Curcumin enhances the membrane trafficking of the sodium iodide symporter and augments radioiodine uptake in dedifferentiated thyroid cancer cells via suppression of the PI3K-AKT signaling pathway-Reference-Cited by-同舟云学术

Curcumin enhances the membrane trafficking of the sodium iodide symporter and augments radioiodine uptake in dedifferentiated thyroid cancer cells via suppression of the PI3K-AKT signaling pathway

Published:2021 Issue:18 Volume:12 Page:8260-8273
ISSN:2042-6496
Container-title:Food & Function
language:en
Short-container-title:Food Funct.

Author:

Zhang Li¹²³^ORCID,Xu Shichen¹,Cheng Xian¹,Wu Jing¹,Wang Xiaowen⁴,Wu Liying⁴,Yu Huixin¹,Bao Jiandong¹

Affiliation:

1. NHC Key Laboratory of Nuclear Medicine, Jiangsu Key Laboratory of Molecular Nuclear Medicine, Jiangsu Institute of Nuclear Medicine, Wuxi, Jiangsu, 214063, China

2. Department of Radiopharmaceuticals, School of Pharmacy, Nanjing Medical University, Nanjing 211166, China

3. School of Life Science and Technology, Southeast University, Nanjing 210096, China

4. School of Food Science and Technology, Jiangnan University, Wuxi, Jiangsu, China

Abstract

Curcumin restores the expression of thyroid functional genes, resulting in a significant improvement of radioiodine uptake in dedifferentiated thyroid cancer cells in vitro.

Funder

National Natural Science Foundation of China

Publisher

Royal Society of Chemistry (RSC)

Subject

General Medicine,Food Science

Link

http://pubs.rsc.org/en/content/articlepdf/2021/FO/D1FO01073E

Reference73 articles.

1. Turmeric and Its Major Compound Curcumin on Health: Bioactive Effects and Safety Profiles for Food, Pharmaceutical, Biotechnological and Medicinal Applications

2. How does curcumin work with poor bioavailability? Clues from experimental and theoretical studies

3. Curcumin induces cell death of human papillary thyroid carcinoma BCPAP cells through endoplasmic reticulum stress

4. Curcumin induces endoplasmic reticulum stress-associated apoptosis in human papillary thyroid carcinoma BCPAP cells via disruption of intracellular calcium homeostasis

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