دورية أكاديمية

Troglitazone Stimulates Cancer Cell Uptake of 18F-FDG by Suppressing Mitochondrial Respiration and Augments Sensitivity to Glucose Restriction.

التفاصيل البيبلوغرافية
العنوان: Troglitazone Stimulates Cancer Cell Uptake of 18F-FDG by Suppressing Mitochondrial Respiration and Augments Sensitivity to Glucose Restriction.
المؤلفون: Moon SH; Department of Nuclear Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea; and., Lee SJ; Department of Nuclear Medicine, Ajou University School of Medicine, Suwon, Korea., Jung KH; Department of Nuclear Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea; and., Quach CH; Department of Nuclear Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea; and., Park JW; Department of Nuclear Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea; and., Lee JH; Department of Nuclear Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea; and., Cho YS; Department of Nuclear Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea; and., Lee KH; Department of Nuclear Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea; and khnm.lee@samsung.com.
المصدر: Journal of nuclear medicine : official publication, Society of Nuclear Medicine [J Nucl Med] 2016 Jan; Vol. 57 (1), pp. 129-35. Date of Electronic Publication: 2015 Oct 08.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Society of Nuclear Medicine Country of Publication: United States NLM ID: 0217410 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1535-5667 (Electronic) Linking ISSN: 01615505 NLM ISO Abbreviation: J Nucl Med Subsets: MEDLINE
أسماء مطبوعة: Publication: Reston, VA : Society of Nuclear Medicine
Original Publication: [Chicago, Ill.] : S.N. Turiel & Assoc.
مواضيع طبية MeSH: Antineoplastic Agents/*pharmacology , Chromans/*pharmacology , Fluorodeoxyglucose F18/*metabolism , Glucose/*metabolism , Mitochondria/*drug effects , Mitochondria/*metabolism , Thiazolidinediones/*pharmacology, Biological Transport/drug effects ; Cell Respiration/drug effects ; Dose-Response Relationship, Drug ; Glycolysis/drug effects ; HCT116 Cells ; Humans ; MAP Kinase Signaling System/drug effects ; Matrix Metalloproteinases/metabolism ; Oxygen/metabolism ; PPAR gamma/metabolism ; Reactive Oxygen Species/metabolism ; Troglitazone
مستخلص: Unlabelled: We evaluated how troglitazone influences cancer cell glucose metabolism and uptake of (18)F-FDG, and we investigated its molecular mechanism and relation to the drug's anticancer effect.
Methods: Human T47D breast and HCT116 colon cancer cells that had been treated with troglitazone were measured for (18)F-FDG uptake, lactate release, oxygen consumption rate, mitochondrial membrane potential, and intracellular reactive oxygen species. Viable cell content was measured by sulforhodamine-B assays.
Results: Treatment with 20 μM troglitazone for 1 h acutely increased (18)F-FDG uptake in multiple breast cancer cell lines, whereas HCT116 cells showed a delayed reaction. In T47D cells, the response occurred in a dose-dependent (threefold increase by 40 μΜ) manner independent of peroxisome proliferator-activated receptor-γ and was accompanied by a twofold increase of lactate production, consistent with enhanced glycolytic flux. Troglitazone-treated cells showed severe reductions of the oxygen consumption rate, indicating suppression of mitochondrial respiration, which was accompanied by significantly decreased mitochondrial membrane potential and increased concentration of reactive oxygen species. Troglitazone dose-dependently reduced T47D and HCT116 cell content, which was significantly potentiated by restriction of glucose availability. In T47D cells, cell reduction closely correlated with the magnitude of increase in relative (18)F-FDG uptake (r = 0.821, P = 0.001).
Conclusion: Troglitazone stimulates cancer cell uptake of (18)F-FDG through a shift of metabolism toward glycolytic flux, likely as an adaptive response to impaired mitochondrial oxidative respiration.
(© 2016 by the Society of Nuclear Medicine and Molecular Imaging, Inc.)
فهرسة مساهمة: Keywords: 18F-FDG; cancer; glycolysis; mitochondria; troglitazone
المشرفين على المادة: 0 (Antineoplastic Agents)
0 (Chromans)
0 (PPAR gamma)
0 (Reactive Oxygen Species)
0 (Thiazolidinediones)
0Z5B2CJX4D (Fluorodeoxyglucose F18)
EC 3.4.24.- (Matrix Metalloproteinases)
I66ZZ0ZN0E (Troglitazone)
IY9XDZ35W2 (Glucose)
S88TT14065 (Oxygen)
تواريخ الأحداث: Date Created: 20151010 Date Completed: 20160514 Latest Revision: 20181202
رمز التحديث: 20240628
DOI: 10.2967/jnumed.115.162016
PMID: 26449833
قاعدة البيانات: MEDLINE