دورية أكاديمية
Upregulation of ZIP14 and Altered Zinc Homeostasis in Muscles in Pancreatic Cancer Cachexia.
| العنوان: | Upregulation of ZIP14 and Altered Zinc Homeostasis in Muscles in Pancreatic Cancer Cachexia. |
|---|---|
| المؤلفون: | Shakri AR; Institute for Cancer Genetics, Columbia University Irving Medical Center, New York, NY 10032, USA., Zhong TJ; Institute for Cancer Genetics, Columbia University Irving Medical Center, New York, NY 10032, USA.; Graduate School of Arts and Sciences, Department of Pathobiology and Mechanisms of Disease, Columbia University Irving Medical Center, New York, NY 10032, USA., Ma W; Institute for Cancer Genetics, Columbia University Irving Medical Center, New York, NY 10032, USA., Coker C; Institute for Cancer Genetics, Columbia University Irving Medical Center, New York, NY 10032, USA., Kim S; Department of Biological Sciences, Columbia University, New York, NY 10027, USA., Calluori S; Barnard College, Columbia University, New York, NY 10027, USA., Scholze H; Barnard College, Columbia University, New York, NY 10027, USA.; Department of Pediatrics, Weill Cornell Medicine, Cornell University, New York, NY 10065, USA., Szabolcs M; Department of Pathology and Cell Biology, Columbia University Irving Medical Center, New York, NY 10032, USA., Caffrey T; Eppley Institute for Research in Cancer and Allied Diseases, Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE 68198, USA., Grandgenett PM; Eppley Institute for Research in Cancer and Allied Diseases, Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE 68198, USA., Hollingsworth MA; Eppley Institute for Research in Cancer and Allied Diseases, Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE 68198, USA., Tanji K; Division of Neuropathology, Department of Pathology and Cell Biology, Columbia University Irving Medical Center, New York, NY 10032, USA., Kluger MD; Department of Surgery, Columbia University Irving Medical Center, New York, NY 10032, USA., Miller G; Department of Surgery, New York University Grossman School of Medicine, New York, NY 10016, USA.; Department of Cell Biology, New York University Grossman School of Medicine, New York, NY 10016, USA., Biswas AK; Institute for Cancer Genetics, Columbia University Irving Medical Center, New York, NY 10032, USA., Acharyya S; Institute for Cancer Genetics, Columbia University Irving Medical Center, New York, NY 10032, USA.; Department of Pathology and Cell Biology, Columbia University Irving Medical Center, New York, NY 10032, USA.; Herbert Irving Comprehensive Cancer Center, Columbia University Irving Medical Center, New York, NY 10032, USA. |
| المصدر: | Cancers [Cancers (Basel)] 2019 Dec 18; Vol. 12 (1). Date of Electronic Publication: 2019 Dec 18. |
| نوع المنشور: | Journal Article |
| اللغة: | English |
| بيانات الدورية: | Publisher: MDPI Country of Publication: Switzerland NLM ID: 101526829 Publication Model: Electronic Cited Medium: Print ISSN: 2072-6694 (Print) Linking ISSN: 20726694 NLM ISO Abbreviation: Cancers (Basel) Subsets: PubMed not MEDLINE |
| أسماء مطبوعة: | Original Publication: Basel, Switzerland : MDPI |
| مستخلص: | Pancreatic ductal adenocarcinoma (PDAC) is a lethal cancer type in which the mortality rate approaches the incidence rate. More than 85% of PDAC patients experience a profound loss of muscle mass and function, known as cachexia. PDAC patients with this condition suffer from decreased tolerance to anti-cancer therapies and often succumb to premature death due to respiratory and cardiac muscle wasting. Yet, there are no approved therapies available to alleviate cachexia. We previously found that upregulation of the metal ion transporter, Zip14 , and altered zinc homeostasis are critical mediators of cachexia in metastatic colon, lung, and breast cancer models. Here, we show that a similar mechanism is likely driving the development of cachexia in PDAC. In two independent experimental metastasis models generated from the murine PDAC cell lines, Pan02 and FC1242, we observed aberrant Zip14 expression and increased zinc ion levels in cachectic muscles. Moreover, in advanced PDAC patients, high levels of ZIP14 in muscles correlated with the presence of cachexia. These studies underscore the importance of altered ZIP14 function in PDAC-associated cachexia development and highlight a potential therapeutic opportunity for improving the quality of life and prolonging survival in PDAC patients. |
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| معلومات مُعتمدة: | NYU 18-S1-00-006678 New York University; P30 CA013696 United States CA NCI NIH HHS; CTSA grant UL1TR001873 Irving Institute; 5P30CA013696-43 Herbert Irving Comprehensive Cancer Center; R01 CA231239 United States CA NCI NIH HHS; NCI R01 CA231239 United States CA NCI NIH HHS; P50 CA127297 United States CA NCI NIH HHS; R50 CA211462 United States CA NCI NIH HHS |
| فهرسة مساهمة: | Keywords: Slc39a14; ZIP14; cachexia; metastasis; muscle atrophy; pancreatic cancer; pancreatic ductal adenocarcinoma; zinc homeostasis; zinc transporter |
| تواريخ الأحداث: | Date Created: 20191222 Latest Revision: 20210226 |
| رمز التحديث: | 20240628 |
| مُعرف محوري في PubMed: | PMC7016633 |
| DOI: | 10.3390/cancers12010003 |
| PMID: | 31861290 |
| قاعدة البيانات: | MEDLINE |
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