Effects of GDF11 on apoptosis of human papillary thyroid cancer K1 cells under high glucose conditions

YOU Yan; TIAN Xiaoyu; ZENG Lang; DANG Ruijie; ZENG Bangbin; ZHU Biao; LI Yunxia

PDF(822 KB)

Medical Journal of the Chinese People Armed Police Forces ›› 2021, Vol. 32 ›› Issue (10) : 852-855.

ORIGINAL ARTICLES

Effects of GDF11 on apoptosis of human papillary thyroid cancer K1 cells under high glucose conditions

YOU Yan^1,2, TIAN Xiaoyu^2,3, ZENG Lang¹, DANG Ruijie^2,3, ZENG Bangbin¹, ZHU Biao³, LI Yunxia³

Author information +

History +

Abstract

Objective To investigate the effects of GDF11 on apoptosis of human papillary thyroid cancer K1 cells under high glucose conditions. Methods Human papillary thyroid cancer K1 cells from the vehicle, HG (high glucose), and GDF11 (HG plus GDF11 administration) groups were cultured for 3 days. Flow cytometry was used to evaluate the apoptotic rate, while Western blot was used to investigate protein levels of Bax and Bcl-2. The expression levels of Nrf2 were determined via qRT-PCR while ROS levels in K1 cells were detected by ROS kit. Results Compared with the vehicle group, the apoptotic rate of HG was decreased, Bcl-2/Bax was increased, expression levels of Nrf2 were up-regulated, and ROS levels were significantly decreased. GDF11 administration increased K1 apoptosis, reduced Bcl-2/Bax protein levels, down-regulated Nrf2 expression levels, and increased ROS levels. Conclusions GDF11 may promote K1 cell apoptosis under high glucose conditions by activating intracellular oxidative stress.

Key words

DGF11 / diabetes / human papillary thyroid cancer K1 cells / cell apoptosis

Cite this article

EndNote

Ris (Procite)

Bibtex

Download Citations

YOU Yan, TIAN Xiaoyu, ZENG Lang, DANG Ruijie, ZENG Bangbin, ZHU Biao, LI Yunxia. Effects of GDF11 on apoptosis of human papillary thyroid cancer K1 cells under high glucose conditions[J]. Medical Journal of the Chinese People Armed Police Forces. 2021, 32(10): 852-855

References

[1] Li H, Qian J. Association of diabetes mellitus with thyroid cancer risk: a meta-analysis of cohort studies[J]. Medicine (Baltimore), 2017,96(47):e8230.
[2] Paulus Y M, Riedel E R, Sabra M M, et al. Prevalence of diabetes mellitus in patients with newly evaluated papillary thyroid cancer[J]. Thyroid Res, 2014,7:7.
[3] 倪静,乐岭,向光大,等. 甲状腺恶性结节与代谢综合征组分及尿碘的相关性研究[J]. 华南国防医学杂志, 2016,30(11):714-717.
[4] 倪静,乐岭,王永,等. 高糖对甲状腺乳头状癌K1细胞增殖及Nrf2表达和转位影响[J]. 中华肿瘤防治杂志, 2017,24(19):1335-1341.
[5] 叶丽姿,乐岭,李静,等. 高糖状态下Nrf2在人甲状腺乳头状癌K1细胞凋亡中的作用及其机制[J]. 华南国防医学杂志, 2019,33(4):223-227.
[6] Li H, Li Y, Xiang L, et al. GDF11 Attenuates development of type 2 diabetes via improvement of islet β-cell function and survival[J]. Diabetes, 2017,66(7):1914-1927.
[7] Zhang J, Li Y, Li H, et al. GDF11 improves angiogenic function of EPCs in diabetic limb ischemia[J]. Diabetes, 2018,67(10):2084-2095.
[8] Mei W, Xiang G, Li Y, et al. GDF11 Protects against endothelial injury and reduces atherosclerotic lesion formation in apolipoprotein E-null mice[J]. Mol Ther, 2016,24(11):1926-1938.
[9] Song F, Zhang L, Yu H X, et al. The mechanism underlying proliferation-inhibitory and apoptosis-inducing effects of curcumin on papillary thyroid cancer cells[J]. Food Chem, 2012,132(1):43-50.
[10] 翟羽,吴方丽,田萧羽,等. GDF11对糖尿病小鼠骨髓间充质干细胞细胞凋亡的影响及其信号机制[J]. 武警医学, 2021,32(1):19-21.
[11] Brasil F B, de Almeida F, Luckachaki M D, et al. Astaxanthin prevents mitochondrial impairment in the dopaminergic SH-SY5Y cell line exposed to glutamate-mediated excitotoxicity: Role for the Nrf2/HO-1/CO-BR axis[J]. Eur J Pharmacol, 2021:174336.
[12] Loboda A, Damulewicz M, Pyza E, et al. Role of Nrf2/HO-1 system in development, oxidative stress response and diseases: an evolutionarily conserved mechanism[J]. Cell Mol Life Sci, 2016,73(17):3221-3247.
[13] Leinonen H M, Kansanen E, Pölönen P, et al. Role of the Keap1-Nrf2 pathway in cancer[J]. Adv Cancer Res, 2014,122:281-320.
[14] Du Z X, Yan Y, Zhang H Y, et al. Proteasome inhibition induces a p38 MAPK pathway-dependent antiapoptotic program via Nrf2 in thyroid cancer cells[J]. J Clin Endocrinol Metab, 2011,96(5):E763-E771.
[15] Cha H Y, Lee B S, Chang J W, et al. Downregulation of Nrf2 by the combination of trail and valproic acid induces apoptotic cell death of TRAIL-resistant papillary thyroid cancer cells via suppression of Bcl-xL[J]. Cancer Lett, 2016,372(1):65-74.
[16] Ziros P G, Manolakou S D, Habeos I G, et al. Nrf2 is commonly activated in papillary thyroid carcinoma, and it controls antioxidant transcriptional responses and viability of cancer cells[J]. J Clin Endocrinol Metab, 2013,98(8):E1422-E1427.
[17] Kaczanowski S. Apoptosis: its origin, history, maintenance and the medical implications for cancer and aging[J]. Phys Biol, 2016,13(3):31001.
[18] Delbridge A R, Grabow S, Strasser A, et al. Thirty years of BCL-2: translating cell death discoveries into novel cancer therapies[J]. Nat Rev Cancer, 2016,16(2):99-109.
[19] Khalifeh S, Oryan S, Digaleh H, et al. Involvement of Nrf2 in development of anxiety-like behavior by linking Bcl2 to oxidative phosphorylation: estimation in rat hippocampus, amygdala, and prefrontal cortex[J]. J Mol Neurosci, 2015,55(2):492-499.
[20] Chakraborty S, Balan M, Flynn E, et al. Activation of c-Met in cancer cells mediates growth-promoting signals against oxidative stress through Nrf2-HO-1[J]. Oncogenesis, 2019,8(2):7.