1. Academic Validation
  2. Celastrol promotes apoptotic cell death in thyroid cancer cells through a caspases-dependent pathway

Celastrol promotes apoptotic cell death in thyroid cancer cells through a caspases-dependent pathway

  • Thyroid Res. 2025 Feb 26;18(1):9. doi: 10.1186/s13044-024-00222-7.
Ruoyi Yang # 1 2 Jie Yao # 3 Hong Ma 1 Chunyan Shui 2 Teng Li 1 Sicheng Zhang 4 Chao Li 5 6
Affiliations

Affiliations

  • 1 Department of Oral and Maxillofacial Surgery, School of Stomatology, Guizhou Medical University, Guiyang, 550004, China.
  • 2 Department of Head and Neck Surgery, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Hospital & Institute, Sichuan Cancer Center, University of Electronic Science and Technology of China, Chengdu, 610041, China.
  • 3 Department of Centre for Translational Research in Cancer, Radiation Oncology Key Laboratory of Sichuan Province, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Center, University of Electronic Science and Technology of China, Chengdu, 610041, China.
  • 4 Department of Head and Neck Surgery, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Hospital & Institute, Sichuan Cancer Center, University of Electronic Science and Technology of China, Chengdu, 610041, China. zhangsicheng@scszlyy.org.cn.
  • 5 Department of Oral and Maxillofacial Surgery, School of Stomatology, Guizhou Medical University, Guiyang, 550004, China. lichao@scszlyy.org.cn.
  • 6 Department of Head and Neck Surgery, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Hospital & Institute, Sichuan Cancer Center, University of Electronic Science and Technology of China, Chengdu, 610041, China. lichao@scszlyy.org.cn.
  • # Contributed equally.
Abstract

Background: Celastrol, a naturally occurring bioactive compound, has demonstrated potential in treating inflammation, obesity, and tumors, particularly in colorectal, gastric, and breast cancers. However, its therapeutic effects on thyroid Cancer (TC), which have poor clinical outcomes, remain unclear. This study aimed to investigate Celastrol's potential in treating thyroid Cancer using cell lines.

Methods: The viability and proliferation of thyroid Cancer cells treated with or without Celastrol were analyzed by CCK-8 and colony formation assay. The state of thyroid Cancer cells treated with or without Celastrol were observed by microscopy. Further evidence from flow cytometry and TUNEL staining demonstrated the induction of apoptotic processes in thyroid Cancer cells. The expression of PARP1, Caspase-3, Bax, BCL2 in thyroid Cancer cells after indicated treatment was analyzed by Western blot and Caspase-3 expression in thyroid Cancer cells after 12 and 24 h of Celastrol treatment was detected by immunofuorescence assay. Anaplastic thyroid Cancer growth-limiting of Celastrol was evaluated in nude mice.

Results: Celastrol induction promoted apoptotic in TC cells, increased the expression of PARP1, Bax and Caspase-3 and reduces expression of BCL2 by Western Blot. The expression of Caspase-3 was increased by immunofluorescence, which indicating that Celastrol may serve as an Adjuvant therapeutic agent for thyroid Cancer treatment by inducing Apoptosis through the Caspase-3 pathway. Celastrol treatment of mice implanted with anaplastic thyroid Cancer cells also inhibited tumor growth, associated with reduced Ki-67 and increased Caspase-3.

Conclusions: Celastrol promotes apoptotic cell death in thyroid carcinoma cells by the Caspase-3 pathway.

Keywords

Anaplastic thyroid cancer; Apoptotic; Caspase-3; Celastrol; Medullary thyroid carcinoma; Papillary thyroid carcinoma.

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