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环状 RNA Circ_0067934 通过 miR-545-3p/SLC7A11 信号通路减轻甲状腺癌细胞的铁死亡。

Circular RNA Circ_0067934 Attenuates Ferroptosis of Thyroid Cancer Cells by miR-545-3p/SLC7A11 Signaling.

机构信息

Department of Endocrinology, The First Affiliated Hospital of Harbin Medical University, Harbin, China.

Department of Endocrinology, Qiqihar First Hospital, Qiqihar, China.

出版信息

Front Endocrinol (Lausanne). 2021 Jul 5;12:670031. doi: 10.3389/fendo.2021.670031. eCollection 2021.

DOI:10.3389/fendo.2021.670031
PMID:34290668
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8287831/
Abstract

Ferroptosis is an emerging programmed cell death distinguished from apoptosis and autophagy and plays essential roles in tumorigenesis. Thyroid cancer is a prevalent endocrine tumor, but the molecular mechanism of ferroptosis during thyroid cancer development remains unclear. Here, we identified the critical function of circular RNA circ_0067934 in repressing ferroptosis of thyroid cancer cells. Our data showed that the ferroptosis activator erastin decreased thyroid cancer cell viabilities, while the circ_0067934 shRNA further attenuated erastin-inhibited cell viabilities. The silencing of circ_0067934 enhanced the levels of ferroptosis-related markers, including Fe, iron, and ROS in the cells. The knockdown of circ_0067934 induced thyroid cancer cell apoptosis and repressed thyroid cancer cell proliferation and . Circ_0067934 upregulated the expression of the ferroptosis-negative regulator SLC7A11 by sponging and inhibiting miR-545-3p in thyroid cancer cells. The overexpression of SLC7A11 or the inhibitor of miR-545-3p reversed circ_0067934 silencing-regulated thyroid cancer cell proliferation. Therefore, we concluded that Circ_0067934 attenuated ferroptosis of thyroid cancer cells by miR-545-3p/SLC7A11 signaling. Circ_0067934 may serve as a potential therapeutic target by regulating ferroptosis for the treatment of thyroid cancer.

摘要

铁死亡是一种区别于细胞凋亡和自噬的新兴程序性细胞死亡，在肿瘤发生中发挥重要作用。甲状腺癌是一种常见的内分泌肿瘤，但铁死亡在甲状腺癌发展过程中的分子机制尚不清楚。在这里，我们鉴定了环状 RNA circ_0067934 在抑制甲状腺癌细胞铁死亡中的关键作用。我们的数据表明，铁死亡激活剂 erastin 降低了甲状腺癌细胞活力，而 circ_0067934 shRNA 进一步减弱了 erastin 抑制的细胞活力。circ_0067934 的沉默增强了细胞中与铁死亡相关的标志物的水平，包括 Fe、铁和 ROS。circ_0067934 的敲低诱导了甲状腺癌细胞凋亡，并抑制了甲状腺癌细胞的增殖和。circ_0067934 通过海绵吸附和抑制甲状腺癌细胞中的 miR-545-3p 上调了铁死亡负调节剂 SLC7A11 的表达。SLC7A11 的过表达或 miR-545-3p 的抑制剂逆转了 circ_0067934 沉默调节的甲状腺癌细胞增殖。因此，我们得出结论，circ_0067934 通过 miR-545-3p/SLC7A11 信号通路减弱了甲状腺癌细胞的铁死亡。circ_0067934 可能通过调节铁死亡作为一种潜在的治疗靶点，用于治疗甲状腺癌。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f0e/8287831/3f102309d9bf/fendo-12-670031-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f0e/8287831/511f66ff040b/fendo-12-670031-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f0e/8287831/e73ab541828f/fendo-12-670031-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f0e/8287831/3da8457b4c8b/fendo-12-670031-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f0e/8287831/34fb8e890ddd/fendo-12-670031-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f0e/8287831/3f102309d9bf/fendo-12-670031-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f0e/8287831/511f66ff040b/fendo-12-670031-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f0e/8287831/cd7708938741/fendo-12-670031-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f0e/8287831/097b833626ff/fendo-12-670031-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f0e/8287831/e730f89a9f41/fendo-12-670031-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f0e/8287831/e73ab541828f/fendo-12-670031-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f0e/8287831/3da8457b4c8b/fendo-12-670031-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f0e/8287831/34fb8e890ddd/fendo-12-670031-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f0e/8287831/3f102309d9bf/fendo-12-670031-g008.jpg

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