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Article: CD44: A metastasis driver and therapeutic target.

Sottnik, Joseph L / Theodorescu, Dan

Oncoscience

2016 Volume 3, Issue 11-12, Page(s) 320–321

Language	English
Publishing date	2016-12-30
Publishing country	United States
Document type	Editorial
ISSN	2331-4737
ISSN	2331-4737
DOI	10.18632/oncoscience.335
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Article ; Online: Androgen Receptor Regulates CD44 Expression in Bladder Cancer.

Sottnik, Joseph L / Vanderlinden, Lauren / Joshi, Molishree / Chauca-Diaz, Ana / Owens, Charles / Hansel, Donna E / Sempeck, Colin / Ghosh, Debashis / Theodorescu, Dan

Cancer research

2021 Volume 81, Issue 11, Page(s) 2833–2846

Abstract: The androgen receptor (AR) is important in the development of both experimental and human bladder cancer. However, the role of AR in bladder cancer growth and progression is less clear, with literature indicating that more advanced stage and grade ... ...

Abstract	The androgen receptor (AR) is important in the development of both experimental and human bladder cancer. However, the role of AR in bladder cancer growth and progression is less clear, with literature indicating that more advanced stage and grade disease are associated with reduced AR expression. To determine the mechanisms underlying these relationships, we profiled AR-expressing human bladder cancer cells by AR chromatin immunoprecipitation sequencing and complementary transcriptomic approaches in response to
MeSH term(s)	Animals ; Apoptosis ; Biomarkers, Tumor/genetics ; Biomarkers, Tumor/metabolism ; Cell Proliferation ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Humans ; Hyaluronan Receptors/genetics ; Hyaluronan Receptors/metabolism ; Male ; Mice ; Mice, Nude ; Prognosis ; Receptors, Androgen/genetics ; Receptors, Androgen/metabolism ; Tumor Cells, Cultured ; Urinary Bladder Neoplasms/genetics ; Urinary Bladder Neoplasms/metabolism ; Urinary Bladder Neoplasms/pathology ; Xenograft Model Antitumor Assays
Chemical Substances	AR protein, human ; Biomarkers, Tumor ; CD44 protein, human ; Hyaluronan Receptors ; Receptors, Androgen
Language	English
Publishing date	2021-03-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-20-3095
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Article ; Online: Mediator of DNA Damage Checkpoint 1 (MDC1) Is a Novel Estrogen Receptor Coregulator in Invasive Lobular Carcinoma of the Breast.

Sottnik, Joseph L / Bordeaux, Evelyn K / Mehrotra, Sanjana / Ferrara, Sarah E / Goodspeed, Andrew E / Costello, James C / Sikora, Matthew J

Molecular cancer research : MCR

2021 Volume 19, Issue 8, Page(s) 1270–1282

Abstract: Invasive lobular carcinoma (ILC) is the most common special histologic subtype of breast cancer, and nearly all ILC tumors express estrogen receptor alpha (ER). However, clinical and laboratory data suggest ILC are strongly estrogen-driven but not ... ...

Abstract	Invasive lobular carcinoma (ILC) is the most common special histologic subtype of breast cancer, and nearly all ILC tumors express estrogen receptor alpha (ER). However, clinical and laboratory data suggest ILC are strongly estrogen-driven but not equally antiestrogen-sensitive. We hypothesized ILC-specific ER coregulators mediate ER functions and antiestrogen resistance in ILC, and profiled ER-associated proteins by mass spectrometry. Three ER
MeSH term(s)	Adaptor Proteins, Signal Transducing/genetics ; Breast/pathology ; Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Carcinoma, Lobular/drug therapy ; Carcinoma, Lobular/genetics ; Carcinoma, Lobular/pathology ; Cell Cycle Proteins/genetics ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cell Proliferation/genetics ; Female ; Humans ; MCF-7 Cells ; Promoter Regions, Genetic/drug effects ; Promoter Regions, Genetic/genetics ; Receptors, Estrogen/genetics ; Signal Transduction/genetics ; Tamoxifen/therapeutic use ; Transcriptome/drug effects ; Transcriptome/genetics
Chemical Substances	Adaptor Proteins, Signal Transducing ; Cell Cycle Proteins ; MDC1 protein, human ; Receptors, Estrogen ; Tamoxifen (094ZI81Y45)
Language	English
Publishing date	2021-05-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2098788-2
ISSN	1557-3125 ; 1541-7786
ISSN (online)	1557-3125
ISSN	1541-7786
DOI	10.1158/1541-7786.MCR-21-0025
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Article ; Online: WNT4 Regulates Cellular Metabolism via Intracellular Activity at the Mitochondria in Breast and Gynecologic Cancers.

Sottnik, Joseph L / Shackleford, Madeleine T / Robinson, Sydney K / Villagomez, Fabian R / Bahnassy, Shaymaa / Oesterreich, Steffi / Hu, Junxiao / Madak-Erdogan, Zeynep / Riggins, Rebecca B / Corr, Bradley R / Cook, Linda S / Treviño, Lindsey S / Bitler, Benjamin G / Sikora, Matthew J

Cancer research communications

2023 Volume 4, Issue 1, Page(s) 134–151

Abstract: Wnt ligand WNT4 is critical in female reproductive tissue development, with WNT4 dysregulation linked to related pathologies including breast cancer (invasive lobular carcinoma, ILC) and gynecologic cancers. WNT4 signaling in these contexts is distinct ... ...

Abstract	Wnt ligand WNT4 is critical in female reproductive tissue development, with WNT4 dysregulation linked to related pathologies including breast cancer (invasive lobular carcinoma, ILC) and gynecologic cancers. WNT4 signaling in these contexts is distinct from canonical Wnt signaling yet inadequately understood. We previously identified atypical intracellular activity of WNT4 (independent of Wnt secretion) regulating mitochondrial function, and herein examine intracellular functions of WNT4. We further examine how convergent mechanisms of WNT4 dysregulation impact cancer metabolism. In ILC, WNT4 is co-opted by estrogen receptor α (ER) via genomic binding in WNT4 intron 1, while in gynecologic cancers, a common genetic polymorphism (rs3820282) at this ER binding site alters WNT4 regulation. Using proximity biotinylation (BioID), we show canonical Wnt ligand WNT3A is trafficked for secretion, but WNT4 is localized to the cytosol and mitochondria. We identified DHRS2, mTOR, and STAT1 as putative WNT4 cytosolic/mitochondrial signaling partners. Whole metabolite profiling, and integrated transcriptomic data, support that WNT4 mediates metabolic reprogramming via fatty acid and amino acid metabolism. Furthermore, ovarian cancer cell lines with rs3820282 variant genotype are WNT4 dependent and have active WNT4 metabolic signaling. In protein array analyses of a cohort of 103 human gynecologic tumors enriched for patient diversity, germline rs3820282 genotype is associated with metabolic remodeling. Variant genotype tumors show increased AMPK activation and downstream signaling, with the highest AMPK signaling activity in variant genotype tumors from non-White patients. Taken together, atypical intracellular WNT4 signaling, in part via genetic dysregulation, regulates the distinct metabolic phenotypes of ILC and gynecologic cancers. Significance: WNT4 regulates breast and gynecologic cancer metabolism via a previously unappreciated intracellular signaling mechanism at the mitochondria, with WNT4 mediating metabolic remodeling. Understanding WNT4 dysregulation by estrogen and genetic polymorphism offers new opportunities for defining tumor biology, precision therapeutics, and personalized cancer risk assessment.
MeSH term(s)	Humans ; Female ; Ligands ; AMP-Activated Protein Kinases/metabolism ; Genital Neoplasms, Female/genetics ; Signal Transduction ; Breast Neoplasms/genetics ; Wnt4 Protein/genetics ; Carbonyl Reductase (NADPH)/metabolism
Chemical Substances	Ligands ; AMP-Activated Protein Kinases (EC 2.7.11.31) ; WNT4 protein, human ; Wnt4 Protein ; DHRS2 protein, human (EC 1.1.1.184) ; Carbonyl Reductase (NADPH) (EC 1.1.1.184)
Language	English
Publishing date	2023-12-19
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2767-9764
ISSN (online)	2767-9764
DOI	10.1158/2767-9764.CRC-23-0275
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Article: Estrogen Regulation of mTOR Signaling and Mitochondrial Function in Invasive Lobular Carcinoma Cell Lines Requires WNT4.

Shackleford, Madeleine T / Rao, Deviyani M / Bordeaux, Evelyn K / Hicks, Hannah M / Towers, Christina G / Sottnik, Joseph L / Oesterreich, Steffi / Sikora, Matthew J

Cancers

2020 Volume 12, Issue 10

Abstract: Invasive lobular carcinoma of the breast (ILC) is strongly estrogen-driven and represents a unique context for estrogen receptor (ER) signaling. In ILC, ER controls the expression of the Wnt ligand WNT4, which is critical for endocrine response and anti- ... ...

Abstract	Invasive lobular carcinoma of the breast (ILC) is strongly estrogen-driven and represents a unique context for estrogen receptor (ER) signaling. In ILC, ER controls the expression of the Wnt ligand WNT4, which is critical for endocrine response and anti-estrogen resistance. However, signaling mediated by WNT4 is cell type- and tissue-specific, and has not been explored in ILC. We utilized reverse phase protein array (RPPA) to characterize ER and WNT4-driven signaling in ILC cells and identified that WNT4 mediates downstream mTOR signaling via phosphorylation of S6 Kinase. Additionally, ER and WNT4 control levels of MCL-1, which is associated with regulation of mitochondrial function. In this context, WNT4 knockdown led to decreased ATP production and increased mitochondrial fragmentation. WNT4 regulation of both mTOR signaling and MCL-1 were also observed in anti-estrogen resistant models of ILC. We identified that high WNT4 expression is associated with similar mTOR pathway activation in ILC and serous ovarian cancer tumors, suggesting that WNT4 signaling is active in multiple tumor types. The identified downstream pathways offer insight into WNT4 signaling and represent potential targets to overcome anti-estrogen resistance for patients with ILC.
Language	English
Publishing date	2020-10-12
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers12102931
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Article ; Online: Tumor-induced pressure in the bone microenvironment causes osteocytes to promote the growth of prostate cancer bone metastases.

Sottnik, Joseph L / Dai, Jinlu / Zhang, Honglai / Campbell, Brittany / Keller, Evan T

Cancer research

2015 Volume 75, Issue 11, Page(s) 2151–2158

Abstract: Cross-talk between tumor cells and their microenvironment is critical for malignant progression. Cross-talk mediators, including soluble factors and direct cell contact, have been identified, but roles for the interaction of physical forces between tumor ...

Abstract	Cross-talk between tumor cells and their microenvironment is critical for malignant progression. Cross-talk mediators, including soluble factors and direct cell contact, have been identified, but roles for the interaction of physical forces between tumor cells and the bone microenvironment have not been described. Here, we report preclinical evidence that tumor-generated pressure acts to modify the bone microenvironment to promote the growth of prostate cancer bone metastases. Tumors growing in mouse tibiae increased intraosseous pressure. Application of pressure to osteocytes, the main mechanotransducing cells in bone, induced prostate cancer growth and invasion. Mechanistic investigations revealed that this process was mediated in part by upregulation of CCL5 and matrix metalloproteinases in osteocytes. Our results defined the critical contribution of physical forces to tumor cell growth in the tumor microenvironment, and they identified osteocytes as a critical mediator in the bone metastatic niche.
MeSH term(s)	Animals ; Bone Neoplasms/pathology ; Bone Neoplasms/secondary ; Cell Proliferation/physiology ; Chemokine CCL5/biosynthesis ; Gene Expression Regulation, Neoplastic ; Humans ; Male ; Matrix Metalloproteinases/biosynthesis ; Mice ; Neoplasm Metastasis ; Osteocytes/metabolism ; Osteocytes/pathology ; Pressure ; Prostatic Neoplasms/pathology ; Tumor Microenvironment
Chemical Substances	CCL5 protein, human ; Chemokine CCL5 ; Matrix Metalloproteinases (EC 3.4.24.-)
Language	English
Publishing date	2015-06-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-14-2493
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Article ; Online: Wnt family member 4 (WNT4) and WNT3A activate cell-autonomous Wnt signaling independent of porcupine

Rao, Deviyani M / Shackleford, Madeleine T / Bordeaux, Evelyn K / Sottnik, Joseph L / Ferguson, Rebecca L / Yamamoto, Tomomi M / Wellberg, Elizabeth A / Bitler, Benjamin G / Sikora, Matthew J

The Journal of biological chemistry

2019 Volume 294, Issue 52, Page(s) 19950–19966

Abstract: ... ...

Abstract	Porcupine
MeSH term(s)	Acyltransferases/antagonists & inhibitors ; Acyltransferases/genetics ; Acyltransferases/metabolism ; Cell Line, Tumor ; Cell Proliferation ; Coculture Techniques ; Culture Media, Conditioned/chemistry ; Fulvestrant/pharmacology ; Humans ; Intracellular Signaling Peptides and Proteins/antagonists & inhibitors ; Intracellular Signaling Peptides and Proteins/genetics ; Intracellular Signaling Peptides and Proteins/metabolism ; Membrane Proteins/antagonists & inhibitors ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Paracrine Communication ; Protein Transport ; RNA Interference ; RNA, Small Interfering/metabolism ; Receptors, G-Protein-Coupled/antagonists & inhibitors ; Receptors, G-Protein-Coupled/genetics ; Receptors, G-Protein-Coupled/metabolism ; Wnt Signaling Pathway/drug effects ; Wnt3A Protein/antagonists & inhibitors ; Wnt3A Protein/genetics ; Wnt3A Protein/metabolism ; Wnt4 Protein/antagonists & inhibitors ; Wnt4 Protein/genetics ; Wnt4 Protein/metabolism
Chemical Substances	Culture Media, Conditioned ; Intracellular Signaling Peptides and Proteins ; Membrane Proteins ; RNA, Small Interfering ; Receptors, G-Protein-Coupled ; WLS protein, human ; Wnt3A Protein ; Wnt4 Protein ; Fulvestrant (22X328QOC4) ; Acyltransferases (EC 2.3.-) ; PORCN protein, human (EC 2.3.1.-)
Language	English
Publishing date	2019-11-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.RA119.009615
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Article: Wnt and Wnt inhibitors in bone metastasis.

Sottnik, Joseph L / Hall, Christopher L / Zhang, Jian / Keller, Evan T

BoneKEy reports

2012 Volume 1, Page(s) 101

Abstract: Bone metastasis is a clinically devastating development of progressive cancers including prostate carcinoma, breast carcinoma and multiple myeloma. Bone metastases are typically painful, lead to adverse skeletal-related events, such as fracture, and are ... ...

Abstract	Bone metastasis is a clinically devastating development of progressive cancers including prostate carcinoma, breast carcinoma and multiple myeloma. Bone metastases are typically painful, lead to adverse skeletal-related events, such as fracture, and are highly resistant to therapy. A major contribution to the ability of cancers to successfully establish bone metastases is their ability to exploit mechanisms of normal bone remodeling. Wnts are a large family of morphogenic proteins that are critical for bone development and contribute to maintaining bone mass in the mature organism. Wnt function is balanced by the presence of a variety of endogenous inhibitors, such as the dickkopf family members, secreted frizzled related proteins and sclerostin. Together, these factors contribute to normal bone homeostasis, allowing for dynamic changes in bone to withstand alterations in physical forces and physiological needs. In this review, we describe the role that Wnts and their inhibitors have in normal bone biology and cancer-related bone pathology. An overview of Wnt signaling pathways is discussed and key bone microenvironment cellular players, as they pertain to Wnt biology, are examined. Finally, we describe clinical trials of several Wnt inhibitor antagonists for patients with tumor-related bone disease. As few options currently exist for the treatment of bone-metastatic disease, Wnt proteins and their inhibitors offer promise for the development of novel therapeutics.
Language	English
Publishing date	2012-07-04
Publishing country	England
Document type	Journal Article
ZDB-ID	2816308-4
ISSN	2047-6396
ISSN	2047-6396
DOI	10.1038/bonekey.2012.101
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Article ; Online: The PCa Tumor Microenvironment.

Sottnik, Joseph L / Zhang, Jian / Macoska, Jill A / Keller, Evan T

Cancer microenvironment : official journal of the International Cancer Microenvironment Society

2011 Volume 4, Issue 3, Page(s) 283–297

Abstract: The tumor microenvironment (TME) is a very complex niche that consists of multiple cell types, supportive matrix and soluble factors. Cells in the TME consist of both host cells that are present at tumor site at the onset of tumor growth and cells that ... ...

Abstract	The tumor microenvironment (TME) is a very complex niche that consists of multiple cell types, supportive matrix and soluble factors. Cells in the TME consist of both host cells that are present at tumor site at the onset of tumor growth and cells that are recruited in either response to tumor- or host-derived factors. PCa (PCa) thrives on crosstalk between tumor cells and the TME. Crosstalk results in an orchestrated evolution of both the tumor and microenvironment as the tumor progresses. The TME reacts to PCa-produced soluble factors as well as direct interaction with PCa cells. In return, the TME produces soluble factors, structural support and direct contact interactions that influence the establishment and progression of PCa. In this review, we focus on the host side of the equation to provide a foundation for understanding how different aspects of the TME contribute to PCa progression. We discuss immune effector cells, specialized niches, such as the vascular and bone marrow, and several key protein factors that mediate host effects on PCa. This discussion highlights the concept that the TME offers a potentially very fertile target for PCa therapy.
Language	English
Publishing date	2011-07-05
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2422345-1
ISSN	1875-2284 ; 1875-2292
ISSN (online)	1875-2284
ISSN	1875-2292
DOI	10.1007/s12307-011-0073-8
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Article ; Online: Glycolysis inhibition by 2-deoxy-D-glucose reverts the metastatic phenotype in vitro and in vivo.

Sottnik, Joseph L / Lori, Janet C / Rose, Barbara J / Thamm, Douglas H

Clinical & experimental metastasis

2011 Volume 28, Issue 8, Page(s) 865–875

Abstract: ... associated with cytoskeletal rearrangement and inhibition of cathepsin L expression. A dose-dependent shift ...

Abstract	Metastasis is the primary cause of death from many tumors, and novel anti-metastatic therapies are necessary. Recently, we showed that metastatic tumors down-regulate key oxidative phosphorylation (OXPHOS) genes in favor of glycolysis, a further enhancement of the Warburg effect. Therefore, we sought to determine if restriction of glycolysis using 2-deoxy-D-glucose (2DG) would lead to increased utilization of OXPHOS and inhibition of the metastatic phenotype. Noncytotoxic concentrations of 2DG dose-dependently inhibited in vitro migration and invasion in the highly metastatic DLM8-luc-M1 osteosarcoma (OS) cell line, as well as other metastatic human, canine, and murine cancer cells of different histotypes. This was associated with cytoskeletal rearrangement and inhibition of cathepsin L expression. A dose-dependent shift toward OXPHOS was confirmed by demonstrating increased oxygen utilization and decreased lactate production in 2DG treated cells. Finally, 2DG treatment significantly delayed metastasis and prolonged survival in an orthotopic postsurgical OS model. In conclusion, this work suggests that forcing cells away from glycolysis may inhibit key components of the metastatic phenotype, providing a novel avenue for metastasis prevention.
MeSH term(s)	Animals ; Antimetabolites/pharmacology ; Blotting, Western ; Bone Neoplasms/metabolism ; Bone Neoplasms/prevention & control ; Bone Neoplasms/secondary ; Cathepsin L/metabolism ; Cell Adhesion/drug effects ; Cell Movement/drug effects ; Cell Proliferation/drug effects ; Deoxyglucose/pharmacology ; Dogs ; Female ; Fluorescent Antibody Technique ; Glycolysis/drug effects ; Humans ; In Vitro Techniques ; Mice ; Mice, Inbred C3H ; Osteosarcoma/drug therapy ; Osteosarcoma/metabolism ; Osteosarcoma/pathology ; Oxidative Phosphorylation/drug effects ; Oxygen Consumption/drug effects ; Phenotype ; Survival Rate ; Tumor Cells, Cultured
Chemical Substances	Antimetabolites ; Deoxyglucose (9G2MP84A8W) ; Cathepsin L (EC 3.4.22.15)
Language	English
Publishing date	2011-08-14
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	604952-7
ISSN	1573-7276 ; 0262-0898
ISSN (online)	1573-7276
ISSN	0262-0898
DOI	10.1007/s10585-011-9417-5
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