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2,273 results on '"Lisanti, Michael P"'

3. ALDH High Breast Cancer Stem Cells Exhibit a Mesenchymal–Senescent Hybrid Phenotype, with Elevated Metabolic and Migratory Activities.

Author

Larrea Murillo, Luis, Sugden, Conor J., Ozsvari, Bela, Moftakhar, Zahra, Hassan, Ghada S., Sotgia, Federica, and Lisanti, Michael P.

Subjects
CANCER stem cells, ALDEHYDE dehydrogenase, CELL populations, METABOLIC reprogramming, CANCER cells
Abstract

Cancer stem cells (CSCs) account for 0.01 to 2% of the total tumor mass; however, they play a key role in tumor progression, metastasis and resistance to current cancer therapies. The generation and maintenance of CSCs are usually linked to the epithelial–mesenchymal transition (EMT), a dynamic process involved in reprogramming cancer cells towards a more aggressive and motile phenotype with increased stemness potential. Cells that undergo an EMT process have shown to be more resistant to conventional chemo/radiotherapies. In this context, aldehyde dehydrogenase (ALDH) enzymes, known for their role in the cellular detoxification of aldehydes and enhancement of cell survival, are often upregulated in cancer cells, promoting their resistance to conventional cancer treatments. Indeed, high ALDH levels have become a hallmark biomarker of CSCs and are often used to isolate this sub-population from the more abundant cancer cell populations. Herein, we isolated human breast cancer epithelial cells with higher ALDH abundance (ALDHHigh) and compared them to those with low ALDH abundance (ALDHLow). ALDHHigh sub-populations exhibited more characteristic EMT biomarkers by adopting a more mesenchymal phenotype with increased stemness and enhanced migratory potential. Furthermore, ALDHHigh sub-populations displayed elevated senescent markers. Moreover, these cells also demonstrated higher levels of mitochondria DNA/mass, as well as greater mitochondrial and glycolytic metabolic function. Conversely, ALDHLow sub-populations showed a higher efficiency of mammosphere/colony formation and an increased proliferative capacity. Therefore, we demonstrated that these ALDH sub-populations have distinct characteristics, underscoring their role in EMT, the formation of tumors and the mechanisms of metastasis. [ABSTRACT FROM AUTHOR]

Published
2024
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5. Kinase-independent role of cyclin D1 in chromosomal instability and mammary tumorigenesis

Author

Casimiro, Mathew C, Di Sante, Gabriele, Crosariol, Marco, Loro, Emanuele, Dampier, William, Ertel, Adam, Yu, Zuoren, Saria, Elizabeth A, Papanikolaou, Alexandros, Li, Zhiping, Wang, Chenguang, Addya, Sankar, Lisanti, Michael P, Fortina, Paolo, Cardiff, Robert D, Tozeren, Aydin, Knudsen, Erik S, Arnold, Andrew, and Pestell, Richard G

Subjects
Human Genome, Genetics, Cancer, Breast Cancer, 2.1 Biological and endogenous factors, Aetiology, Adenocarcinoma, Amino Acid Substitution, Aneuploidy, Animals, Catalytic Domain, Cell Transformation, Neoplastic, Cells, Cultured, Centrosome, Chromosomal Instability, Cyclin D1, Female, Fibroblasts, Genes, bcl-1, Humans, Mammary Neoplasms, Experimental, Mammary Tumor Virus, Mouse, Mice, Mice, Knockout, Mice, Transgenic, Mutation, Piperazines, Pyridines, Recombinant Fusion Proteins, Spindle Apparatus, Transduction, Genetic, breast cancer, chromosomal instability, cyclin D1, Oncology and Carcinogenesis
Abstract

Cyclin D1 is an important molecular driver of human breast cancer but better understanding of its oncogenic mechanisms is needed, especially to enhance efforts in targeted therapeutics. Currently, pharmaceutical initiatives to inhibit cyclin D1 are focused on the catalytic component since the transforming capacity is thought to reside in the cyclin D1/CDK activity. We initiated the following study to directly test the oncogenic potential of catalytically inactive cyclin D1 in an in vivo mouse model that is relevant to breast cancer. Herein, transduction of cyclin D1(-/-) mouse embryonic fibroblasts (MEFs) with the kinase dead KE mutant of cyclin D1 led to aneuploidy, abnormalities in mitotic spindle formation, autosome amplification, and chromosomal instability (CIN) by gene expression profiling. Acute transgenic expression of either cyclin D1(WT) or cyclin D1(KE) in the mammary gland was sufficient to induce a high CIN score within 7 days. Sustained expression of cyclin D1(KE) induced mammary adenocarcinoma with similar kinetics to that of the wild-type cyclin D1. ChIP-Seq studies demonstrated recruitment of cyclin D1(WT) and cyclin D1(KE) to the genes governing CIN. We conclude that the CDK-activating function of cyclin D1 is not necessary to induce either chromosomal instability or mammary tumorigenesis.

Published
2015

10. FoxO3a Drives the Metabolic Reprogramming in Tamoxifen-Resistant Breast Cancer Cells Restoring Tamoxifen Sensitivity

Author

Fiorillo, Marco, primary, Ricci, Elena, additional, Fava, Mariarosa, additional, Longobucco, Camilla, additional, Sotgia, Federica, additional, Rizza, Pietro, additional, Lanzino, Marilena, additional, Bonofiglio, Daniela, additional, Conforti, Francesca Luisa, additional, Catalano, Stefania, additional, Barone, Ines, additional, Morelli, Catia, additional, Aquila, Saveria, additional, Lisanti, Michael P., additional, and Sisci, Diego, additional

Published
2023
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17. In Vitro Investigation of Therapy-Induced Senescence and Senescence Escape in Breast Cancer Cells Using Novel Flow Cytometry-Based Methods.

Author

Tóth, Fanni, Moftakhar, Zahra, Sotgia, Federica, and Lisanti, Michael P.

Subjects
CELLULAR aging, CANCER cells, AGING, BREAST cancer, CELL cycle, DRUG target
Abstract

Although cellular senescence was originally defined as an irreversible form of cell cycle arrest, in therapy-induced senescence models, the emergence of proliferative senescence-escaped cancer cells has been reported by several groups, challenging the definition of senescence. Indeed, senescence-escaped cancer cells may contribute to resistance to cancer treatment. Here, to study senescence escape and isolate senescence-escaped cells, we developed novel flow cytometry-based methods using the proliferation marker Ki-67 and CellTrace CFSE live-staining. We investigated the role of a novel senescence marker (DPP4/CD26) and a senolytic drug (azithromycin) on the senescence-escaping ability of MCF-7 and MDA-MB-231 breast cancer cells. Our results show that the expression of DPP4/CD26 is significantly increased in both senescent MCF-7 and MDA-MB-231 cells. While not essential for senescence induction, DPP4/CD26 contributed to promoting senescence escape in MCF-7 cells but not in MDA-MB-231 cells. Our results also confirmed the potential senolytic effect of azithromycin in senescent cancer cells. Importantly, the combination of azithromycin and a DPP4 inhibitor (sitagliptin) demonstrated a synergistic effect in senescent MCF-7 cells and reduced the number of senescence-escaped cells. Although further research is needed, our results and novel methods could contribute to the investigation of the mechanisms of senescence escape and the identification of potential therapeutic targets. Indeed, DPP4/CD26 could be a promising marker and a novel target to potentially decrease senescence escape in cancer. [ABSTRACT FROM AUTHOR]

Published
2024
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22. Recent Developments in the Interactions Between Caveolin and Pathogens

Author

Machado, Fabiana S., Rodriguez, Nilda E., Adesse, Daniel, Garzoni, Luciana R., Esper, Lisia, Lisanti, Michael P., Burk, Robert D., Albanese, Chris, Van Doorslaer, Koenraad, Weiss, Louis M., Nagajyothi, Fnu, Nosanchuk, Joshua D., Wilson, Mary E., Tanowitz, Herbert B., Jasmin, Jean-François, editor, Frank, Philippe G., editor, and Lisanti, Michael P., editor

Published
2012
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23. Atherosclerosis, Caveolae and Caveolin-1

Author

Pavlides, Stephanos, Gutierrez-Pajares, Jorge L., Danilo, Christiane, Lisanti, Michael P., Frank, Philippe G., Jasmin, Jean-François, editor, Frank, Philippe G., editor, and Lisanti, Michael P., editor

Published
2012
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28. Preferred apical distribution of glycosyl-phosphatidylinositol (GPI) anchored proteins: A highly conserved feature of the polarized epithelial cell phenotype

Author

Lisanti, Michael P, Le Bivic, André, Saltiel, Alan R, and Rodriguez-Boulan, Enrique

Subjects
Biochemistry and Cell Biology, Biological Sciences, Animals, Cell Line, Dogs, Epithelium, Glycolipids, Glycosylphosphatidylinositols, Humans, Immunoblotting, Intestinal Mucosa, Kidney, Membrane Proteins, Phenotype, Phosphatidylinositols, Microbiology, Medical Microbiology, Physiology, Biochemistry and cell biology
Abstract

We use a sensitive biotin polarity assay to survey the surface distribution of glycosyl-phosphatidylinositol (GPI) anchored proteins in five model epithelial cell lines derived from different species (dog, pig, man) and tissues, i.e., kidney (MDCK I, MDCK II, LLC-PK1) and intestine (Caco-2 and SK-CO15). After biotinylation of apical or basolateral surfaces of confluent monolayers grown on polycarbonate filters, GPI-anchored proteins are identified by their shift from a Triton X-114 detergent-rich phase to a detergent-poor phase in the presence of phosphatidylinositol-specific phospholipase C. All GPI-anchored proteins detected (3-9 per cell type, at least 13 different proteins) are found to be apically polarized; no GPI-anchored protein is observed preferentially localized to the basal surface. One of the GPI-anchored proteins is identified as carcinoembryonic antigen (CEA). Survey of MDCK II-RCAr, a mutant cell line with a pleiotropic defect in galactosylation of glycoproteins and glycolipids (that presumably affects GPI anchors) also reveals an apical polarization of all GPI-anchored proteins. In contrast, analysis of MDCK II-ConAr (a mutant cell line with an unknown defect in glycosylation) revealed five GPI-anchored proteins, two of which appeared relatively unpolarized. Our results indicate that the polarized apical distribution of GPI-anchored proteins is highly conserved across species and tissue-type and may depend on glycosylation.

Published
1990

29. Data from v-Src Oncogene Induces Trop2 Proteolytic Activation via Cyclin D1

Author

Ju, Xiaoming, primary, Jiao, Xuanmao, primary, Ertel, Adam, primary, Casimiro, Mathew C., primary, Di Sante, Gabriele, primary, Deng, Shengqiong, primary, Li, Zhiping, primary, Di Rocco, Agnese, primary, Zhan, Tingting, primary, Hawkins, Adam, primary, Stoyanova, Tanya, primary, Andò, Sebastiano, primary, Fatatis, Alessandro, primary, Lisanti, Michael P., primary, Gomella, Leonard G., primary, Languino, Lucia R., primary, and Pestell, Richard G., primary

Published
2023
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30. Supplemental Methos from v-Src Oncogene Induces Trop2 Proteolytic Activation via Cyclin D1

Author

Ju, Xiaoming, primary, Jiao, Xuanmao, primary, Ertel, Adam, primary, Casimiro, Mathew C., primary, Di Sante, Gabriele, primary, Deng, Shengqiong, primary, Li, Zhiping, primary, Di Rocco, Agnese, primary, Zhan, Tingting, primary, Hawkins, Adam, primary, Stoyanova, Tanya, primary, Andò, Sebastiano, primary, Fatatis, Alessandro, primary, Lisanti, Michael P., primary, Gomella, Leonard G., primary, Languino, Lucia R., primary, and Pestell, Richard G., primary

Published
2023
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31. Supplemental Figures from v-Src Oncogene Induces Trop2 Proteolytic Activation via Cyclin D1

Author

Ju, Xiaoming, primary, Jiao, Xuanmao, primary, Ertel, Adam, primary, Casimiro, Mathew C., primary, Di Sante, Gabriele, primary, Deng, Shengqiong, primary, Li, Zhiping, primary, Di Rocco, Agnese, primary, Zhan, Tingting, primary, Hawkins, Adam, primary, Stoyanova, Tanya, primary, Andò, Sebastiano, primary, Fatatis, Alessandro, primary, Lisanti, Michael P., primary, Gomella, Leonard G., primary, Languino, Lucia R., primary, and Pestell, Richard G., primary

Published
2023
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32. Data from CCR5 Receptor Antagonists Block Metastasis to Bone of v-Src Oncogene–Transformed Metastatic Prostate Cancer Cell Lines

Author

Sicoli, Daniela, primary, Jiao, Xuanmao, primary, Ju, Xiaoming, primary, Velasco-Velazquez, Marco, primary, Ertel, Adam, primary, Addya, Sankar, primary, Li, Zhiping, primary, Andò, Sebastiano, primary, Fatatis, Alessandro, primary, Paudyal, Bishnuhari, primary, Cristofanilli, Massimo, primary, Thakur, Mathew L., primary, Lisanti, Michael P., primary, and Pestell, Richard G., primary

Published
2023
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35. Supplementary Figure 4 from Identification of a Cyclin D1 Network in Prostate Cancer That Antagonizes Epithelial–Mesenchymal Restraint

Author

Ju, Xiaoming, primary, Casimiro, Mathew C., primary, Gormley, Michael, primary, Meng, Hui, primary, Jiao, Xuanmao, primary, Katiyar, Sanjay, primary, Crosariol, Marco, primary, Chen, Ke, primary, Wang, Min, primary, Quong, Andrew A., primary, Lisanti, Michael P., primary, Ertel, Adam, primary, and Pestell, Richard G., primary

Published
2023
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38. Supplementary Figure Legends from CCR5 Receptor Antagonists Block Metastasis to Bone of v-Src Oncogene–Transformed Metastatic Prostate Cancer Cell Lines

Author

Sicoli, Daniela, primary, Jiao, Xuanmao, primary, Ju, Xiaoming, primary, Velasco-Velazquez, Marco, primary, Ertel, Adam, primary, Addya, Sankar, primary, Li, Zhiping, primary, Andò, Sebastiano, primary, Fatatis, Alessandro, primary, Paudyal, Bishnuhari, primary, Cristofanilli, Massimo, primary, Thakur, Mathew L., primary, Lisanti, Michael P., primary, and Pestell, Richard G., primary

Published
2023
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41. Supplementary Table 1 from Dachshund Binds p53 to Block the Growth of Lung Adenocarcinoma Cells

Author

Chen, Ke, primary, Wu, Kongming, primary, Cai, Shaoxin, primary, Zhang, Wei, primary, Zhou, Jie, primary, Wang, Jing, primary, Ertel, Adam, primary, Li, Zhiping, primary, Rui, Hallgeir, primary, Quong, Andrew, primary, Lisanti, Michael P., primary, Tozeren, Aydin, primary, Tanes, Ceylan, primary, Addya, Sankar, primary, Gormley, Michael, primary, Wang, Chenguang, primary, McMahon, Steven B., primary, and Pestell, Richard G., primary

Published
2023
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42. Data from Genetic Ablation of Cav1 Differentially Affects Melanoma Tumor Growth and Metastasis in Mice: Role of Cav1 in Shh Heterotypic Signaling and Transendothelial Migration

Author

Capozza, Franco, primary, Trimmer, Casey, primary, Castello-Cros, Remedios, primary, Katiyar, Sanjay, primary, Whitaker-Menezes, Diana, primary, Follenzi, Antonia, primary, Crosariol, Marco, primary, Llaverias, Gemma, primary, Sotgia, Federica, primary, Pestell, Richard G., primary, and Lisanti, Michael P., primary

Published
2023
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43. Supplementary Figure Legend from Genetic Ablation of Cav1 Differentially Affects Melanoma Tumor Growth and Metastasis in Mice: Role of Cav1 in Shh Heterotypic Signaling and Transendothelial Migration

Author

Capozza, Franco, primary, Trimmer, Casey, primary, Castello-Cros, Remedios, primary, Katiyar, Sanjay, primary, Whitaker-Menezes, Diana, primary, Follenzi, Antonia, primary, Crosariol, Marco, primary, Llaverias, Gemma, primary, Sotgia, Federica, primary, Pestell, Richard G., primary, and Lisanti, Michael P., primary

Published
2023
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44. Data from The Canonical NF-κB Pathway Governs Mammary Tumorigenesis in Transgenic Mice and Tumor Stem Cell Expansion

Author

Liu, Manran, primary, Sakamaki, Toshiyuki, primary, Casimiro, Mathew C., primary, Willmarth, Nicole E., primary, Quong, Andrew A., primary, Ju, Xiaoming, primary, Ojeifo, John, primary, Jiao, Xuanmao, primary, Yeow, Wen-Shuz, primary, Katiyar, Sanjay, primary, Shirley, L. Andrew, primary, Joyce, David, primary, Lisanti, Michael P., primary, Albanese, Christopher, primary, and Pestell, Richard G., primary

Published
2023
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45. Supplementary Table 2 from Identification of a Cyclin D1 Network in Prostate Cancer That Antagonizes Epithelial–Mesenchymal Restraint

Author

Ju, Xiaoming, primary, Casimiro, Mathew C., primary, Gormley, Michael, primary, Meng, Hui, primary, Jiao, Xuanmao, primary, Katiyar, Sanjay, primary, Crosariol, Marco, primary, Chen, Ke, primary, Wang, Min, primary, Quong, Andrew A., primary, Lisanti, Michael P., primary, Ertel, Adam, primary, and Pestell, Richard G., primary

Published
2023
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48. Supplementary Figures 1 - 4 from Dachshund Binds p53 to Block the Growth of Lung Adenocarcinoma Cells

Author

Chen, Ke, primary, Wu, Kongming, primary, Cai, Shaoxin, primary, Zhang, Wei, primary, Zhou, Jie, primary, Wang, Jing, primary, Ertel, Adam, primary, Li, Zhiping, primary, Rui, Hallgeir, primary, Quong, Andrew, primary, Lisanti, Michael P., primary, Tozeren, Aydin, primary, Tanes, Ceylan, primary, Addya, Sankar, primary, Gormley, Michael, primary, Wang, Chenguang, primary, McMahon, Steven B., primary, and Pestell, Richard G., primary

Published
2023
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50. Supplementary Methods, Figure Legend from Identification of a Cyclin D1 Network in Prostate Cancer That Antagonizes Epithelial–Mesenchymal Restraint

Author

Ju, Xiaoming, primary, Casimiro, Mathew C., primary, Gormley, Michael, primary, Meng, Hui, primary, Jiao, Xuanmao, primary, Katiyar, Sanjay, primary, Crosariol, Marco, primary, Chen, Ke, primary, Wang, Min, primary, Quong, Andrew A., primary, Lisanti, Michael P., primary, Ertel, Adam, primary, and Pestell, Richard G., primary

Published
2023
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