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2. Directed cell migration towards softer environments

Author

Isomursu, Aleksi, Park, Keun-Young, Hou, Jay, Cheng, Bo, Mathieu, Mathilde, Shamsan, Ghaidan A., Fuller, Benjamin, Kasim, Jesse, Mahmoodi, M. Mohsen, Lu, Tian Jian, Genin, Guy M., Xu, Feng, Lin, Min, Distefano, Mark D., Ivaska, Johanna, and Odde, David J.

Published
2022
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3. Mutual antagonism between CD44 and integrins in glioblastoma cell traction and migration.

Author

Kelly, Marcus D., Pawlak, Matthew R., Zhan, Kevin H., Shamsan, Ghaidan A., Gordon, Wendy R., and Odde, David J.

Subjects
CELL migration, CD44 antigen, EXTRACELLULAR matrix, HYALURONIC acid, CANCER invasiveness
Abstract

Cell migration is the major driver of invasion and metastasis during cancer progression. For cells to migrate, they utilize the actin–myosin cytoskeleton and adhesion molecules, such as integrins and CD44, to generate traction forces in their environment. CD44 primarily binds to hyaluronic acid (HA) and integrins primarily bind to extracellular matrix (ECM) proteins such as collagen. However, the role of CD44 under integrin-mediated conditions and vice versa is not well known. Here, we performed traction force microscopy (TFM) on U251 cells seeded on collagen I-coated polyacrylamide gels to assess the functional mechanical relationship between integrins and CD44. Performing TFM on integrin-mediated adhesion conditions, i.e., collagen, we found that CD44KO U251 cells exerted more traction force than wild-type (WT) U251 cells. Furthermore, untreated WT and CD44-blocked WT exhibited comparable results. Conversely, in CD44-mediated adhesive conditions, integrin-blocked WT cells exerted a higher traction force than untreated WT cells. Our data suggest that CD44 and integrins have a mutually antagonistic relationship where one receptor represses the other's ability to generate traction force on its cognate substrate. [ABSTRACT FROM AUTHOR]

Published
2024
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7. Supplementary Figures 4-7 from Sleeping Beauty Insertional Mutagenesis Reveals Important Genetic Drivers of Central Nervous System Embryonal Tumors

Author

Beckmann, Pauline J., primary, Larson, Jon D., primary, Larsson, Alex T., primary, Ostergaard, Jason P., primary, Wagner, Sandra, primary, Rahrmann, Eric P., primary, Shamsan, Ghaidan A., primary, Otto, George M., primary, Williams, Rory L., primary, Wang, Jun, primary, Lee, Catherine, primary, Tschida, Barbara R., primary, Das, Paramita, primary, Dubuc, Adrian M., primary, Moriarity, Branden S., primary, Picard, Daniel, primary, Wu, Xiaochong, primary, Rodriguez, Fausto J., primary, Rosemarie, Quincy, primary, Krebs, Ryan D., primary, Molan, Amy M., primary, Demer, Addison M., primary, Frees, Michelle M., primary, Rizzardi, Anthony E., primary, Schmechel, Stephen C., primary, Eberhart, Charles G., primary, Jenkins, Robert B., primary, Wechsler-Reya, Robert J., primary, Odde, David J., primary, Huang, Annie, primary, Taylor, Michael D., primary, Sarver, Aaron L., primary, and Largaespada, David A., primary

Published
2023
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8. Data from Sleeping Beauty Insertional Mutagenesis Reveals Important Genetic Drivers of Central Nervous System Embryonal Tumors

Author

Beckmann, Pauline J., primary, Larson, Jon D., primary, Larsson, Alex T., primary, Ostergaard, Jason P., primary, Wagner, Sandra, primary, Rahrmann, Eric P., primary, Shamsan, Ghaidan A., primary, Otto, George M., primary, Williams, Rory L., primary, Wang, Jun, primary, Lee, Catherine, primary, Tschida, Barbara R., primary, Das, Paramita, primary, Dubuc, Adrian M., primary, Moriarity, Branden S., primary, Picard, Daniel, primary, Wu, Xiaochong, primary, Rodriguez, Fausto J., primary, Rosemarie, Quincy, primary, Krebs, Ryan D., primary, Molan, Amy M., primary, Demer, Addison M., primary, Frees, Michelle M., primary, Rizzardi, Anthony E., primary, Schmechel, Stephen C., primary, Eberhart, Charles G., primary, Jenkins, Robert B., primary, Wechsler-Reya, Robert J., primary, Odde, David J., primary, Huang, Annie, primary, Taylor, Michael D., primary, Sarver, Aaron L., primary, and Largaespada, David A., primary

Published
2023
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9. Supplementary Tables 1-9 from Sleeping Beauty Insertional Mutagenesis Reveals Important Genetic Drivers of Central Nervous System Embryonal Tumors

Author

Beckmann, Pauline J., primary, Larson, Jon D., primary, Larsson, Alex T., primary, Ostergaard, Jason P., primary, Wagner, Sandra, primary, Rahrmann, Eric P., primary, Shamsan, Ghaidan A., primary, Otto, George M., primary, Williams, Rory L., primary, Wang, Jun, primary, Lee, Catherine, primary, Tschida, Barbara R., primary, Das, Paramita, primary, Dubuc, Adrian M., primary, Moriarity, Branden S., primary, Picard, Daniel, primary, Wu, Xiaochong, primary, Rodriguez, Fausto J., primary, Rosemarie, Quincy, primary, Krebs, Ryan D., primary, Molan, Amy M., primary, Demer, Addison M., primary, Frees, Michelle M., primary, Rizzardi, Anthony E., primary, Schmechel, Stephen C., primary, Eberhart, Charles G., primary, Jenkins, Robert B., primary, Wechsler-Reya, Robert J., primary, Odde, David J., primary, Huang, Annie, primary, Taylor, Michael D., primary, Sarver, Aaron L., primary, and Largaespada, David A., primary

Published
2023
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10. Supplementary Figures 1-3 from Sleeping Beauty Insertional Mutagenesis Reveals Important Genetic Drivers of Central Nervous System Embryonal Tumors

Author

Beckmann, Pauline J., primary, Larson, Jon D., primary, Larsson, Alex T., primary, Ostergaard, Jason P., primary, Wagner, Sandra, primary, Rahrmann, Eric P., primary, Shamsan, Ghaidan A., primary, Otto, George M., primary, Williams, Rory L., primary, Wang, Jun, primary, Lee, Catherine, primary, Tschida, Barbara R., primary, Das, Paramita, primary, Dubuc, Adrian M., primary, Moriarity, Branden S., primary, Picard, Daniel, primary, Wu, Xiaochong, primary, Rodriguez, Fausto J., primary, Rosemarie, Quincy, primary, Krebs, Ryan D., primary, Molan, Amy M., primary, Demer, Addison M., primary, Frees, Michelle M., primary, Rizzardi, Anthony E., primary, Schmechel, Stephen C., primary, Eberhart, Charles G., primary, Jenkins, Robert B., primary, Wechsler-Reya, Robert J., primary, Odde, David J., primary, Huang, Annie, primary, Taylor, Michael D., primary, Sarver, Aaron L., primary, and Largaespada, David A., primary

Published
2023
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12. A role for genetic susceptibility in sporadic focal segmental glomerulosclerosis

Author

Yu, Haiyang, Artomov, Mykyta, Brahler, Sebastian, Stander, M. Christine, Shamsan, Ghaidan, Sampson, Matthew G., White, J. Michael, Kretzler, Matthias, Miner, Jeffrey H., Jain, Sanjay, Winkler, Cheryl A., Mitra, Robi D., Kopp, Jeffrey B., Daly, Mark J., and Shaw, Andrey S.

Subjects
Genetic research, Glomerulonephritis -- Genetic aspects -- Risk factors, Genetic variation -- Identification and classification -- Health aspects, Genetic susceptibility -- Research, Health care industry
Abstract

Focal segmental glomerulosclerosis (FSGS) is a syndrome that involves kidney podocyte dysfunction and causes chronic kidney disease. Multiple factors including chemical toxicity, inflammation, and infection underlie FSGS; however, highly penetrant disease genes have been identified in a small fraction of patients with a family history of FSGS. Variants of apolipoprotein L1 (APOL1) have been linked to FSGS in African Americans with HIV or hypertension, supporting the proposal that genetic factors enhance FSGS susceptibility. Here, we used sequencing to investigate whether genetics plays a role in the majority of FSGS cases that are identified as primary or sporadic FSGS and have no known cause. Given the limited number of biopsy-proven cases with ethnically matched controls, we devised an analytic strategy to identify and rank potential candidate genes and used an animal model for validation. Nine candidate FSGS susceptibility genes were identified in our patient cohort, and three were validated using a high-throughput mouse method that we developed. Specifically, we introduced a podocyte-specific, doxycycline-inducible transactivator into a murine embryonic stem cell line with an FSGS-susceptible genetic background that allows shRNA-mediated targeting of candidate genes in the adult kidney. Our analysis supports a broader role for genetic susceptibility of both sporadic and familial cases of FSGS and provides a tool to rapidly evaluate candidate FSGS-associated genes., Introduction The glomerulus of the kidney is a specialized capillary bed that generates an ultrafiltrate that, after modification by the kidney tubule system, becomes urine. Diseases of the glomerulus often [...]

Published
2016
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13. Differential migration mechanics and immune responses of glioblastoma subtypes

Author

Shamsan, Ghaidan A., primary, Liu, Chao J., additional, Braman, Brooke C., additional, Rathe, Susan K., additional, Sarver, Aaron L., additional, Ghaderi, Nima, additional, McMahon, Mariah M., additional, Klank, Rebecca L., additional, Tschida, Barbara R., additional, McFarren, S. Joey, additional, Rosato, Pamela C., additional, Masopust, David, additional, Sarkaria, Jann N., additional, Clark, H. Brent, additional, Rosenfeld, Steven S., additional, Largaespada, David A., additional, and Odde, David J., additional

Published
2022
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14. TAMI-28. DIFFERENTIAL MIGRATION MECHANICS AND IMMUNE RESPONSES OF GLIOMA SUBTYPES

Author

Shamsan, Ghaidan, primary, Liu, Chao, additional, Braman, Brooke, additional, Rathe, Susan, additional, Sarver, Aaron, additional, Ghaderi, Nima, additional, McMahon, Mariah, additional, Klank, Rebecca, additional, Tschida, Barbara, additional, McFarren, Joey, additional, Sarkaria, Jann, additional, Clark, H Brent, additional, Rosenfeld, Steven, additional, Largaespada, David, additional, and Odde, David, additional

Published
2020
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15. Negative durotaxis: cell movement toward softer environments

Author

Isomursu, Aleksi, primary, Park, Keun-Young, additional, Hou, Jay, additional, Cheng, Bo, additional, Shamsan, Ghaidan, additional, Fuller, Benjamin, additional, Kasim, Jesse, additional, Mahmoodi, M. Mohsen, additional, Lu, Tian Jian, additional, Genin, Guy M., additional, Xu, Feng, additional, Lin, Min, additional, Distefano, Mark, additional, Ivaska, Johanna, additional, and Odde, David J., additional

Published
2020
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17. SEMA4C is a novel target to limit osteosarcoma growth, progression, and metastasis

Author

Smeester, Branden A., primary, Slipek, Nicholas J., additional, Pomeroy, Emily J., additional, Bomberger, Heather E., additional, Shamsan, Ghaidan A., additional, Peterson, Joseph J., additional, Crosby, Margaret R., additional, Draper, Garrett M., additional, Becklin, Kelsie L., additional, Rahrmann, Eric P., additional, McCarthy, James B., additional, Odde, David J., additional, Wood, David K., additional, Largaespada, David A., additional, and Moriarity, Branden S., additional

Published
2019
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18. Sleeping Beauty Insertional Mutagenesis Reveals Important Genetic Drivers of Central Nervous System Embryonal Tumors

Author

Beckmann, Pauline J., primary, Larson, Jon D., additional, Larsson, Alex T., additional, Ostergaard, Jason P., additional, Wagner, Sandra, additional, Rahrmann, Eric P., additional, Shamsan, Ghaidan A., additional, Otto, George M., additional, Williams, Rory L., additional, Wang, Jun, additional, Lee, Catherine, additional, Tschida, Barbara R., additional, Das, Paramita, additional, Dubuc, Adrian M., additional, Moriarity, Branden S., additional, Picard, Daniel, additional, Wu, Xiaochong, additional, Rodriguez, Fausto J., additional, Rosemarie, Quincy, additional, Krebs, Ryan D., additional, Molan, Amy M., additional, Demer, Addison M., additional, Frees, Michelle M., additional, Rizzardi, Anthony E., additional, Schmechel, Stephen C., additional, Eberhart, Charles G., additional, Jenkins, Robert B., additional, Wechsler-Reya, Robert J., additional, Odde, David J., additional, Huang, Annie, additional, Taylor, Michael D., additional, Sarver, Aaron L., additional, and Largaespada, David A., additional

Published
2019
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20. Shifting the optimal stiffness for cell migration

Author

Bangasser, Benjamin L., primary, Shamsan, Ghaidan A., additional, Chan, Clarence E., additional, Opoku, Kwaku N., additional, Tüzel, Erkan, additional, Schlichtmann, Benjamin W., additional, Kasim, Jesse A., additional, Fuller, Benjamin J., additional, McCullough, Brannon R., additional, Rosenfeld, Steven S., additional, and Odde, David J., additional

Published
2017
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21. Slit-Robo GTPase-Activating Protein 2 as a metastasis suppressor in osteosarcoma

Author

Marko, Tracy A., primary, Shamsan, Ghaidan A., additional, Edwards, Elizabeth N., additional, Hazelton, Paige E., additional, Rathe, Susan K., additional, Cornax, Ingrid, additional, Overn, Paula R., additional, Varshney, Jyotika, additional, Diessner, Brandon J., additional, Moriarity, Branden S., additional, O’Sullivan, M. Gerard, additional, Odde, David J., additional, and Largaespada, David A., additional

Published
2016
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24. Mutations in the Gene That Encodes the F-Actin Binding Protein Anillin Cause FSGS

Author

Gbadegesin, Rasheed A., primary, Hall, Gentzon, additional, Adeyemo, Adebowale, additional, Hanke, Nils, additional, Tossidou, Irini, additional, Burchette, James, additional, Wu, Guanghong, additional, Homstad, Alison, additional, Sparks, Matthew A., additional, Gomez, Jose, additional, Jiang, Ruiji, additional, Alonso, Andrea, additional, Lavin, Peter, additional, Conlon, Peter, additional, Korstanje, Ron, additional, Stander, M. Christine, additional, Shamsan, Ghaidan, additional, Barua, Moumita, additional, Spurney, Robert, additional, Singhal, Pravin C., additional, Kopp, Jeffrey B., additional, Haller, Hermann, additional, Howell, David, additional, Pollak, Martin R., additional, Shaw, Andrey S., additional, Schiffer, Mario, additional, and Winn, Michelle P., additional

Published
2014
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25. Mechanical Regulation of Glioma Cell Migration

Author

Shamsan, Ghaidan

Abstract

Glioblastoma is an incurable aggressive brain tumor with median survival of less than 17 months. In Glioblastoma, tumor spreading is driven by tumor cells’ ability to infiltrate healthy brain parenchyma, which prevents complete surgical resection and contributes to tumor recurrence. Thus, understanding the mechanisms driving glioblastoma cancer cell migration is critical for the development of effective anti-migratory therapies. Through extensive genomic analyses, distinct molecular subtypes were identified—proneural, classical and mesenchymal— and were shown to strongly correlate with specific genetic alterations (Mesenchymal: NF1; Classical: EGFRvIII; Proneural: PDGFRA). In this dissertation, I developed genetically induced tumor mouse models of human glioblastoma subtypes to study the migration behavior of mesenchymal and proneural cancer cells. Using a multidisciplinary approach, I identified key mechanistic differences between glioblastoma molecular subtypes involving cancer cell migration and immune cell infiltration. Using mathematical modeling, we demonstrated the elevation of adhesion molecules, notably the glycoprotein CD44, leads to enhanced cancer cell migration and force generation. In the second part of my thesis, I developed a 2-dimensional compliant substrate to study the biophysics of CD44-dependent adhesion. Using immobilized anti-CD44 antibody, I demonstrated the ability of CD44 to support cell adhesion, migration and force transmission. Furthermore, I showed CD44-mediated migration and force transmission are stiffness and adhesion sensitive as predicted by a motor-clutch mechanism. In summary, this dissertation supports the role of CD44 as an adhesion molecule mediating glioblastoma cancer cell migration and highlights its therapeutic potential as an anti-migratory target. In addition, the work in this thesis informs future studies to explore targeting CD44 to slow glioblastoma cancer cell migration and to identify the factors driving immune cell infiltration in mesenchymal glioblastoma.

Published
2021

26. A role for genetic susceptibility in sporadic focal segmental glomerulosclerosis.

Author

Haiyang Yu, Mykyta Artomov, Brähler, Sebastian, Stander, M. Christine, Shamsan, Ghaidan, Sampson, Matthew G., White, J. Michael, Kretzler, Matthias, Miner, Jeffrey H., Jain, Sanjay, Winkler, Cheryl A., Mitra, Robi D., Kopp, Jeffrey B., Daly, Mark J., Shaw, Andrey S., Yu, Haiyang, and Artomov, Mykyta

Subjects
*GLOMERULOSCLEROSIS, *DISEASE susceptibility, *KIDNEY diseases, *APOLIPOPROTEINS, *HEALTH of African Americans, *GENETICS, *ANIMAL experimentation, *CELL culture, *GENETIC polymorphisms, *GENETIC techniques, *GLOMERULONEPHRITIS, *MICE, *RESEARCH funding, *CASE-control method, *SEQUENCE analysis
Abstract

Focal segmental glomerulosclerosis (FSGS) is a syndrome that involves kidney podocyte dysfunction and causes chronic kidney disease. Multiple factors including chemical toxicity, inflammation, and infection underlie FSGS; however, highly penetrant disease genes have been identified in a small fraction of patients with a family history of FSGS. Variants of apolipoprotein L1 (APOL1) have been linked to FSGS in African Americans with HIV or hypertension, supporting the proposal that genetic factors enhance FSGS susceptibility. Here, we used sequencing to investigate whether genetics plays a role in the majority of FSGS cases that are identified as primary or sporadic FSGS and have no known cause. Given the limited number of biopsy-proven cases with ethnically matched controls, we devised an analytic strategy to identify and rank potential candidate genes and used an animal model for validation. Nine candidate FSGS susceptibility genes were identified in our patient cohort, and three were validated using a high-throughput mouse method that we developed. Specifically, we introduced a podocyte-specific, doxycycline-inducible transactivator into a murine embryonic stem cell line with an FSGS-susceptible genetic background that allows shRNA-mediated targeting of candidate genes in the adult kidney. Our analysis supports a broader role for genetic susceptibility of both sporadic and familial cases of FSGS and provides a tool to rapidly evaluate candidate FSGS-associated genes. [ABSTRACT FROM AUTHOR]

Published
2016
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