RPL22 Promotes Anaplastic Thyroid Carcinoma Progression by Regulating the cGAS/STING pathway-associated Autophagy

Jie Liu; Xiong Zheng; Guiren Fang; Yunpeng Bai; Shuping Wu; Wensi Gao

doi:10.32604/biocell.2026.088129

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RPL22 Promotes Anaplastic Thyroid Carcinoma Progression by Regulating the cGAS/STING pathway-associated Autophagy

Jie Liu¹, Xiong Zheng¹, Guiren Fang¹, Yunpeng Bai², Shuping Wu¹, Wensi Gao^3,*
1 Department of Head and Neck Surgery, Clinical Oncology School of Fujian Medical University, Fujian Cancer Hospital, Fuzhou, China
2 Laboratory Animal Center, Clinical Oncology School of Fujian Medical University, Fujian Cancer Hospital, Fuzhou, China
3 Department of Breast Surgery, Clinical Oncology School of Fujian Medical University, Fujian Cancer Hospital, Fuzhou, China
* Corresponding Author: Wensi Gao. Email: email

BIOCELL https://doi.org/10.32604/biocell.2026.088129

Received 29 June 2026; Accepted 11 September 2026; Published online 20 September 2026

Abstract

Background: Anaplastic thyroid carcinoma (ATC) is a highly aggressive malignancy with limited therapeutic options. Although ribosomal protein L22 (RPL22) has been implicated in tumorigenesis, its specific roles and underlying mechanisms in ATC remain unclear. This study aimed to investigate the biological functions and molecular mechanisms of RPL22 in ATC. Methods: RPL22 expression was assessed in ATC clinical specimens and cell lines utilizing immunohistochemistry (IHC), quantitative reverse transcription PCR (qRT-PCR), and Western blotting. shRNA was employed to knock down RPL22 in CAL-62 cells. Cell proliferation, apoptosis, and autophagy were evaluated by CCK-8, TUNEL, and immunofluorescence assays. Western blotting was used to monitor the cyclic GMP-AMP synthase (cGAS)/stimulator of interferon genes (STING) pathway. A cGAS inhibitor (Cladophorol A, Clad A) and an in vivo xenograft model were used to validate the mechanistic roles. Results: RPL22 was overexpressed in both ATC tissues (p < 0.01) and cell lines (p < 0.01). RPL22 knockdown reduced cell viability (p < 0.01), induced apoptosis (p < 0.01) and autophagy (p < 0.01), and activated the cGAS/STING pathway (p < 0.01). Pharmacological inhibition of cGAS/STING reversed these RPL22 knockdown-induced effects (p < 0.01). In vivo, RPL22 silencing suppressed tumor growth, an effect largely abolished by Clad A treatment (p < 0.01). Conclusion: RPL22 promotes ATC progression by modulating proliferation, apoptosis, and autophagy via the cGAS/STING signaling axis. These findings identify RPL22 as a potential therapeutic target in ATC, offering a novel avenue for future treatment strategies.

Keywords

Anaplastic thyroid carcinoma; ribosomal protein L22; cyclic GMP-AMP synthase (cGAS)/stimulator of interferon genes (STING); autophagy; tumor progression

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RPL22 Promotes Anaplastic Thyroid Carcinoma Progression by Regulating the cGAS/STING pathway-associated Autophagy

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