Daniel E. Frigo

ORCID: 0000-0002-0713-471X
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About
Contact & Profiles
Research Areas
  • Cancer, Lipids, and Metabolism
  • Prostate Cancer Treatment and Research
  • Cancer, Hypoxia, and Metabolism
  • Metabolism, Diabetes, and Cancer
  • Estrogen and related hormone effects
  • Lipid metabolism and biosynthesis
  • Adipose Tissue and Metabolism
  • Cancer-related Molecular Pathways
  • Autophagy in Disease and Therapy
  • PI3K/AKT/mTOR signaling in cancer
  • Amino Acid Enzymes and Metabolism
  • Mitochondrial Function and Pathology
  • Hormonal and reproductive studies
  • Melanoma and MAPK Pathways
  • Prostate Cancer Diagnosis and Treatment
  • Cancer-related molecular mechanisms research
  • Advanced NMR Techniques and Applications
  • Protein Kinase Regulation and GTPase Signaling
  • Advanced MRI Techniques and Applications
  • Molecular Biology Techniques and Applications
  • Hormonal Regulation and Hypertension
  • Retinoids in leukemia and cellular processes
  • Metabolomics and Mass Spectrometry Studies
  • Ferroptosis and cancer prognosis
  • Pancreatic function and diabetes

The University of Texas MD Anderson Cancer Center
2017-2025

University of Houston
2015-2024

Duke University Hospital
2008-2023

Duke Medical Center
2008-2023

Houston Methodist
2012-2022

Methodist Hospital
2021

The University of Texas Health Science Center at Houston
2020

Methodist Hospital
2020

Florey Institute of Neuroscience and Mental Health
2020

Baylor College of Medicine
2015

Transmitochondrial cybrids and multiple OMICs approaches were used to understand mitochondrial reprogramming mitochondria-regulated cancer pathways in triple-negative breast (TNBC). Analysis of established (BC) cell lines showed that metastatic TNBC maintains high levels ATP through fatty acid β oxidation (FAO) activates Src oncoprotein autophosphorylation at Y419. Manipulation FAO including the knocking down carnitine palmitoyltransferase-1A (CPT1) 2 (CPT2), rate-limiting proteins FAO,...

10.1016/j.celrep.2016.02.004 article EN cc-by-nc-nd Cell Reports 2016-02-25

Abstract Androgens, through their actions on the androgen receptor (AR), are required for development of prostate and contribute to pathologic growth dysregulation observed in cancers. Consequently, ablation has become an essential component pharmacotherapy cancer. In this study, we explored utility targeting processes downstream AR as alternate approach therapy. Specifically, show that serum glucocorticoid-regulated kinase 1 (SGK1) gene is androgen-regulated target cellular models...

10.1158/0008-5472.can-08-1047 article EN Cancer Research 2008-09-14

Abstract Cancer cells display an increased demand for glucose. Therefore, identifying the specific aspects of glucose metabolism that are involved in pathogenesis cancer may uncover novel therapeutic nodes. Recently, there has been a renewed interest role pentose phosphate pathway cancer. This metabolic is advantageous rapidly growing because it provides nucleotide precursors and helps regenerate reducing agent NADPH, which can contribute to reactive oxygen species (ROS) scavenging....

10.1038/oncsis.2014.18 article EN cc-by Oncogenesis 2014-05-26

While patients with advanced prostate cancer initially respond favorably to androgen ablation therapy, most experience a relapse of the disease within 1-2 years. Although hormone-refractory is unresponsive androgen-deprivation, receptor (AR)-regulated signaling pathways remain active and are necessary for progression. Thus, both AR itself processes downstream viable targets therapeutic intervention. Microarray analysis multiple clinical cohorts showed that serine/threonine kinase...

10.1158/0008-5472.can-10-2581 article EN Cancer Research 2010-11-23

// Sanchaika Gaur 1,2,9 , Yunfei Wen 3 Jian H. Song 1 Nila U. Parikh Lingegowda S. Mangala 3,4 Alicia M. Blessing 5 Cristina Ivan Sherry Y. Wu Andreas Varkaris Yan Shi Gabriel Lopez-Berestein 4,6 Daniel E. Frigo 5,7 Anil K. Sood 2,3,4,8 and Gary Gallick 1,2 Department of Genitourinary Medical Oncology, David Koch Center for Applied Research Cancers, The University Texas, MD Anderson Cancer Center, Houston, TX, USA 2 Program in Biology Metastasis, Texas Graduate School Biomedical Sciences at...

10.18632/oncotarget.4971 article EN Oncotarget 2015-07-22

Triple-negative breast cancer (TNBC) is characterized by aggressiveness and affects 10-20% of patients. Since TNBC lacks expression ERα, PR HER2, existing targeted treatments are not effective the survival poor. In this study, we demonstrate that tumor suppressor microRNA miR-200a directly regulates oncogene EPH receptor A2 (EPHA2) modulates migration. We show EPHA2 correlated with poor specifically in basal-like its repressed through direct interaction 3'UTR EPHA2. This regulation...

10.1093/carcin/bgv087 article EN Carcinogenesis 2015-06-18

AR (androgen receptor) signaling is crucial for the development and maintenance of prostate as well initiation progression cancer. Despite AR's central role in cancer progression, it still unclear which AR-mediated processes drive disease. Here, we identified 4 core autophagy genes: ATG4B, ATG4D, ULK1, ULK2, addition to transcription factor TFEB, a master regulator lysosomal biogenesis function, transcriptional targets These findings were significant light our recent observation that...

10.1080/15548627.2016.1268300 article EN Autophagy 2016-12-19

Abstract Androgens regulate both the physiological development of prostate and pathology prostatic diseases. However, mechanisms by which androgens exert their regulatory activities on these processes are poorly understood. In this study, we have determined that overall cell metabolism growth, in part, increasing autophagy cancer cells. Importantly, inhibition using either pharmacological or molecular inhibitors significantly abrogated androgen-induced growth. Mechanistically,...

10.1210/me.2012-1260 article EN Molecular Endocrinology 2012-12-19

Despite the known importance of androgen receptor (AR) signaling in prostate cancer, processes downstream AR that drive disease development and progression remain poorly understood. This knowledge gap has thus limited ability to treat cancer. Here, it is demonstrated androgens increase metabolism glutamine cancer cells. was required for maximal cell growth under conditions serum starvation. Mechanistically, promoted by increasing expression transporters SLC1A4 SLC1A5, genes commonly...

10.1158/1541-7786.mcr-16-0480 article EN Molecular Cancer Research 2017-05-16

// Ayesha A. Shafi 1 , Vasanta Putluri 1,2,3 James M. Arnold 2 Efrosini Tsouko 4 Suman Maity Justin Roberts Cristian Coarfa 1,3 Daniel E. Frigo 4,5 Nagireddy Arun Sreekumar and Nancy L. Weigel 1,6 Department of Molecular Cellular Biology, Baylor College Medicine, Houston, TX, USA Verna Marrs McLean Biochemistry, 3 Alkek Center for Discovery, Nuclear Receptors Cell Signaling, Biology University 5 Genomic Medicine Program, Houston Methodist Research Institute, 6 Scott Urology, Correspondence...

10.18632/oncotarget.5585 article EN Oncotarget 2015-09-10

Abstract The precise molecular alterations driving castration-resistant prostate cancer (CRPC) are not clearly understood. Using a novel network-based integrative approach, here, we show distinct in the hexosamine biosynthetic pathway (HBP) to be critical for CRPC. Expression of HBP enzyme glucosamine-phosphate N-acetyltransferase 1 ( GNPNAT1 ) is found significantly decreased CRPC compared with localized (PCa). Genetic loss-of-function CRPC-like cells increases proliferation and...

10.1038/ncomms11612 article EN cc-by Nature Communications 2016-05-19

Despite altered metabolism being an accepted hallmark of cancer, it is still not completely understood which signaling pathways regulate these processes. Given the central role androgen receptor (AR) in prostate we hypothesized that AR could promote cancer cell growth part through increasing glucose uptake via expression distinct transporters. Here, determined directly increased SLC2A12 , gene encodes transporter GLUT12. In support findings, signatures activity correlated with multiple...

10.1530/erc-17-0051 article EN Endocrine Related Cancer 2018-02-08

The therapeutic efficacy of histone deacetylase inhibitors (HDACI) is generally attributed to their ability alter gene expression secondary effects on the acetylation status transcription factors and histones. However, because HDACIs exhibit similar transcriptional in most cells, molecular basis for selectivity toward malignant cells largely unknown. In this study, we report that HDACI, distinct chemotypes, quantitatively inhibit glucose transporter 1 (GLUT1)-mediated transport into multiple...

10.1210/me.2008-0179 article EN Molecular Endocrinology 2008-12-23

Male mice lacking the androgen receptor (AR) in pancreatic β cells exhibit blunted glucose-stimulated insulin secretion (GSIS), leading to hyperglycemia. Testosterone activates an extranuclear AR amplify glucagon-like peptide-1 (GLP-1) insulinotropic action. Here, we examined architecture of targets that regulate GLP-1 action male cells. cooperates with enhance cAMP production at plasma membrane and endosomes via: (1) increased mitochondrial CO2, activating HCO3−-sensitive soluble adenylate...

10.1016/j.celrep.2023.112529 article EN cc-by-nc-nd Cell Reports 2023-05-01

Organochlorine compounds have been demonstrated to detrimental health effects in both wildlife and humans, an effect largely attributed their ability mimic the hormone estrogen. Our laboratory has studied cell signaling by environmental chemicals associated with estrogen receptor (ER) more recently via ER-independent mechanisms. Here, we show that organochlorine pesticide dichlorodiphenyltrichloroethane (DDT) its metabolites induce a stress mitogen-activated protein kinase (MAPK) leads AP-1...

10.1093/carcin/bgh009 article EN Carcinogenesis 2003-10-24

Advanced prostate cancers preferentially metastasize to bone, suggesting that this tissue produces factors provide a suitable microenvironment for cancer cells. Recently, it has become clear even in antiandrogen-resistant cancers, the androgen receptor (AR)-signaling axis is required progression. Therefore, we hypothesized AR may be involved regulation of pathways are responsible homing cells select microenvironments. In support hypothesis, have determined chemokine (C-X-C motif) 4 (CXCR4),...

10.1210/me.2009-0010 article EN Molecular Endocrinology 2009-05-21

116 Background: Androgen deprivation therapy (ADT) and androgen receptor signaling inhibitors (ARSIs) indirectly increase CV risk. There are no risk estimation tools specific to men with prostate cancer undergoing HT. Current practice utilizes designed for the general population, such as AHA/ACC ASCVD score. Herein, we investigate applicability of population in receiving pre-operative HT LHRPC. Methods: We conducted a retrospective analysis LHRPCa who received 6 months ADT + apalutamide +/-...

10.1200/jco.2025.43.5_suppl.116 article EN Journal of Clinical Oncology 2025-02-10
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