دورية أكاديمية

The cross-talk between estrogen receptor and peroxisome proliferator-activated receptor gamma in thyroid cancer.

التفاصيل البيبلوغرافية
العنوان: The cross-talk between estrogen receptor and peroxisome proliferator-activated receptor gamma in thyroid cancer.
المؤلفون: Chu R; Department of Otorhinolaryngology, Head and Neck Surgery, The Chinese University of Hong Kong, Hong Kong, China., van Hasselt A, Vlantis AC, Ng EK, Liu SY, Fan MD, Ng SK, Chan AB, Liu Z, Li XY, Chen GG
المصدر: Cancer [Cancer] 2014 Jan 01; Vol. 120 (1), pp. 142-53. Date of Electronic Publication: 2013 Oct 02.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Wiley Country of Publication: United States NLM ID: 0374236 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1097-0142 (Electronic) Linking ISSN: 0008543X NLM ISO Abbreviation: Cancer Subsets: MEDLINE
أسماء مطبوعة: Publication: <2005- >: Hoboken, NJ : Wiley
Original Publication: New York [etc.] Published for the American Cancer Society by J. Wiley [etc.]
مواضيع طبية MeSH: Estrogen Receptor alpha/*metabolism , Estrogen Receptor beta/*metabolism , PPAR gamma/*metabolism , Thyroid Neoplasms/*metabolism, Apoptosis/drug effects ; Apoptosis/physiology ; Cell Growth Processes/physiology ; Cell Line, Tumor ; Cell Movement/drug effects ; Cell Movement/physiology ; Estrogen Receptor alpha/biosynthesis ; Estrogen Receptor alpha/deficiency ; Estrogen Receptor beta/biosynthesis ; Estrogen Receptor beta/deficiency ; Gene Knockdown Techniques ; Humans ; PPAR gamma/biosynthesis ; Receptor Cross-Talk ; Rosiglitazone ; Signal Transduction ; Thiazolidinediones/pharmacology ; Thyroid Neoplasms/pathology ; Transfection
مستخلص: Background: Estrogen receptor (ER) and peroxisome proliferator-activated receptor gamma (PPARγ) are associated with thyroid tumorigenesis and treatment. However, the interaction between them has not been studied.
Methods: The impact of ER over-expression or down-expression by DNA/small interfering RNA (siRNA) transfection, ERα agonists, and the ERβ agonist diarylpropiolnitrile (DPN) on PPARγ expression/activity was examined in papillary thyroid carcinoma (PTC) and anaplastic thyroid carcinoma (ATC) cells. The effects of PPARγ modulation by rosiglitazone (RTZ), a PPARγ ligand, and of PPARγ siRNA on ER expression were determined. Cellular functions reflected by cell proliferation and migration were assayed. Apoptosis was analyzed by terminal deoxynucleotidyl transferase dUTP nick-end labeling, and apoptotic-related proteins were evaluated by Western blot analysis.
Results: PPARγ protein and activity were reduced by the over-expression of either ERα or ERβ, whereas repression of ERα or ERβ increased PPARγ expression. The administration of RTZ counteracted the effects of ER and also reduced their expression, particularly in PTC cells. Moreover, knockdown of PPARγ increased ER expression and activity. Functionally, ERα activation offset the inhibitory effect of PPARγ on cellular functions, but ERβ activation aggregated it and induced apoptosis, particularly in PTC cells. Finally, the interaction between ERβ and PPARγ enhanced the expression of proapoptotic molecules, such as caspase-3 and apoptosis-inducing factor.
Conclusions: This study provides evidence supporting a cross-talk between ER and PPARγ. The reciprocal interaction between PPARγ and ERβ significantly inhibits the proliferation and migration of thyroid cancer cells, providing a new therapeutic strategy against thyroid cancer.
(© 2013 American Cancer Society.)
فهرسة مساهمة: Keywords: apoptosis; estrogen receptors; peroxisome proliferator-activated receptor gamma; rosiglitazone; thyroid cancer
المشرفين على المادة: 0 (ESR1 protein, human)
0 (Estrogen Receptor alpha)
0 (Estrogen Receptor beta)
0 (PPAR gamma)
0 (Thiazolidinediones)
05V02F2KDG (Rosiglitazone)
تواريخ الأحداث: Date Created: 20131012 Date Completed: 20140513 Latest Revision: 20210816
رمز التحديث: 20240513
DOI: 10.1002/cncr.28383
PMID: 24114184
قاعدة البيانات: MEDLINE
الوصف
تدمد:1097-0142
DOI:10.1002/cncr.28383