Molecular Oncology and Biomarkers Program
Associate Professor, Biochemistry & Molecular Biology
Georgia Cancer Center
1410 Laney Walker Blvd., Office: CN-3150
Phone: 706-723-0029 office 706-721-4121 laboratory
My laboratory research is mainly focused on obesity/cachexia, liver cancer and cancer metabolism studies. We are specifically interested in identifying novel cytokines and transcription factors and investigating their function in the liver and adipose tissue metabolic pathways and their potential role in the initiation and progression of liver cancer, obesity and cachexia.
Liver cancer is one of the leading causes of cancer deaths worldwide. Therefore, it is very essential to study and understand liver cancer at the cellular and molecular levels to discover specific molecular targets for reducing the cancer burden. My laboratory utilizes advanced techniques such as RNAseq, Mass-Spec and cytokine 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.
Obesity is a significant risk factor for various diseases such as hypertension, type 2 diabetes, dyslipidemia, chronic heart disease, fatty liver disease and degenerative disorders and various cancers such as liver, colon, breast, gastric, gallbladder, endometrial, esophagus, pancreas and renal cell carcinoma. Obesity results from lack of physical activity, increased energy consumption and reduced energy expenditure. My laboratory is actively investigating the role of specific cytokines and transcription factors in the energy storage and expenditure pathways. Specifically, we are studying these pathways in the liver and adipose tissues. Obesity and cachexia are the opposite sides of the same coin. Cachexia is a complex condition of tissue wasting that affects up to 80% of cancer patients. Other end-stage diseases such as AIDS, congestive heart failure, rheumatoid arthritis, tuberculosis, and cystic fibrosis are also associated with cachexia. Cachexia is characterized by systemic inflammation, hyper-metabolism, increased energy expenditure, loss of skeletal muscle and white adipose tissue (WAT). Therefore, understanding how the energy expenditure and energy storage pathways operate in two completely opposite diseases, obesity and cachexia, will provide significant insights into how these pathways are regulated and which proteins play critical roles in body energy expenditure versus energy storage.
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.
Elattar S, Dimri M, Satyanarayana A. The Tumor Secretory Factor Zag Promotes White Adipose Tissue Browning and Energy Wasting, FASEB J 2018 Mar 23: fj201701465RR. doi: 10. 1096/fj.201701465RR. [Epub ahead of print]
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 Mar 7. [Epub ahead of print].
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.
Satyanarayana A. Brown adipose tissue and the genetics of obesity. Heart and Metabolism 2016, 69; 4-8.
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.
Elattar S, Satyanarayana A. Can brown fat win the battle against white fat? J Cell Physiol 2015, Oct;230(10):2311-7.
Patil M, Sharma BK, Satyanarayana A. Id transcriptional regulators in adipogenesis and adipose tissue metabolism. Frontiers in Bioscience 2014, Jun; 19: 1386-97.
Sharma BK, Patil M, Satyanarayana A. Negative regulators of brown adipose tissue (BAT)-mediated thermogenesis. J Cell Physiol 2014, Dec; 229 (12): 1901-7
Satyanarayana A, Klarmann KD, Gavrilova O, Keller Jr. Ablation of the transcriptional regulator Id1 enhances energy expenditure and increases insulin sensitivity and protects against age and diet induced insulin resistance and hepatosteatosis. FASEB J 2012, Jan; 26 (1): 309-323.
Sirma H, Kumar M, Meena JK, Witt B, Weise JM, Lechel A, Satyanarayana A, Sakk V, Guguen-Guillouzo C, Zender L, Rudolph KL, Gunes C. The promoter of human telomerase reverse transcriptase is activated during liver regeneration and hepatocyte proliferation. Gastroenterology 2011, Jul; 141 (1): 326-337.
Satyanarayana A*, Gudmundsson KO*, Chen X*, Coppala V, Tessarollo L, KellerJ, Hou SX. RapGEF2 is essential for embryonic hematopoiesis but dispensable for adult hematopoiesis. Blood 2010, Oct 21; 116 (16): 2921-2931. (* equal contribution)
Satyanarayana A, Kaldis P. Mammalian Cell Cycle Regulation: several Cdks, numerous cyclins and diverse compensatory mechanisms. Oncogene 2009, Aug; 28 (33):2925-39.
Satyanarayana A, Kaldis P. A dual role of Cdk2 in DNA damage response. Cell Division 2009 May; 18; 4:9.
Satyanarayana A, Berthet C, Lopez-Molina J, Coppala V, Tessarolo L, Kaldis P. Genetic substitution of Cdk1 by Cdk2 leads to embryonic lethality and loss of meiotic function of Cdk2. Development 2008 Oct; 135 (20): 3389-400. # cover page article of the issue #
Satyanarayana A, Hilton MB & Kaldis P. P21 inhibits Cdk1 in the absence ofCdk2 to maintain G1/S phase DNA damage checkpoint. Mol Biol Cell 2008 Jan;19(1):65-77. Epub 2007 Oct 17.
Lechel A, Satyanarayana A, Ju Z, Plentz RR, Schaetzlein S, Rudolph C, Wilkens L, Wiemann SU, Saretzki G, Malek NP, Manns MP, Buer J, Rudolph KL. The cellular level of telomere dysfunction determines induction of senescence or apoptosis in vivo. EMBO Rep. 2005 Mar;6(3):275-81.
Wiemann SU, Satyanarayana A, Buer J, Kamino K, Manns MP, Rudolph KL. Contrasting effects of telomere shortening on organ homeostasis, tumor suppression, and survival during chronic liver damage. Oncogene 2005 Feb 24;24(9):1501-9.
Satyanarayana A, Geffers R, Manns MP, Buer J, Rudolph KL. Gene expression profile at the G1/S transition of liver regeneration after partial hepatectomy in mice. Cell Cycle 2004 Nov;3(11):1405-17.
Satyanarayana A, Rudolph KL. p16 and ARF: activation of teenage proteins in old age. J Clin Invest. 2004 Nov;114(9):1237-40.
Satyanarayana A, Manns MP, Rudolph KL. Telomeres, telomerase and cancer: An endless search to target the ends. Cell Cycle 2004 Sep;3(9):1138-50.
Satyanarayana A, Manns MP, Rudolph KL. Telomeres and Telomerase: A dual role in Hepatocarcinogenesis. Hepatology 2004 Aug;40(2):276-83.
Satyanarayana A, Greenberg RA, Schaetzlein S, Buer J, Masutomi K, Hahn WC,Zimmermann S, Martens U, Manns MP, Rudolph KL. Mitogen stimulation co-operates with telomere shortening to activate DNA damage responses and senescence signaling. Mol Cell Biol 2004 Jun;24(12):5459-74.
Satyanarayana A, Wiemann SU, Buer J, Lauber J, Dittmar KEJ, Wüstefeld T,Blasco M, Manns MP, Rudolph KL. Telomere shortening impairs organ regeneration by inhibiting cell cycle re-entry of a sub-population of cells. EMBO J 2003 Aug 1;22(15):4003-4013.
Wiemann SU*, Satyanarayana A*, Tsahuridu M*, Tillmann HL, Zender L, Klempnauer J, Flemming P, Franco S, Blasco MA, Manns MP, Rudolph KL. Hepatocyte telomere shortening and senescence are general markers of human liver cirrhosis. FASEB J 2002 Jul;16(9):935-42 (* equal contribution).