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6,774 results on '"Li, Shun"'

78. Caveolin-1 controls mitochondrial damage and ROS production by regulating fission - fusion dynamics and mitophagy

Author

Jiang, Ying, Krantz, Sarah, Qin, Xiang, Li, Shun, Gunasekara, Hirushi, Kim, Young-Mee, Zimnicka, Adriana, Bae, Misuk, Ma, Ke, Toth, Peter T, Hu, Ying, Shajahan-Haq, Ayesha N, Patel, Hemal H, Gentile, Saverio, Bonini, Marcelo G, Rehman, Jalees, Liu, Yiyao, and Minshall, Richard D

Subjects
Biochemistry and Cell Biology, Biological Sciences, Cancer, Aetiology, 2.1 Biological and endogenous factors, Underpinning research, 1.1 Normal biological development and functioning, Generic health relevance, Caveolin 1, Mitochondria, Mitochondrial Dynamics, Mitochondrial Proteins, Mitophagy, Reactive Oxygen Species, Cav-1, Mitochondrial dynamics, mtROS, Mitofusin 2, Dynamin-related protein 1, Medical Biochemistry and Metabolomics, Pharmacology and Pharmaceutical Sciences, Biochemistry and cell biology, Medicinal and biomolecular chemistry
Abstract

As essential regulators of mitochondrial quality control, mitochondrial dynamics and mitophagy play key roles in maintenance of metabolic health and cellular homeostasis. Here we show that knockdown of the membrane-inserted scaffolding and structural protein caveolin-1 (Cav-1) and expression of tyrosine 14 phospho-defective Cav-1 mutant (Y14F), as opposed to phospho-mimicking Y14D, altered mitochondrial morphology, and increased mitochondrial matrix mixing, mitochondrial fusion and fission dynamics as well as mitophagy in MDA-MB-231 triple negative breast cancer cells. Further, we found that interaction of Cav-1 with mitochondrial fusion/fission machinery Mitofusin 2 (Mfn2) and Dynamin related protein 1 (Drp1) was enhanced by Y14D mutant indicating Cav-1 Y14 phosphorylation prevented Mfn2 and Drp1 translocation to mitochondria. Moreover, limiting mitochondrial recruitment of Mfn2 diminished formation of the PINK1/Mfn2/Parkin complex required for initiation of mitophagy resulting in accumulation of damaged mitochondria and ROS (mtROS). Thus, these studies indicate that phospho-Cav-1 may be an important switch mechanism in cancer cell survival which could lead to novel strategies for complementing cancer therapies.

Published
2022

92. Interleukin-13 and its receptor are synaptic proteins involved in plasticity and neuroprotection

Author

Li, Shun, olde Heuvel, Florian, Rehman, Rida, Aousji, Oumayma, Froehlich, Albrecht, Li, Zhenghui, Jark, Rebecca, Zhang, Wanhong, Conquest, Alison, Woelfle, Sarah, Schoen, Michael, O´Meara, Caitlin C., Reinhardt, Richard Lee, Voehringer, David, Kassubek, Jan, Ludolph, Albert, Huber-Lang, Markus, Knöll, Bernd, Morganti-Kossmann, Maria Cristina, Brockmann, Marisa M., Boeckers, Tobias, and Roselli, Francesco

Published
2023
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95. Case report: Therapy-related myeloid neoplasms in three pediatric cases with medulloblastoma

Author

Li Shun Mak, Xiuling Li, Wilson Y. K. Chan, Alex W. K. Leung, Daniel K. L. Cheuk, Liz Y. P. Yuen, Jason C. C. So, Shau Yin Ha, and Anthony P. Y. Liu

Subjects
case report, medulloblastoma (MB), therapy-related myelodysplastic syndrome/acute myeloid leukemia, chemotherapy, alkylating agent, genetic predisposition, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

IntroductionMedulloblastoma is the most common malignant brain tumor in children, often requiring intensive multimodal therapy, including chemotherapy with alkylating agents. However, therapy-related complications, such as therapy-related myeloid neoplasms (t-MNs), can arise, particularly in patients with genetic predisposition syndromes. This case report presents three pediatric cases of medulloblastoma with subsequent development of t-MNs, highlighting the potential role of genetic predisposition and the importance of surveillance for hematological abnormalities in long-term survivors.Case presentationWe describe three cases of pediatric medulloblastoma who developed t-MNs after receiving chemotherapy, including alkylating agents. Two of the patients had underlying genetic predisposition syndromes (TP53 pathologic variants). The latency period between initial diagnosis of medulloblastoma and the development of secondary cancer varied among the cases, ranging from 17 to 65 months. The three cases eventually succumbed from secondary malignancy, therapy-related complications and progression of primary disease, respectively.ConclusionsThis report highlights the potential association between genetic predisposition syndromes and the development of therapy-related myeloid neoplasms in pediatric medulloblastoma survivors. It underscores the importance of surveillance for hematological abnormalities among such patients.

Published
2024
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