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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Huang, Zhi-ming Sviderskaya, Elena V. Patel, Mira P. Cleaver, James E. Xie, Tong Zhong, Lily Scherzer, Rebecca Wei, Maria L. Chinen, Milka Demetriou, Stephanie Oh, Dennis H. Chang, Philip J. Millhauser, Glenn L. Bennett, Dorothy C. |
| Description | Author Affiliation: Huang ZM ( Department of Dermatology, University of California, San Francisco, CA 94115, USA.); |
| Abstract | Protein-trafficking pathways are targeted here in human melanoma cells using methods independent of oncogene mutational status, and the ability to up-regulate and down-regulate tumor treatment sensitivity is demonstrated. Sensitivity of melanoma cells to cis-diaminedichloroplatinum II (cDDP, cis-platin), carboplatin, dacarbazine, or temozolomide together with velaparib, an inhibitor of poly (ADP ribose) polymerase 1, is increased by up to 10-fold by targeting genes that regulate both protein trafficking and the formation of melanosomes, intracellular organelles unique to melanocytes and melanoma cells. Melanoma cells depleted of either of the protein-trafficking regulators vacuolar protein sorting 33A protein (VPS33A) or cappuccino protein (CNO) have increased nuclear localization of cDDP, increased nuclear DNA damage by platination, and increased apoptosis, resulting in increased treatment sensitivity. Depleted cells also exhibit a decreased proportion of intracellular, mature melanosomes compared with undepleted cells. Modulation of protein trafficking via cell-surface signaling by binding the melanocortin 1 receptor with the antagonist agouti-signaling protein decreased the proportion of mature melanosomes formed and increased cDDP sensitivity, whereas receptor binding with the agonist melanocyte-stimulating hormone resulted in an increased proportion of mature melanosomes formed and in decreased sensitivity (i.e., increased resistance) to cDDP. Mutation of the protein-trafficking gene Hps6, known to impair the formation of mature melanosomes, also increased cDDP sensitivity. Together, these results indicate that targeting protein-trafficking molecules markedly increases melanoma treatment sensitivity and influences the degree of melanosomes available for sequestration of therapeutic agents. |
| ISSN | 00278424 |
| e-ISSN | 10916490 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Issue Number | 2 |
| Volume Number | 109 |
| Language | English |
| Publisher | National Academy of Sciences |
| Publisher Date | 2012-01-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Antineoplastic Agents Pharmacology Cisplatin Drug Resistance, Neoplasm Drug Effects Intracellular Signaling Peptides And Proteins Genetics Melanoma Drug Therapy Melanosomes Vesicular Transport Proteins Deficiency Amino Acid Sequence Carboplatin Cell Line, Tumor DNA Repair Dacarbazine Analogs & Derivatives Down-Regulation Physiology Immunoblotting Microscopy, Electron Microscopy, Fluorescence Molecular Sequence Data Mutation Protein Transport RNA Interference Receptor, Melanocortin, Type 1 Metabolism Up-Regulation Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S. Multidisciplinary |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
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