Satyanarayana Ande, PhD
Associate Professor, Biochemistry and Molecular Biology
Member, Molecular Oncology and Biomarkers Program
Georgia Cancer Center at Augusta University
My laboratory research is mainly focused on liver cancer and obesity-associated liver disease. We are specifically interested in identifying novel cytokines and transcription factors and investigating their specific function in the liver and adipose tissues and their potential involvement in the initiation and progression of liver cancer and obesity-associated fatty liver disease.
The Satyanarayana Ande Lab
Health Sciences Campus
GCC - M. Bert Storey Research Building
1410 Laney Walker Blvd., CN-3327, Augusta, GA 30912
(706) 723-0029
Liver cancer is one of the leading causes of cancer deaths worldwide. Therefore, it is very essential to investigate and understand liver cancer at the cellular and molecular levels to discover specific molecular targets for this deadly cancer. My laboratory utilizes advanced techniques such as RNAseq, Mass-Spec and cytokine/protein arrays to identify genes that are differentially expressed in the liver cancer compared to normal liver. Subsequently, we generate gene knockout and transgenic mouse models to investigate the specific functions of these genes in the initiation and progression of liver cancer and liver cancer cell metabolic adaptation.
Metabolic reprogramming is one of the central hallmarks of cancer, and the majority of cancer cells, including liver cancer cells, depend on high rates of glycolysis and glutaminolysis for their growth and survival. Therefore, identifying and targeting proteins that play critically important roles in metabolic reprogramming is a very valid strategy to suppress tumor growth. By utilizing RNAseq, Mass-Spec and cytokine arrays we identify genes that are differentially expressed in the liver cancer compared to normal liver. We then investigate the function of these genes in cancer cell metabolic reprogramming. Subsequently, we generate gene knockout and transgenic mouse models and explore the specific functions of these genes in the progression of liver cancer.
Obesity is a significant risk factor for various diseases such as hypertension, type 2 diabetes, dyslipidemia, chronic heart disease, fatty liver disease and various cancers. Recently, obesity-induced non-alcoholic fatty liver disease (NAFLD), and its progression to non-alcoholic steatohepatitis (NASH), have emerged as critical promoters of hepatocellular carcinoma (HCC). Adipose tissue dysfunction and subsequent infiltration of inflammatory cells to the adipose tissues and the resulting chronic low grade inflammation play central role in the development and progression of NAFLD. My laboratory is very actively investigating the role of specific cytokines and transcription factors in adipose tissue dysfunction, hepatosteatosis and its progression to NASH and HCC.
Dimri M, Humphries A, Laknaur A, Elattar S, Lee TJ, Sharma A, Kolhe R, Satyanarayana A. NADP(P)H quinone dehydrogenase 1 ablation inhibits activation of the phosphoinositide 3-kinase/Akt serine/threonine kinase and mitogen-activated protein kinase/extracellular signal-regulated kinase pathways and blocks metabolic adaptation in hepatocellular carcinoma. Hepatology, 2020; Feb;71(2):549-568.
Elattar S, Dimri M, Satyanarayana A. The tumor secretory factor ZAG promotes white adipose tissue browning and energy wasting. FASEB J, 2018; Sep; 32(9): 4727-4743.
Patil M, Sharma BK, Elattar S, Chang J, Kapil S, Yuan J, Satyanarayana A. Id1 promotes obesity by suppressing brown adipose thermogenesis and white adipose browning. Diabetes 2017 Jun; 66(6): 1611-1625.
Kapil S*, Sharma BK*, Patil M*, Elattar S, Yuan J, Hou SX, Kolhe R, Satyanarayana A. The cell polarity protein Scrib functions as a tumor suppressor in liver cancer. Oncotarget 2017, Feb 24; 15713. (* equal contribution)
Tu Z, Bayazit MB, Liu H, Zhang J, Busayavalasa K, Risal S, Shao J, Satyanarayana A, Coppola V, Tessarollo L, Singh M, Zheng C, Han C, Chen Z, Kaldis P, Gustafsson JÅ, Liu K. Speedy A-Cdk2 binding mediates initial telomere-nuclear envelope attachment during meiotic prophase I independent of Cdk2 activation. Proc Natl Acad Sci U S A. 2017, Jan 17;114(3):592-597.
Sharma BK, Kolhe R, Black SM, Keller JR, Mivechi NF, Satyanarayana A. Inhibitor of differentiation 1 transcription factor promotes metabolic reprogramming in hepatocellular carcinoma cells. FASEB J 2016, Jan; 30(1):262-75.
