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4. Metabolic Reprogramming by MYCN Confers Dependence on the Serine-Glycine-One-Carbon Biosynthetic Pathway

Author

Xia, Yingfeng, Ye, Bingwei, Ding, Jane, Yu, Yajie, Alptekin, Ahmet, Thangaraju, Muthusamy, Prasad, Puttur D, Ding, Zhi-Chun, Park, Eun Jeong, Choi, Jeong-Hyeon, Gao, Bei, Fiehn, Oliver, Yan, Chunhong, Dong, Zheng, Zha, Yunhong, and Ding, Han-Fei

Subjects
Neurosciences, Genetics, Neuroblastoma, Cancer, Rare Diseases, Clinical Research, Pediatric, 5.1 Pharmaceuticals, Development of treatments and therapeutic interventions, Biosynthetic Pathways, Carbon, Cell Line, Tumor, Child, Glycine, Humans, N-Myc Proto-Oncogene Protein, Serine, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

MYCN amplification drives the development of neuronal cancers in children and adults. Given the challenge in therapeutically targeting MYCN directly, we searched for MYCN-activated metabolic pathways as potential drug targets. Here we report that neuroblastoma cells with MYCN amplification show increased transcriptional activation of the serine-glycine-one-carbon (SGOC) biosynthetic pathway and an increased dependence on this pathway for supplying glucose-derived carbon for serine and glycine synthesis. Small molecule inhibitors that block this metabolic pathway exhibit selective cytotoxicity to MYCN-amplified cell lines and xenografts by inducing metabolic stress and autophagy. Transcriptional activation of the SGOC pathway in MYCN-amplified cells requires both MYCN and ATF4, which form a positive feedback loop, with MYCN activation of ATF4 mRNA expression and ATF4 stabilization of MYCN protein by antagonizing FBXW7-mediated MYCN ubiquitination. Collectively, these findings suggest a coupled relationship between metabolic reprogramming and increased sensitivity to metabolic stress, which could be exploited as a strategy for selective cancer therapy. SIGNIFICANCE: This study identifies a MYCN-dependent metabolic vulnerability and suggests a coupled relationship between metabolic reprogramming and increased sensitivity to metabolic stress, which could be exploited for cancer therapy.See related commentary by Rodriguez Garcia and Arsenian-Henriksson, p. 3818.

Published
2019

8. Cytotoxic Autophagy: A Novel Treatment Paradigm against Breast Cancer Using Oleanolic Acid and Ursolic Acid.

Author

Gupta, Kunj Bihari, Gao, Jie, Li, Xin, Thangaraju, Muthusamy, Panda, Siva S., and Lokeshwar, Bal L.

Subjects
THERAPEUTIC use of antineoplastic agents, TRITERPENES, PROTEIN kinase inhibitors, URSOLIC acid, AUTOPHAGY, RESEARCH funding, PROTEIN kinases, PHOSPHORYLATION, BREAST tumors, ANTINEOPLASTIC agents, APOPTOSIS, CELL proliferation, CELLULAR signal transduction, CELL lines, PARADIGMS (Social sciences), GENE expression, DRUG efficacy, CELL survival, PHARMACODYNAMICS
Abstract

Simple Summary: Cancer chemotherapy is dominated by cytotoxic drugs that non-selectively kill proliferating cells by blocking DNA replication and inducing apoptosis. Some natural anticancer products are less toxic to normal, slow-replicating cells but kill aggressive tumor cells. The combination of two structural isomers of pentacyclic triterpenes, oleanolic acid and ursolic acid, showed potent cytotoxic activity in human breast cancer cells in vitro by inducing cytotoxic autophagy at a significantly lower dose than previously reported. They were nontoxic to breast epithelial cells. Their activity was mainly due to the inhibition of AKT-mediated cell survival and the inhibition of the mammalian target of rapamycin (mTOR) signaling pathway, a central regulator of cell metabolism, growth, and proliferation. The compounds were equally effective against ER+ and triple-negative breast cancer cells. Combining low doses of nontoxic inhibitors of PI3k kinase increased the activities of these compounds. In contrast, inhibition of autophagy by 3-methyl adenine annulled their activity, demonstrating that cytotoxic autophagy may be the dominant mechanism of cell death. These compounds have potential for cancer therapy in neoadjuvant or adjuvant settings. Background: Oleanolic acid (OA) and Ursolic acid (UA) are bioactive triterpenoids. Reported activities vary with the dose used for testing their activities in vitro. Studies using doses of ≥20 µM showed apoptosis activities in cancer cells. However, reported drug levels in circulation achieved by oral administration of UA and OA are ≤2 µM, thus limiting their use for treatment or delivering a combination treatment. Materials and Methods: The present report demonstrates the efficacy of OA, UA, and OA + UA on tumor cell-specific cytotoxicity at low doses (5 µM to 10 µM) in breast cancer (BrCa) cell lines MCF7 and MDA-MB231. Results: The data show that both OA and UA killed BrCa cells at low doses, but were significantly less toxic to MCF-12A, a non-tumorigenic cell line. Moreover, OA + UA at ≤10 µM was lethal to BrCa cells. Mechanistic studies unraveled the significant absence of apoptosis, but their cytotoxicity was due to the induction of excessive autophagy at a OA + UA dose of 5 µM each. A link to drug-induced cytotoxic autophagy was established by demonstrating a lack of their cytotoxicity by silencing the autophagy-targeting genes (ATGs), which prevented OA-, UA-, or OA + UA-induced cell death. Further, UA or OA + UA treatment of BrCa cells caused an inhibition of PI3 kinase-mediated phosphorylation of Akt/mTOR, the key pathways that regulate cancer cell survival, metabolism, and proliferation. Discussion: Combinations of a PI3K inhibitor (LY294002) with OA, UA, or OA + UA synergistically inhibited BrCa cell survival. Therefore, the dominance of cytotoxic autophagy by inhibiting PI3K-mediated autophagy may be the primary mechanism of PTT-induced anticancer activity in BrCa cells. Conclusion: These results suggest it would be worthwhile testing combined OA and UA in clinical settings. [ABSTRACT FROM AUTHOR]

Published
2024
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9. Curcumin-Dichloroacetate Hybrid Molecule as an Antitumor Oral Drug against Multidrug-Resistant Advanced Bladder Cancers.

Author

Gupta, Kunj Bihari, Taylor, Truett L., Panda, Siva S., Thangaraju, Muthusamy, and Lokeshwar, Bal. L.

Subjects
BLADDER tumors, BIOLOGICAL models, DRUG resistance in cancer cells, ACETIC acid, MITOCHONDRIA, RESEARCH funding, ANTINEOPLASTIC agents, APOPTOSIS, MULTIDRUG resistance, ORAL drug administration, TREATMENT effectiveness, IN vivo studies, XENOGRAFTS, IMMUNODIAGNOSIS, DESCRIPTIVE statistics, OXIDATIVE stress, MICE, REACTIVE oxygen species, ACETYLCYSTEINE, CURCUMIN, ANIMAL experimentation, MOLECULAR structure, HYDROXIDES, COMPARATIVE studies, CELL surface antigens, PHARMACODYNAMICS
Abstract

Simple Summary: Advanced urinary bladder cancer (BCa) is characterized by rapid progression and development of therapy resistance. Despite all the available therapies, the five-year survival of metastatic BCa is a dismal 8% or lower. Many conjugates and additives of the natural polyphenol curcumin were developed and tested for potential therapeutic for cancers, with little success in vivo due to their rapid elimination and poor tissue penetrance. We tested a novel molecular hybrid CMC-2 composed of a curcumin scaffold conjugated to two dichloroacetate and glycine molecules. CMC-2 showed significantly higher antiproliferative and anti-survival activities against BCa than its parent compounds. Further, it was equally effective against chemotherapy-naïve and multidrug-resistant BCas (MDR-BCa). When tested in vivo using BCa xenograft in athymic mice, CMC-2 significantly delayed tumor growth without systemic toxicity. The mechanism of anticancer activity of CMC-2 was the induction of excessive oxidative stress in the cancer cells, leading to apoptotic cell death. These results show the potential of CMC-2 as a nontoxic oral treatment for high-grade bladder cancers. Tumor cells produce excessive reactive oxygen species (ROS) but cannot detoxify ROS if they are due to an external agent. An agent that produces toxic levels of ROS, specifically in tumor cells, could be an effective anticancer drug. CMC-2 is a molecular hybrid of the bioactive polyphenol curcumin conjugated to dichloroacetate (DCA) via a glycine bridge. The CMC-2 was tested for its cytotoxic antitumor activities and killed both naïve and multidrug-resistant (MDR) bladder cancer (BCa) cells with equal potency (<1.0 µM); CMC-2 was about 10–15 folds more potent than curcumin or DCA. Growth of human BCa xenograft in mice was reduced by >50% by oral gavage of 50 mg/kg of CMC-2 without recognizable systemic toxicity. Doses that used curcumin or DCA showed minimum antitumor effects. In vitro, the toxicity of CMC-2 in both naïve and MDR cells depended on increased intracellular ROS in tumor cells but not in normal cells at comparable doses. Increased ROS caused the permeabilization of mitochondria and induced apoptosis. Further, adding N-Acetyl cysteine (NAC), a hydroxyl radical scavenger, abolished excessive ROS production and CMC-2's cytotoxicity. The lack of systemic toxicity, equal potency against chemotherapy -naïve and resistant tumors, and oral bioavailability establish the potential of CMC-2 as a potent drug against bladder cancers. [ABSTRACT FROM AUTHOR]

Published
2024
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13. List of Contributors

Author

Aghi, Andrea, primary, Akdad, Mourad, additional, Andres, Emmanuel, additional, Bartolini, Desirée, additional, Brandão, Paula, additional, Bridges, Allison, additional, Casanello, Paola, additional, Castaño-Moreno, Erika, additional, Chailyan, S.G., additional, Ciceri, Paola, additional, Conte, Ferruccio, additional, Cozzolino, Mario, additional, Cruciani, Gabriele, additional, Cunningham, John, additional, Dali-Youcef, Nassim, additional, Dalto, Danyel Bueno, additional, Danielyan, K.E., additional, De Santis, Domenica, additional, Dontaraju, Venkata Satish, additional, Dronamraju, Venkateshwara, additional, El Bouhali, Bachir, additional, Emmerson, Joshua T., additional, Fichna, Jakub, additional, Friso, Simonetta, additional, Fusaro, Maria, additional, Galarini, Roberta, additional, Galassi, Andrea, additional, Galli, Francesco, additional, Gallieni, Maurizio, additional, Geier, Andreas, additional, Gioiello, Antimo, additional, Giusepponi, Danilo, additional, Gomes, Cláudio M., additional, Gonçalves, Álisson de Carvalho, additional, Guieu, Samuel, additional, Hagiwara, Shin-ichiro, additional, Hajiluian, Ghazaleh, additional, Henriques, Bárbara J., additional, Iervasi, Giorgio, additional, Jadavji, Nafisa M., additional, Jahn, Daniel, additional, Jankowska, Magdalena, additional, Karmin, O, additional, Kato, Norihisa, additional, Khallouki, Farid, additional, Kruk, Jerzy, additional, Kumrungsee, Thanutchaporn, additional, Labudzinskyi, Dmytro, additional, Laganà, Antonio Simone, additional, Lisakovska, Olha, additional, Llanos, Miguel, additional, Locatelli, Francesco, additional, Marinelli, Rita, additional, Matte, Jean-Jacques, additional, Mazanova, Anna, additional, Mereu, Maria Cristina, additional, Millan-Linares, Maria C., additional, Moftah, Mahira, additional, Montserrat-de la Paz, Sergio, additional, Munirathinam, Gnanasekar, additional, Mustafi, Sushmita, additional, Mutalip, Siti Syairah Mohd, additional, Naranjo, Maria C., additional, Nowicka, Beatrycze, additional, Owen, Robert Wyn, additional, Parkhomenko, Yuliya, additional, Peñailillo, Reyna, additional, Piñuñuri, Raúl, additional, Pizzolo, Francesca, additional, Plebani, Mario, additional, Poirot, Marc, additional, Portari, Guilherme Vannucchi, additional, Prasad, Puttur D., additional, Preedy, Victor R., additional, Price, Mina Yamazaki, additional, Protasova, Zoya, additional, Rajpurohit, Pragya, additional, Rizzo, Gianluca, additional, Ronco, Ana María, additional, Sebastiani, Bartolomeo, additional, Shidfar, Farzad, additional, Shymanskyi, Ihor, additional, Sid, Victoria, additional, Silvente-Poirot, Sandrine, additional, Siow, Yaw L., additional, Siragusa, Lydia, additional, Soldi, Luiz Ricardo, additional, Stucchi, Andrea, additional, Suda, Takashi, additional, Suidasari, Sofya, additional, Sylvester, Paul William, additional, Szymaszkiewicz, Agata, additional, Szymańska, Renata, additional, Thakur, Kiran, additional, Thangaraju, Muthusamy, additional, Tomar, Sudhir Kumar, additional, Torquato, Pierangelo, additional, Trela, Agnieszka, additional, Tripepi, Giovanni, additional, Udali, Silvia, additional, Veliky, Mykola, additional, Vinjamuri, Smita, additional, Vovk, Andriy, additional, Wang, Gaofeng, additional, Wei, Zhao-Jun, additional, Woo, Connie W.H., additional, Yanaka, Noriyuki, additional, Zaninotto, Martina, additional, Zhang, Peipei, additional, and Świerczyński, Mikołaj, additional

Published
2020
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18. Supplementary Figure S1 from IFNγ Induces DNA Methylation–Silenced GPR109A Expression via pSTAT1/p300 and H3K18 Acetylation in Colon Cancer

Author

Bardhan, Kankana, primary, Paschall, Amy V., primary, Yang, Dafeng, primary, Chen, May R., primary, Simon, Priscilla S., primary, Bhutia, Yangzom D., primary, Martin, Pamela M., primary, Thangaraju, Muthusamy, primary, Browning, Darren D., primary, Ganapathy, Vadivel, primary, Heaton, Christopher M., primary, Gu, Keni, primary, Lee, Jeffrey R., primary, and Liu, Kebin, primary

Published
2023
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19. Supplementary Table S1 from IFNγ Induces DNA Methylation–Silenced GPR109A Expression via pSTAT1/p300 and H3K18 Acetylation in Colon Cancer

Author

Bardhan, Kankana, primary, Paschall, Amy V., primary, Yang, Dafeng, primary, Chen, May R., primary, Simon, Priscilla S., primary, Bhutia, Yangzom D., primary, Martin, Pamela M., primary, Thangaraju, Muthusamy, primary, Browning, Darren D., primary, Ganapathy, Vadivel, primary, Heaton, Christopher M., primary, Gu, Keni, primary, Lee, Jeffrey R., primary, and Liu, Kebin, primary

Published
2023
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20. Supplementary Methods from RAD51AP1 Loss Attenuates Colorectal Cancer Stem Cell Renewal and Sensitizes to Chemotherapy

Author

Bridges, Allison E., primary, Ramachandran, Sabarish, primary, Tamizhmani, Kavin, primary, Parwal, Utkarsh, primary, Lester, Adrienne, primary, Rajpurohit, Pragya, primary, Morera, Daley S., primary, Hasanali, Sarrah L., primary, Arjunan, Pachiappan, primary, Jedeja, Ravirajsinh N., primary, Patel, Nikhil, primary, Martin, Pamela M., primary, Korkaya, Hasan, primary, Singh, Nagendra, primary, Manicassamy, Santhakumar, primary, Prasad, Puttur D., primary, Lokeshwar, Vinata B., primary, Lokeshwar, Bal L., primary, Ganapathy, Vadivel, primary, and Thangaraju, Muthusamy, primary

Published
2023
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21. Data from IFNγ Induces DNA Methylation–Silenced GPR109A Expression via pSTAT1/p300 and H3K18 Acetylation in Colon Cancer

Author

Bardhan, Kankana, primary, Paschall, Amy V., primary, Yang, Dafeng, primary, Chen, May R., primary, Simon, Priscilla S., primary, Bhutia, Yangzom D., primary, Martin, Pamela M., primary, Thangaraju, Muthusamy, primary, Browning, Darren D., primary, Ganapathy, Vadivel, primary, Heaton, Christopher M., primary, Gu, Keni, primary, Lee, Jeffrey R., primary, and Liu, Kebin, primary

Published
2023
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22. Supplementary Figure S3 from Promoter Methylation Modulates Indoleamine 2,3-Dioxygenase 1 Induction by Activated T Cells in Human Breast Cancers

Author

Noonepalle, Satish K., primary, Gu, Franklin, primary, Lee, Eun-Joon, primary, Choi, Jeong-Hyeon, primary, Han, Qimei, primary, Kim, Jaejik, primary, Ouzounova, Maria, primary, Shull, Austin Y., primary, Pei, Lirong, primary, Hsu, Pei-Yin, primary, Kolhe, Ravindra, primary, Shi, Fang, primary, Choi, Jiseok, primary, Chiou, Katie, primary, Huang, Tim H.M., primary, Korkaya, Hasan, primary, Deng, Libin, primary, Xin, Hong-Bo, primary, Huang, Shuang, primary, Thangaraju, Muthusamy, primary, Sreekumar, Arun, primary, Ambs, Stefan, primary, Tang, Shou-Ching, primary, Munn, David H., primary, and Shi, Huidong, primary

Published
2023
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23. Data from RAD51AP1 Loss Attenuates Colorectal Cancer Stem Cell Renewal and Sensitizes to Chemotherapy

Author

Bridges, Allison E., primary, Ramachandran, Sabarish, primary, Tamizhmani, Kavin, primary, Parwal, Utkarsh, primary, Lester, Adrienne, primary, Rajpurohit, Pragya, primary, Morera, Daley S., primary, Hasanali, Sarrah L., primary, Arjunan, Pachiappan, primary, Jedeja, Ravirajsinh N., primary, Patel, Nikhil, primary, Martin, Pamela M., primary, Korkaya, Hasan, primary, Singh, Nagendra, primary, Manicassamy, Santhakumar, primary, Prasad, Puttur D., primary, Lokeshwar, Vinata B., primary, Lokeshwar, Bal L., primary, Ganapathy, Vadivel, primary, and Thangaraju, Muthusamy, primary

Published
2023
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24. Supplementary Figure Legends from Promoter Methylation Modulates Indoleamine 2,3-Dioxygenase 1 Induction by Activated T Cells in Human Breast Cancers

Author

Noonepalle, Satish K., primary, Gu, Franklin, primary, Lee, Eun-Joon, primary, Choi, Jeong-Hyeon, primary, Han, Qimei, primary, Kim, Jaejik, primary, Ouzounova, Maria, primary, Shull, Austin Y., primary, Pei, Lirong, primary, Hsu, Pei-Yin, primary, Kolhe, Ravindra, primary, Shi, Fang, primary, Choi, Jiseok, primary, Chiou, Katie, primary, Huang, Tim H.M., primary, Korkaya, Hasan, primary, Deng, Libin, primary, Xin, Hong-Bo, primary, Huang, Shuang, primary, Thangaraju, Muthusamy, primary, Sreekumar, Arun, primary, Ambs, Stefan, primary, Tang, Shou-Ching, primary, Munn, David H., primary, and Shi, Huidong, primary

Published
2023
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25. Data from Promoter Methylation Modulates Indoleamine 2,3-Dioxygenase 1 Induction by Activated T Cells in Human Breast Cancers

Author

Noonepalle, Satish K., primary, Gu, Franklin, primary, Lee, Eun-Joon, primary, Choi, Jeong-Hyeon, primary, Han, Qimei, primary, Kim, Jaejik, primary, Ouzounova, Maria, primary, Shull, Austin Y., primary, Pei, Lirong, primary, Hsu, Pei-Yin, primary, Kolhe, Ravindra, primary, Shi, Fang, primary, Choi, Jiseok, primary, Chiou, Katie, primary, Huang, Tim H.M., primary, Korkaya, Hasan, primary, Deng, Libin, primary, Xin, Hong-Bo, primary, Huang, Shuang, primary, Thangaraju, Muthusamy, primary, Sreekumar, Arun, primary, Ambs, Stefan, primary, Tang, Shou-Ching, primary, Munn, David H., primary, and Shi, Huidong, primary

Published
2023
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26. Supplementary Tables 1 through 5 from Promoter Methylation Modulates Indoleamine 2,3-Dioxygenase 1 Induction by Activated T Cells in Human Breast Cancers

Author

Noonepalle, Satish K., primary, Gu, Franklin, primary, Lee, Eun-Joon, primary, Choi, Jeong-Hyeon, primary, Han, Qimei, primary, Kim, Jaejik, primary, Ouzounova, Maria, primary, Shull, Austin Y., primary, Pei, Lirong, primary, Hsu, Pei-Yin, primary, Kolhe, Ravindra, primary, Shi, Fang, primary, Choi, Jiseok, primary, Chiou, Katie, primary, Huang, Tim H.M., primary, Korkaya, Hasan, primary, Deng, Libin, primary, Xin, Hong-Bo, primary, Huang, Shuang, primary, Thangaraju, Muthusamy, primary, Sreekumar, Arun, primary, Ambs, Stefan, primary, Tang, Shou-Ching, primary, Munn, David H., primary, and Shi, Huidong, primary

Published
2023
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27. Supplementary Data from RAD51AP1 Loss Attenuates Colorectal Cancer Stem Cell Renewal and Sensitizes to Chemotherapy

Author

Bridges, Allison E., primary, Ramachandran, Sabarish, primary, Tamizhmani, Kavin, primary, Parwal, Utkarsh, primary, Lester, Adrienne, primary, Rajpurohit, Pragya, primary, Morera, Daley S., primary, Hasanali, Sarrah L., primary, Arjunan, Pachiappan, primary, Jedeja, Ravirajsinh N., primary, Patel, Nikhil, primary, Martin, Pamela M., primary, Korkaya, Hasan, primary, Singh, Nagendra, primary, Manicassamy, Santhakumar, primary, Prasad, Puttur D., primary, Lokeshwar, Vinata B., primary, Lokeshwar, Bal L., primary, Ganapathy, Vadivel, primary, and Thangaraju, Muthusamy, primary

Published
2023
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28. Supplemental Figure Legend from IFNγ Induces DNA Methylation–Silenced GPR109A Expression via pSTAT1/p300 and H3K18 Acetylation in Colon Cancer

Author

Bardhan, Kankana, primary, Paschall, Amy V., primary, Yang, Dafeng, primary, Chen, May R., primary, Simon, Priscilla S., primary, Bhutia, Yangzom D., primary, Martin, Pamela M., primary, Thangaraju, Muthusamy, primary, Browning, Darren D., primary, Ganapathy, Vadivel, primary, Heaton, Christopher M., primary, Gu, Keni, primary, Lee, Jeffrey R., primary, and Liu, Kebin, primary

Published
2023
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29. Table S2 from Metabolic Reprogramming by MYCN Confers Dependence on the Serine-Glycine-One-Carbon Biosynthetic Pathway

Author

Xia, Yingfeng, primary, Ye, Bingwei, primary, Ding, Jane, primary, Yu, Yajie, primary, Alptekin, Ahmet, primary, Thangaraju, Muthusamy, primary, Prasad, Puttur D., primary, Ding, Zhi-Chun, primary, Park, Eun Jeong, primary, Choi, Jeong-Hyeon, primary, Gao, Bei, primary, Fiehn, Oliver, primary, Yan, Chunhong, primary, Dong, Zheng, primary, Zha, Yunhong, primary, and Ding, Han-Fei, primary

Published
2023
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30. Data from Metabolic Reprogramming by MYCN Confers Dependence on the Serine-Glycine-One-Carbon Biosynthetic Pathway

Author

Xia, Yingfeng, primary, Ye, Bingwei, primary, Ding, Jane, primary, Yu, Yajie, primary, Alptekin, Ahmet, primary, Thangaraju, Muthusamy, primary, Prasad, Puttur D., primary, Ding, Zhi-Chun, primary, Park, Eun Jeong, primary, Choi, Jeong-Hyeon, primary, Gao, Bei, primary, Fiehn, Oliver, primary, Yan, Chunhong, primary, Dong, Zheng, primary, Zha, Yunhong, primary, and Ding, Han-Fei, primary

Published
2023
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31. Supplementary Data from Metabolic Reprogramming by MYCN Confers Dependence on the Serine-Glycine-One-Carbon Biosynthetic Pathway

Author

Xia, Yingfeng, primary, Ye, Bingwei, primary, Ding, Jane, primary, Yu, Yajie, primary, Alptekin, Ahmet, primary, Thangaraju, Muthusamy, primary, Prasad, Puttur D., primary, Ding, Zhi-Chun, primary, Park, Eun Jeong, primary, Choi, Jeong-Hyeon, primary, Gao, Bei, primary, Fiehn, Oliver, primary, Yan, Chunhong, primary, Dong, Zheng, primary, Zha, Yunhong, primary, and Ding, Han-Fei, primary

Published
2023
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32. Data from The Niacin/Butyrate Receptor GPR109A Suppresses Mammary Tumorigenesis by Inhibiting Cell Survival

Author

Elangovan, Selvakumar, primary, Pathania, Rajneesh, primary, Ramachandran, Sabarish, primary, Ananth, Sudha, primary, Padia, Ravi N., primary, Lan, Ling, primary, Singh, Nagendra, primary, Martin, Pamela M., primary, Hawthorn, Lesleyann, primary, Prasad, Puttur D., primary, Ganapathy, Vadivel, primary, and Thangaraju, Muthusamy, primary

Published
2023
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33. Data from Combined Inhibition of DNMT and HDAC Blocks the Tumorigenicity of Cancer Stem-like Cells and Attenuates Mammary Tumor Growth

Author

Pathania, Rajneesh, primary, Ramachandran, Sabarish, primary, Mariappan, Gurusamy, primary, Thakur, Priyanka, primary, Shi, Huidong, primary, Choi, Jeong-Hyeon, primary, Manicassamy, Santhakumar, primary, Kolhe, Ravindra, primary, Prasad, Puttur D., primary, Sharma, Suash, primary, Lokeshwar, Bal L., primary, Ganapathy, Vadivel, primary, and Thangaraju, Muthusamy, primary

Published
2023
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34. Supplementary Table 1 from Combined Inhibition of DNMT and HDAC Blocks the Tumorigenicity of Cancer Stem-like Cells and Attenuates Mammary Tumor Growth

Author

Pathania, Rajneesh, primary, Ramachandran, Sabarish, primary, Mariappan, Gurusamy, primary, Thakur, Priyanka, primary, Shi, Huidong, primary, Choi, Jeong-Hyeon, primary, Manicassamy, Santhakumar, primary, Kolhe, Ravindra, primary, Prasad, Puttur D., primary, Sharma, Suash, primary, Lokeshwar, Bal L., primary, Ganapathy, Vadivel, primary, and Thangaraju, Muthusamy, primary

Published
2023
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35. Supplementary Figure Legends 1-5 from GPR109A Is a G-protein–Coupled Receptor for the Bacterial Fermentation Product Butyrate and Functions as a Tumor Suppressor in Colon

Author

Thangaraju, Muthusamy, primary, Cresci, Gail A., primary, Liu, Kebin, primary, Ananth, Sudha, primary, Gnanaprakasam, Jaya P., primary, Browning, Darren D., primary, Mellinger, John D., primary, Smith, Sylvia B., primary, Digby, Gregory J., primary, Lambert, Nevin A., primary, Prasad, Puttur D., primary, and Ganapathy, Vadivel, primary

Published
2023
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36. Supplemental Materials and Methods from Combined Inhibition of DNMT and HDAC Blocks the Tumorigenicity of Cancer Stem-like Cells and Attenuates Mammary Tumor Growth

Author

Pathania, Rajneesh, primary, Ramachandran, Sabarish, primary, Mariappan, Gurusamy, primary, Thakur, Priyanka, primary, Shi, Huidong, primary, Choi, Jeong-Hyeon, primary, Manicassamy, Santhakumar, primary, Kolhe, Ravindra, primary, Prasad, Puttur D., primary, Sharma, Suash, primary, Lokeshwar, Bal L., primary, Ganapathy, Vadivel, primary, and Thangaraju, Muthusamy, primary

Published
2023
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38. Supplementary Figures 1-5 from GPR109A Is a G-protein–Coupled Receptor for the Bacterial Fermentation Product Butyrate and Functions as a Tumor Suppressor in Colon

Author

Thangaraju, Muthusamy, primary, Cresci, Gail A., primary, Liu, Kebin, primary, Ananth, Sudha, primary, Gnanaprakasam, Jaya P., primary, Browning, Darren D., primary, Mellinger, John D., primary, Smith, Sylvia B., primary, Digby, Gregory J., primary, Lambert, Nevin A., primary, Prasad, Puttur D., primary, and Ganapathy, Vadivel, primary

Published
2023
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39. Supplementary Figures 1 - 5, Table 1 from The Niacin/Butyrate Receptor GPR109A Suppresses Mammary Tumorigenesis by Inhibiting Cell Survival

Author

Elangovan, Selvakumar, primary, Pathania, Rajneesh, primary, Ramachandran, Sabarish, primary, Ananth, Sudha, primary, Padia, Ravi N., primary, Lan, Ling, primary, Singh, Nagendra, primary, Martin, Pamela M., primary, Hawthorn, Lesleyann, primary, Prasad, Puttur D., primary, Ganapathy, Vadivel, primary, and Thangaraju, Muthusamy, primary

Published
2023
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40. Supplementary Figure legends from Combined Inhibition of DNMT and HDAC Blocks the Tumorigenicity of Cancer Stem-like Cells and Attenuates Mammary Tumor Growth

Author

Pathania, Rajneesh, primary, Ramachandran, Sabarish, primary, Mariappan, Gurusamy, primary, Thakur, Priyanka, primary, Shi, Huidong, primary, Choi, Jeong-Hyeon, primary, Manicassamy, Santhakumar, primary, Kolhe, Ravindra, primary, Prasad, Puttur D., primary, Sharma, Suash, primary, Lokeshwar, Bal L., primary, Ganapathy, Vadivel, primary, and Thangaraju, Muthusamy, primary

Published
2023
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41. Supplementary Table 3 from The Niacin/Butyrate Receptor GPR109A Suppresses Mammary Tumorigenesis by Inhibiting Cell Survival

Author

Elangovan, Selvakumar, primary, Pathania, Rajneesh, primary, Ramachandran, Sabarish, primary, Ananth, Sudha, primary, Padia, Ravi N., primary, Lan, Ling, primary, Singh, Nagendra, primary, Martin, Pamela M., primary, Hawthorn, Lesleyann, primary, Prasad, Puttur D., primary, Ganapathy, Vadivel, primary, and Thangaraju, Muthusamy, primary

Published
2023
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42. Supplementary Table 2 from The Niacin/Butyrate Receptor GPR109A Suppresses Mammary Tumorigenesis by Inhibiting Cell Survival

Author

Elangovan, Selvakumar, primary, Pathania, Rajneesh, primary, Ramachandran, Sabarish, primary, Ananth, Sudha, primary, Padia, Ravi N., primary, Lan, Ling, primary, Singh, Nagendra, primary, Martin, Pamela M., primary, Hawthorn, Lesleyann, primary, Prasad, Puttur D., primary, Ganapathy, Vadivel, primary, and Thangaraju, Muthusamy, primary

Published
2023
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43. Supplemental Figures from Combined Inhibition of DNMT and HDAC Blocks the Tumorigenicity of Cancer Stem-like Cells and Attenuates Mammary Tumor Growth

Author

Pathania, Rajneesh, primary, Ramachandran, Sabarish, primary, Mariappan, Gurusamy, primary, Thakur, Priyanka, primary, Shi, Huidong, primary, Choi, Jeong-Hyeon, primary, Manicassamy, Santhakumar, primary, Kolhe, Ravindra, primary, Prasad, Puttur D., primary, Sharma, Suash, primary, Lokeshwar, Bal L., primary, Ganapathy, Vadivel, primary, and Thangaraju, Muthusamy, primary

Published
2023
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45. Supplementary Table 4 from The Niacin/Butyrate Receptor GPR109A Suppresses Mammary Tumorigenesis by Inhibiting Cell Survival

Author

Elangovan, Selvakumar, primary, Pathania, Rajneesh, primary, Ramachandran, Sabarish, primary, Ananth, Sudha, primary, Padia, Ravi N., primary, Lan, Ling, primary, Singh, Nagendra, primary, Martin, Pamela M., primary, Hawthorn, Lesleyann, primary, Prasad, Puttur D., primary, Ganapathy, Vadivel, primary, and Thangaraju, Muthusamy, primary

Published
2023
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46. Data from GPR109A Is a G-protein–Coupled Receptor for the Bacterial Fermentation Product Butyrate and Functions as a Tumor Suppressor in Colon

Author

Thangaraju, Muthusamy, primary, Cresci, Gail A., primary, Liu, Kebin, primary, Ananth, Sudha, primary, Gnanaprakasam, Jaya P., primary, Browning, Darren D., primary, Mellinger, John D., primary, Smith, Sylvia B., primary, Digby, Gregory J., primary, Lambert, Nevin A., primary, Prasad, Puttur D., primary, and Ganapathy, Vadivel, primary

Published
2023
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48. Supplementary Table 2 from Combined Inhibition of DNMT and HDAC Blocks the Tumorigenicity of Cancer Stem-like Cells and Attenuates Mammary Tumor Growth

Author

Pathania, Rajneesh, primary, Ramachandran, Sabarish, primary, Mariappan, Gurusamy, primary, Thakur, Priyanka, primary, Shi, Huidong, primary, Choi, Jeong-Hyeon, primary, Manicassamy, Santhakumar, primary, Kolhe, Ravindra, primary, Prasad, Puttur D., primary, Sharma, Suash, primary, Lokeshwar, Bal L., primary, Ganapathy, Vadivel, primary, and Thangaraju, Muthusamy, primary

Published
2023
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49. Exacerbation of AMD Phenotype in Lasered CNV Murine Model by Dysbiotic Oral Pathogens

Author

Pachiappan Arjunan, Radhika Swaminathan, Jessie Yuan, Mohamed Elashiry, Amany Tawfik, Mohamed Al-Shabrawey, Pamela M. Martin, Thangaraju Muthusamy, and Christopher W. Cutler

Subjects
age-related macular degeneration, retinal inflammation, oxidative stress, antioxidants, retinal degeneration, periodontal disease, Therapeutics. Pharmacology, RM1-950
Abstract

Emerging evidence underscores an association between age-related macular degeneration (AMD) and periodontal disease (PD), yet the biological basis of this linkage and the specific role of oral dysbiosis caused by PD in AMD pathophysiology remains unclear. Furthermore, a simple reproducible model that emulates characteristics of both AMD and PD has been lacking. Hence, we established a novel AMD+PD murine model to decipher the potential role of oral infection (ligature-enhanced) with the keystone periodontal pathogen Porphyromonas gingivalis, in the progression of neovasculogenesis in a laser-induced choroidal-neovascularization (Li-CNV) mouse retina. By a combination of fundus photography, optical coherence tomography, and fluorescein angiography, we documented inflammatory drusen-like lesions, reduced retinal thickness, and increased vascular leakage in AMD+PD mice retinae. H&E further confirmed a significant reduction of retinal thickness and subretinal drusen-like deposits. Immunofluorescence microscopy revealed significant induction of choroidal/retinal vasculogenesis in AMD+PD mice. qPCR identified increased expression of oxidative-stress, angiogenesis, pro-inflammatory mediators, whereas antioxidants and anti-inflammatory genes in AMD+PD mice retinae were notably decreased. Through qPCR, we detected Pg and its fimbrial 16s-RrNA gene expression in the AMD+PD mice retinae. To sum-up, this is the first in vivo study signifying a role of periodontal infection in augmentation of AMD phenotype, with the aid of a pioneering AMD+PD murine model established in our laboratory.

Published
2021
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