dermatol 2015; 135:657-9. PubMed
  • DeRan M, Yang J, Shen CH, Peters EC, Fitamant J, Chan P, Hsieh M, Zhu S, Asara JM, Zheng B, Bardeesy N, Liu J, Wu X. Energy stress regulates hippo-YAP signaling involving AMPK-mediated regulation of angiomotin-like 1 protein. Cell Rep 2014; 9:495-503. PubMed
  • Yuan P, Ito K, Perez-Lorenzo R, Del Guzzo C, Lee JH, Shen CH, Bosenberg MW, McMahon M, Cantley LC, Zheng B. Phenformin enhances the therapeutic benefit of BRAF(V600E) inhibition in melanoma. Proc Natl Acad Sci U S A 2013. PubMed
  • Shen CH, Yuan P, Perez-Lorenzo R, Zhang Y, Lee SX, Ou Y, Asara JM, Cantley LC, Zheng B. Phosphorylation of BRAF by AMPK impairs BRAF-KSR1 association and cell proliferation. Mol Cell 2013. PubMed
  • Wu N, Zheng B, Shaywitz A, Dagon Y, Tower C, Bellinger G, Shen CH, Wen J, Asara J, McGraw TE, Kahn BB, Cantley LC. AMPK-Dependent Degradation of TXNIP upon Energy Stress Leads to Enhanced Glucose Uptake via GLUT1. Mol Cell 2013; 49:1167-75. PubMed
  • Mack HI, Zheng B, Asara J, Thomas SM. AMPK-dependent phosphorylation of ULK1 regulates ATG9 localization. Autophagy 2012; 8:1197-214. PubMed
  • Dagon Y, Hur E, Zheng B, Wellenstein K, Cantley LC, Kahn BB. p70S6 kinase phosphorylates AMPK on serine 491 to mediate leptin's effect on food intake. Cell Metab 2012; 16:104-12. PubMed
  • Li Y, Xu S, Mihaylova MM, Zheng B, Hou X, Jiang B, Park O, Luo Z, Lefai E, Shyy JY, Gao B, Wierzbicki M, Verbeuren TJ, Shaw RJ, Cohen RA, Zang M. AMPK phosphorylates and inhibits SREBP activity to attenuate hepatic steatosis and atherosclerosis in diet-induced insulin-resistant mice. Cell Metab 2011; 13:376-88. PubMed
  • Tsou P, Zheng B, Hsu CH, Sasaki AT, Cantley LC. A Fluorescent Reporter of AMPK Activity and Cellular Energy Stress. Cell Metab 2011; 13:476-86. PubMed
  • Zheng B,Jeong JH,Asara JM,Yuan YY,Granter SR,Chin L,Cantley LC. Oncogenic B-RAF negatively regulates the tumor suppressor LKB1 to promote melanoma cell proliferation. Mol Cell 2009; 33:237-47. PubMed