Subhamoy Dasgupta

Molecular and Cellular Biology

Specializing In:

Cancer Biology Metabolic Signaling Signal Transduction Intermediary Metabolism

Research Interests:

Tumor cell metabolism Transcriptional Regulation Mitochondrial Biology Immunometabolism Cancer Metastasis

About Subhamoy Dasgupta


Dr. Subhamoy Dasgupta joined the faculty of Cell Stress Biology at the Roswell Park Comprehensive Cancer Center in July 2017 as an Assistant Member and Assistant Professor of Oncology. Subho earned his BS in Chemistry and Microbiology from Bangalore University, a MS in Biochemistry from Banaras Hindu University, India, and a PhD in Biomedical Sciences from UNT Health Science Center at Fort Worth, Texas. As a graduate student, he characterized the functional role of a novel oncogene named C17orf37/MIEN1 in prostate and breast cancer invasion-metastasis (Oncogene, 2009) under the mentorship of Dr. JK Vishwanatha. His doctoral thesis revealed how isoprenylation of MIEN1 protein can regulate its translocation to the plasma membrane and activate signaling events leading to increased invasive phenotype (JBC, 2011; Mol Can, 2015).

Dr. Dasgupta performed a postdoctoral fellowship in the laboratory of Dr. Bert W. O'Malley at Baylor College of Medicine, Houston, where he demonstrated that transcriptional coregulator steroid receptor coactivator 2 (SRC-2/NCOA2) regulates metabolic reprogramming to accentuate prostate cancer metastasis (JCI, 2015). As a Susan G. Komen Postdoctoral fellow, he uncovered a novel interplay between a glycolytic enzyme and oncogenic coactivator SRC-3/AIB1 leading to increased proliferation and metastasis of breast tumors.

The Dasgupta laboratory focuses on defining the underlying mechanisms that promote tumor progression and metastasis by taking a systems biology approach investigating metabolic pathways, genetic and epigenetic regulation, and immune evasion mechanisms that selectively sustain aggressive cancer progression. Dr. Dasgupta’s laboratory is funded by grants from the National Cancer Institute (NCI), NIH Director's Award, Susan G. Komen Foundation and Department of Defense (DoD).

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Roswell Park Comprehensive Cancer Center
  • Associate Professor of Oncology, Cell Stress Biology
  • Department of Cell Stress Biology


Education and Training:

  • 2005-2010 - PhD - Biomedical Sciences, University of North Texas Health Science Center, Texas


  • 2011-2015 - Postdoctoral Fellowship, Baylor College of Medicine, Houston, Texas

Professional Memberships:

  • Sigma Xi
  • American Association for Cancer Research (AACR)
  • Endocrine Society

Honors & Awards:

  • 2020 - NIH Director's New Innovator Award (DP2)
  • 2019 Outstanding Young Investigator, Endocrine Society
  • 2018 Career Catalyst Research Award, Susan G. Komen
  • 2017 - The NCI Transition Career Development Award (K22)
  • 2016 - DOD-Idea Development Award, Prostate Cancer Research Program
  • 2014 - Susan G. Komen Breast Cancer Postdoctoral Fellowship
  • 2010 - Outstanding Graduate Student, Biomedical Sciences, UNTHSC
  • 2008 - Department of Defense (DoD)- Predoctoral Fellowship


Research Overview:

Metabolic reprogramming is an essential hallmark of tumor progression and metastasis. Cancer cells use altered metabolic pathways to sustain rapid growth and to overcome enormous stress encountered in tumor microenvironment. Tumor cells constantly alter their metabolic state in response to oncogenic stimuli, nutrient availability, and interaction with immune cells however the precise regulation that precedes the metabolic alteration is poorly understood. We believe information about a tumor cell's metabolic state is integrated into the regulation of transcription, and understanding these regulatory checkpoints will certainly allow us to intervene tumor progression and metastasis. Our lab uses state-of-art facilities such as metabolomics, proteomics, and genomics along with molecular biology techniques to investigate the crosstalk between metabolic signaling and transcriptional networks. Multiple animal model systems including genetically engineered mouse models (GEMMs), patient-derived xenograft (PDX), and syngeneic tumor models are used to investigate metabolic adaptations that promote tumor progression and metastasis.

Discovering Metabolic Dysregulation In Cancer
Metabolic adaptation is one of the essential hallmarks of cancer to sustain replication and survival stress. Based on available nutrients, tumor cells alter their metabolic pathways for the biosynthesis of macromolecules and mitochondrial ATP synthesis. Metabolic reprogramming plays a pivotal role in tumor cell survival during metastatic dissemination, circulation, and colonization in distant organs, thus driving the successful formation of metastatic lesions. Hence, we are understanding the metabolic checkpoints that drive aggressive metastatic cancer that could be exploited as a potential therapeutic target.

Defining Transcriptional and Epigenetic Regulation
Cellular adaptation to fuel availability is critical for major cellular decisions, and it requires alterations in metabolic pathways coupled with differential expression of genes to rewire biochemical processes. Mitochondria lay at the core of cellular metabolism, whereas nucleus integrates cellular and environmental signals to activate gene transcription. Intriguingly, many metabolic enzymes can directly sense the nutrient supply and stimulate gene transcription to establish an adaptive response. However, how the mitochondrial enzymes modulate gene transcription in response to bioenergetic stress is poorly understood, which is an active area of investigation in our lab.

Decoding Tumor Microenvironment and Immune Response
Tumor intrinsic metabolic pathways significantly alter the tumor microenvironment (TME). Metabolic stress in TME influences aggressive tumor phenotype and the hypoxic regions within the tumor exert an increased risk of metastasis by activating transcriptional programs. TME consists of cellular components including stromal cells and immune cells, and characterized by lactic acidosis, hypoxia and secreted tumor-derived factors. We are interested to define whether adaptive changes induced by TME contribute to enhanced invasiveness by allowing cancer cells to acquire cell-autonomous properties favoring site-specific metastatic colonization. In addition, altered tumor metabolism promotes an immunosuppressive TME which may diminish efficacy and response rate of immunotherapy. We are investigating the mechanisms that regulate TME properties compromising anti-tumor immune response.

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Featured on Cancer Talk


Full Publications list on PubMed
  • Sawant Dessai A, Dominguez MP, Chen UI, Hasper J, Prechtl C, Yu C, Katsuta E, Dai T, Zhu B, Jung SY, Putluri N, Takabe K, Zhang XH, O'Malley BW, Dasgupta S. Transcriptional Repression of SIRT3 Potentiates Mitochondrial Aconitase Activation to Drive Aggressive Prostate Cancer to the Bone. Cancer Research. 2021 Jan 1;81(1):50-63.PMID: 33115805; PMCID: PMC7878313.


  • Blundon MA, Dasgupta S. Metabolic Dysregulation Controls Endocrine Therapy-Resistant Cancer Recurrence and Metastasis. Endocrinology. 2019 Aug 1;160(8):1811-1820. PMID: 31157867; PMCID: PMC6620757.


  • Singh R, Karri D, Shen H, Shao J, Dasgupta S, Huang S, Edwards DP, Ittmann MM, O'Malley BW, Yi P. TRAF4-mediated ubiquitination of NGF receptor TrkA regulates prostate cancer metastasis. Journal of Clinical Investigation. 2018 Jul 2;128(7):3129-3143. PMID: 29715200; PMCID: PMC6026011.


  • Dasgupta S, Rajapakshe K, Zhu B, Nikolai BC, Yi P, Putluri N, Choi JM, Jung SY, Coarfa C, Westbrook TF, Zhang XH, Foulds CE, Tsai SY, Tsai MJ, O'Malley BW. Metabolic enzyme PFKFB4 activates transcriptional coactivator SRC-3 to drive breast cancer. Nature. 2018 Apr;556(7700):249-254. PMID: 29615789; PMCID: PMC5895503.

  • Dasgupta S, Putluri N, Long W, Kaushik AK, Zhang B, Bhowmik SK, Wang J, Stashi E, Brennan CA, Ittmann MM, Mitsiades N, Chinnaiyan AM, Sreekumar A, O’Malley BW. Coactivator SRC-2-dependent metabolic reprogramming mediates prostate cancer survival and metastasis. Journal of Clinical Investigation. 2015 Mar 2;125(3):1174-88. PMID:25664849 PMCID: PMC4362260.