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Article ; Online: Single-cell genomics analysis reveals complex genetic interactions in an

Schillo, Jacob L / Feddersen, Charlotte R / Peplinski, Rebekah M / Powell, Lexy S / Varzavand, Afshin / Stipp, Christopher S / Riordan, Jesse D / Dupuy, Adam J

NAR cancer

2024 Volume 6, Issue 1, Page(s) zcad061

Abstract: The evolution of therapeutic resistance is a major obstacle to the success of targeted oncology drugs. While both inter- and intratumoral heterogeneity limit our ability to detect resistant subpopulations that pre-exist or emerge during treatment, our ... ...

Abstract	The evolution of therapeutic resistance is a major obstacle to the success of targeted oncology drugs. While both inter- and intratumoral heterogeneity limit our ability to detect resistant subpopulations that pre-exist or emerge during treatment, our ability to analyze tumors with single-cell resolution is limited. Here, we utilized a cell-based transposon mutagenesis method to identify mechanisms of BRAF inhibitor resistance in a model of cutaneous melanoma. This screen identified overexpression of NEDD4L and VGLL3 as significant drivers of BRAF inhibitor resistance
Language	English
Publishing date	2024-01-11
Publishing country	England
Document type	Journal Article
ISSN	2632-8674
ISSN (online)	2632-8674
DOI	10.1093/narcan/zcad061
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Article: SRC-RAC1 signaling drives drug resistance to BRAF inhibition in de-differentiated cutaneous melanomas.

Zhu, Eliot Y / Riordan, Jesse D / Vanneste, Marion / Henry, Michael D / Stipp, Christopher S / Dupuy, Adam J

NPJ precision oncology

2022 Volume 6, Issue 1, Page(s) 74

Abstract: Rare gain-of-function mutations in RAC1 drive drug resistance to targeted BRAF inhibition in cutaneous melanoma. Here, we show that wildtype RAC1 is a critical driver of growth and drug resistance, but only in a subset of melanomas with elevated markers ... ...

Abstract	Rare gain-of-function mutations in RAC1 drive drug resistance to targeted BRAF inhibition in cutaneous melanoma. Here, we show that wildtype RAC1 is a critical driver of growth and drug resistance, but only in a subset of melanomas with elevated markers of de-differentiation. Similarly, SRC inhibition also selectively sensitized de-differentiated melanomas to BRAF inhibition. One possible mechanism may be the suppression of the de-differentiated state, as SRC and RAC1 maintained markers of de-differentiation in human melanoma cells. The functional differences between melanoma subtypes suggest that the clinical management of cutaneous melanoma can be enhanced by the knowledge of differentiation status. To simplify the task of classification, we developed a binary classification strategy based on a small set of ten genes. Using this gene set, we reliably determined the differentiation status previously defined by hundreds of genes. Overall, our study informs strategies that enhance the precision of BRAFi by discovering unique vulnerabilities of the de-differentiated cutaneous melanoma subtype and creating a practical method to resolve differentiation status.
Language	English
Publishing date	2022-10-21
Publishing country	England
Document type	Journal Article
ISSN	2397-768X
ISSN	2397-768X
DOI	10.1038/s41698-022-00310-7
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Article ; Online: Laminin-binding integrins and their tetraspanin partners as potential antimetastatic targets.

Stipp, Christopher S

Expert reviews in molecular medicine

2010 Volume 12, Page(s) e3

Abstract: Within the integrin family of cell adhesion receptors, integrins alpha3beta1, alpha6beta1, alpha6beta4 and alpha7beta1 make up a laminin-binding subfamily. The literature is divided on the role of these laminin-binding integrins in metastasis, with ... ...

Abstract	Within the integrin family of cell adhesion receptors, integrins alpha3beta1, alpha6beta1, alpha6beta4 and alpha7beta1 make up a laminin-binding subfamily. The literature is divided on the role of these laminin-binding integrins in metastasis, with different studies indicating either pro- or antimetastatic functions. The opposing roles of the laminin-binding integrins in different settings might derive in part from their unusually robust associations with tetraspanin proteins. Tetraspanins organise integrins into multiprotein complexes within discrete plasma membrane domains termed tetraspanin-enriched microdomains (TEMs). TEM association is crucial to the strikingly rapid cell migration mediated by some of the laminin-binding integrins. However, emerging data suggest that laminin-binding integrins also promote the stability of E-cadherin-based cell-cell junctions, and that tetraspanins are essential for this function as well. Thus, TEM association endows the laminin-binding integrins with both pro-invasive functions (rapid migration) and anti-invasive functions (stable cell junctions), and the composition of TEMs in different cell types might help determine the balance between these opposing activities. Unravelling the tetraspanin control mechanisms that regulate laminin-binding integrins will help to define the settings where inhibiting the function of these integrins would be helpful rather than harmful, and may create opportunities to modulate integrin activity in more sophisticated ways than simple functional blockade.
MeSH term(s)	Animals ; Humans ; Integrins/chemistry ; Integrins/metabolism ; Laminin/chemistry ; Laminin/metabolism ; Neoplasm Metastasis/therapy ; Protein Binding
Chemical Substances	Integrins ; Laminin
Language	English
Publishing date	2010-01-18
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ISSN	1462-3994
ISSN (online)	1462-3994
DOI	10.1017/S1462399409001355
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Article: Abl kinases can function as suppressors of tumor progression and metastasis.

Marchal, Melissa A / Moose, Devon L / Varzavand, Afshin / Jordan, Nicole E / Taylor, Destiney / Tanas, Munir R / Brown, James A / Henry, Michael D / Stipp, Christopher S

Frontiers in oncology

2023 Volume 13, Page(s) 1241056

Abstract: Introduction: Abl family kinases function as proto-oncogenes in various leukemias, and pro-tumor functions have been discovered for Abl kinases in many solid tumors as well. However, a growing body of evidence indicates that Abl kinases can function to ... ...

Abstract	Introduction: Abl family kinases function as proto-oncogenes in various leukemias, and pro-tumor functions have been discovered for Abl kinases in many solid tumors as well. However, a growing body of evidence indicates that Abl kinases can function to suppress tumor cell proliferation and motility and tumor growth Methods: To investigate the role of Abl kinases in tumor progression, we used RNAi to generate Abl-deficient cells in a model of androgen receptor-indifferent, metastatic prostate cancer. The effect of Abl kinase depletion on tumor progression and metastasis was studied in an Results: Reduced Abl family kinase expression resulted in a highly aggressive, metastatic phenotype Conclusions: Collectively, our data reveal that Abl family kinases can function to suppress malignant cell phenotypes
Language	English
Publishing date	2023-09-08
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2023.1241056
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Article ; Online: CD151 Maintains Endolysosomal Protein Quality to Inhibit Vascular Inflammation.

Chen, Junxiong / Ding, Yingjun / Jiang, Chao / Qu, Rongmei / Wren, Jonathan D / Georgescu, Constantin / Wang, Xuejun / Reuter, Darlene N / Liu, Beibei / Giles, Cory B / Mayr, Christoph H / Schiller, Herbert B / Dai, Jingxing / Stipp, Christopher S / Subramaniyan, Bharathiraja / Wang, Jie / Zuo, Houjuan / Huang, Chao / Fung, Kar-Ming /

Rice, Heather C / Sonnenberg, Arnoud / Wu, David / Walters, Matthew S / Zhao, You-Yang / Kanie, Tomoharu / Hays, Franklin A / Papin, James F / Wang, Dao Wen / Zhang, Xin A

Circulation research

2024

Abstract: Background: Tetraspanin CD151 is highly expressed in endothelia and reinforces cell adhesion, but its role in vascular inflammation remains largely unknown.: Methods: In vitro molecular and cellular biological analyses on genetically modified ... ...

Abstract	Background: Tetraspanin CD151 is highly expressed in endothelia and reinforces cell adhesion, but its role in vascular inflammation remains largely unknown. Methods: In vitro molecular and cellular biological analyses on genetically modified endothelial cells, in vivo vascular biological analyses on genetically engineered mouse models, and in silico systems biology and bioinformatics analyses on CD151-related events. Results: Endothelial ablation of Conclusions: Distinct from its canonical function in strengthening cell adhesion at cell surface, CD151 maintains endolysosome function by sustaining VCP/p97-mediated protein unfolding and turnover. By supporting protein quality control and protein degradation, CD151 prevents proteins from (1) buildup in endolysosomes and (2) discharge through exosomes, to limit vascular inflammation. Also, our study conceptualizes that balance between degradation and discharge of proteins in endothelial cells determines vascular information. Thus, the IFITM3/V-ATPase-tetraspanin-VCP/p97 complexes on endolysosome, as a protein quality control and inflammation-inhibitory machinery, could be beneficial for therapeutic intervention against vascular inflammation.
Language	English
Publishing date	2024-04-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	80100-8
ISSN	1524-4571 ; 0009-7330 ; 0931-6876
ISSN (online)	1524-4571
ISSN	0009-7330 ; 0931-6876
DOI	10.1161/CIRCRESAHA.123.323190
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Article ; Online: PRC2 loss drives MPNST metastasis and matrix remodeling.

Brockman, Qierra R / Scherer, Amanda / McGivney, Gavin R / Gutierrez, Wade R / Voigt, Andrew P / Isaacson, Alexandra L / Laverty, Emily A / Roughton, Grace / Knepper-Adrian, Vickie / Darbro, Benjamin / Tanas, Munir R / Stipp, Christopher S / Dodd, Rebecca D

JCI insight

2022 Volume 7, Issue 20

Abstract: The histone methyltransferase PRC2 plays a complex role in cancer. Malignant peripheral nerve sheath tumors (MPNSTs) are aggressive sarcomas with frequent loss-of-function mutations in PRC2 that are associated with poor outcome. Here, we identify a ... ...

Abstract	The histone methyltransferase PRC2 plays a complex role in cancer. Malignant peripheral nerve sheath tumors (MPNSTs) are aggressive sarcomas with frequent loss-of-function mutations in PRC2 that are associated with poor outcome. Here, we identify a critical role for PRC2 loss in driving MPNST metastasis. PRC2-dependent metastatic phenotypes included increased collagen-dependent invasion, upregulation of matrix-remodeling enzymes, and elevated lung metastasis in orthotopic mouse models. Furthermore, clinical sample analysis determined that PRC2 loss correlated with metastatic disease, increased fibrosis, and decreased survival in patients with MPNSTs. These results may have broad implications for PRC2 function across multiple cancers and provide a strong rationale for investigating potential therapies targeting ECM-remodeling enzymes and tumor fibrosis to improve outcomes in patients with MPNSTs.
MeSH term(s)	Mice ; Animals ; Neurofibrosarcoma/genetics ; Neurofibrosarcoma/pathology ; Mutation ; Histone Methyltransferases ; Fibrosis
Chemical Substances	Histone Methyltransferases (EC 2.1.1.-)
Language	English
Publishing date	2022-10-24
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.157502
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Article: Functional Genomic Screening Independently Identifies CUL3 as a Mediator of Vemurafenib Resistance via Src-Rac1 Signaling Axis.

Vanneste, Marion / Feddersen, Charlotte R / Varzavand, Afshin / Zhu, Elliot Y / Foley, Tyler / Zhao, Lei / Holt, Kathleen H / Milhem, Mohammed / Piper, Robert / Stipp, Christopher S / Dupuy, Adam J / Henry, Michael D

Frontiers in oncology

2020 Volume 10, Page(s) 442

Abstract: Patients with malignant melanoma have a 5-year survival rate of only 15-20% once the tumor has metastasized to distant tissues. While MAP kinase pathway inhibitors (MAPKi) are initially effective for the majority of patients with melanoma harboring ... ...

Abstract	Patients with malignant melanoma have a 5-year survival rate of only 15-20% once the tumor has metastasized to distant tissues. While MAP kinase pathway inhibitors (MAPKi) are initially effective for the majority of patients with melanoma harboring BRAF
Language	English
Publishing date	2020-04-03
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2020.00442
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Article ; Online: The CD9/CD81 tetraspanin complex and tetraspanin CD151 regulate α3β1 integrin-dependent tumor cell behaviors by overlapping but distinct mechanisms.

Gustafson-Wagner, Elisabeth / Stipp, Christopher S

PloS one

2013 Volume 8, Issue 4, Page(s) e61834

Abstract: Integrin α3β1 potently promotes cell motility on its ligands, laminin-332 and laminin-511, and this may help to explain why α3β1 has repeatedly been linked to breast carcinoma progression and metastasis. The pro-migratory functions of α3β1 depend ... ...

Abstract	Integrin α3β1 potently promotes cell motility on its ligands, laminin-332 and laminin-511, and this may help to explain why α3β1 has repeatedly been linked to breast carcinoma progression and metastasis. The pro-migratory functions of α3β1 depend strongly on lateral interactions with cell surface tetraspanin proteins. Tetraspanin CD151 interacts directly with the α3 integrin subunit and links α3β1 integrin to other tetraspanins, including CD9 and CD81. Loss of CD151 disrupts α3β1 association with other tetraspanins and impairs α3β1-dependent motility. However, the extent to which tetraspanins other than CD151 are required for specific α3β1 functions is unclear. To begin to clarify which aspects of α3β1 function require which tetraspanins, we created breast carcinoma cells depleted of both CD9 and CD81 by RNA interference. Silencing both of these closely related tetraspanins was required to uncover their contributions to α3β1 function. We then directly compared our CD9/CD81-silenced cells to CD151-silenced cells. Both CD9/CD81-silenced cells and CD151-silenced cells showed delayed α3β1-dependent cell spreading on laminin-332. Surprisingly, however, once fully spread, CD9/CD81-silenced cells, but not CD151-silenced cells, displayed impaired α3β1-dependent directed motility and altered front-rear cell morphology. Also unexpectedly, the CD9/CD81 complex, but not CD151, was required to promote α3β1 association with PKCα in breast carcinoma cells, and a PKC inhibitor mimicked aspects of the CD9/CD81-silenced cell motility defect. Our data reveal overlapping, but surprisingly distinct contributions of specific tetraspanins to α3β1 integrin function. Importantly, some of CD9/CD81's α3β1 regulatory functions may not require CD9/CD81 to be physically linked to α3β1 by CD151.
MeSH term(s)	Animals ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Cell Adhesion/drug effects ; Cell Adhesion Molecules/pharmacology ; Cell Line, Tumor ; Cell Movement/drug effects ; Cell Polarity/drug effects ; Cell Proliferation/drug effects ; Cell Shape/drug effects ; Female ; Flow Cytometry ; Gene Silencing/drug effects ; Humans ; Integrin alpha3beta1/metabolism ; Models, Biological ; Protein Binding/drug effects ; Protein Kinase C-alpha/metabolism ; Rats ; Tetraspanin 24/metabolism ; Tetraspanin 28/metabolism ; Tetraspanin 29/metabolism ; Kalinin
Chemical Substances	CD151 protein, human ; CD81 protein, human ; CD9 protein, human ; Cell Adhesion Molecules ; Integrin alpha3beta1 ; Tetraspanin 24 ; Tetraspanin 28 ; Tetraspanin 29 ; Protein Kinase C-alpha (EC 2.7.11.13)
Language	English
Publishing date	2013-04-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0061834
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Article ; Online: PRC2 loss drives MPNST metastasis and matrix remodeling

Qierra R. Brockman / Amanda Scherer / Gavin R. McGivney / Wade R. Gutierrez / Andrew P. Voigt / Alexandra L. Isaacson / Emily A. Laverty / Grace Roughton / Vickie Knepper-Adrian / Benjamin Darbro / Munir R. Tanas / Christopher S. Stipp / Rebecca D. Dodd

JCI Insight, Vol 7, Iss

2022 Volume 20

Abstract	The histone methyltransferase PRC2 plays a complex role in cancer. Malignant peripheral nerve sheath tumors (MPNSTs) are aggressive sarcomas with frequent loss-of-function mutations in PRC2 that are associated with poor outcome. Here, we identify a critical role for PRC2 loss in driving MPNST metastasis. PRC2-dependent metastatic phenotypes included increased collagen-dependent invasion, upregulation of matrix-remodeling enzymes, and elevated lung metastasis in orthotopic mouse models. Furthermore, clinical sample analysis determined that PRC2 loss correlated with metastatic disease, increased fibrosis, and decreased survival in patients with MPNSTs. These results may have broad implications for PRC2 function across multiple cancers and provide a strong rationale for investigating potential therapies targeting ECM-remodeling enzymes and tumor fibrosis to improve outcomes in patients with MPNSTs.
Keywords	Oncology ; Medicine ; R
Language	English
Publishing date	2022-10-01T00:00:00Z
Publisher	American Society for Clinical investigation
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Cancer Cells Resist Mechanical Destruction in Circulation via RhoA/Actomyosin-Dependent Mechano-Adaptation.

Moose, Devon L / Krog, Benjamin L / Kim, Tae-Hyung / Zhao, Lei / Williams-Perez, Sophia / Burke, Gretchen / Rhodes, Lillian / Vanneste, Marion / Breheny, Patrick / Milhem, Mohammed / Stipp, Christopher S / Rowat, Amy C / Henry, Michael D

Cell reports

2020 Volume 30, Issue 11, Page(s) 3864–3874.e6

Abstract: During metastasis, cancer cells are exposed to potentially destructive hemodynamic forces including fluid shear stress (FSS) while en route to distant sites. However, prior work indicates that cancer cells are more resistant to brief pulses of high-level ...

Abstract	During metastasis, cancer cells are exposed to potentially destructive hemodynamic forces including fluid shear stress (FSS) while en route to distant sites. However, prior work indicates that cancer cells are more resistant to brief pulses of high-level FSS in vitro relative to non-transformed epithelial cells. Herein, we identify a mechano-adaptive mechanism of FSS resistance in cancer cells. Our findings demonstrate that cancer cells activate RhoA in response to FSS, which protects them from FSS-induced plasma membrane damage. We show that cancer cells freshly isolated from mouse and human tumors are resistant to FSS, that formin and myosin II activity protects circulating tumor cells (CTCs) from destruction, and that short-term inhibition of myosin II delays metastasis in mouse models. Collectively, our data indicate that viable CTCs actively resist destruction by hemodynamic forces and are likely to be more mechanically robust than is commonly thought.
MeSH term(s)	Actomyosin/metabolism ; Adaptation, Biological ; Animals ; Cell Line, Tumor ; Cell Membrane/metabolism ; Cell Survival ; Hemodynamics ; Humans ; Mice, Inbred C57BL ; Myosin Type II/metabolism ; Neoplasm Metastasis ; Neoplasms/metabolism ; Neoplasms/pathology ; Neoplastic Cells, Circulating/pathology ; Shear Strength ; Stress, Mechanical ; rhoA GTP-Binding Protein/metabolism
Chemical Substances	RHOA protein, human (124671-05-2) ; Actomyosin (9013-26-7) ; Myosin Type II (EC 3.6.1.-) ; rhoA GTP-Binding Protein (EC 3.6.5.2)
Language	English
Publishing date	2020-03-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2020.02.080
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