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CircIQGAP1-CARM1 axis promotes renal cell carcinoma progression through glycolytic reprogramming
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  • Published: 27 March 2026

CircIQGAP1-CARM1 axis promotes renal cell carcinoma progression through glycolytic reprogramming

  • Ruyue Jia1,2 na1,
  • Benkui Zou1 na1,
  • Yiran Liang3,
  • Qingkun Chen1,2,
  • Tao Chen1,
  • Xiangzhi Li4,
  • Chao Zhang1,
  • Fajun Pei1,
  • Xuehua Zhu1,
  • Jiasheng Bian1 &
  • …
  • Renbo Guo1 

Cell Death & Disease , Article number:  (2026) Cite this article

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We are providing an unedited version of this manuscript to give early access to its findings. Before final publication, the manuscript will undergo further editing. Please note there may be errors present which affect the content, and all legal disclaimers apply.

Subjects

  • Renal cell carcinoma
  • RNA splicing

Abstract

Renal cell carcinoma (RCC) relies heavily on aerobic glycolysis for rapid proliferation and metastasis; however, the role of circular RNAs (circRNAs) in this process remains unclear. This study identified circIQGAP1 as a key regulator; its expression was upregulated under glucose deficiency, with U2AF2 promoting its biosynthesis. Functional assays showed that circIQGAP1 enhances RCC cell proliferation, motility, invasion, and glycolytic flux. Mechanistically, circIQGAP1 binds to CARM1, inhibiting its K48-linked ubiquitination and prolonging its half-life. Elevated CARM1 then catalyses COL5A1 promoter dimethylation, driving COL5A1 transcription. Rescue experiments confirmed that both CARM1 and COL5A1 were essential for circIQGAP1-mediated metabolic reprogramming and malignant phenotypes. Clinically, circIQGAP1 is overexpressed in RCC tissues and is correlated with poor outcomes. These findings revealed that circIQGAP1 promotes glycolysis-dependent RCC progression by stabilizing CARM1 to activate COL5A1, highlighting that this regulatory axis may provide an innovative strategy for RCC treatment.

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Data availability

The data underlying the results presented in this paper are available from the corresponding author upon reasonable request. Full and uncropped blots are provided with this paper (Supplemental Material).

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Acknowledgements

We would like to express our gratitude to all members of our laboratory for their participation in this experiment. This work was supported by the National Natural Science Foundation of China (No. 82203815), the Natural Science Foundation of Shandong Province (No. ZR2020LZL011, ZR2022MH308, ZR2022MH003, and ZR2024QH467), Research Funds of the Shandong Provincial Key Laboratory of Animal Cell and Developmental Biology (No. SDKLACDB-2019010), and Key Scientific and Medical Project of Shandong (No. 2011QZ016 and 2016GSF201042).

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  1. These authors contributed equally: Ruyue Jia, Benkui Zou.

Authors and Affiliations

  1. Department of Urology, Shandong Cancer Hospital and Institute, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, China

    Ruyue Jia, Benkui Zou, Qingkun Chen, Tao Chen, Chao Zhang, Fajun Pei, Xuehua Zhu, Jiasheng Bian & Renbo Guo

  2. Shandong Provincial Key Laboratory of Precision Oncology, Cancer Research Center, Shandong Cancer Hospital and Institute, Jinan, Shandong Province, China

    Ruyue Jia & Qingkun Chen

  3. Department of Breast Surgery, General Surgery, Qilu Hospital of Shandong University, Jinan, China

    Yiran Liang

  4. Shandong Provincial Key Laboratory of Animal Cell and Developmental Biology, School of Life Sciences, Shandong University, Qingdao, China

    Xiangzhi Li

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Contributions

RJ and BZ contributed equally to this work. RG, RJ, BZ, and YL conceived of and designed the experiments. RG, RJ, BZ, YL, QC, TC, CZ, FP, and XZ performed the experiments. RG and BZ collected the clinical samples. RG, BZ, XL, and JB analyzed the data. RJ, BZ, YL, and RG wrote and revised the manuscript. All the authors have read and agreed to the published version of the manuscript.

Corresponding author

Correspondence to Renbo Guo.

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The authors declare no competing interests.

Ethics approval and consent to participate

This study was approved by the Ethics Review Committee of Shandong Cancer Hospital and Institute (Approval no. SDTHEC2023001023). All experimental procedures were conducted in strict accordance with relevant guidelines and regulations, and informed consent was obtained from all patients.

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Jia, R., Zou, B., Liang, Y. et al. CircIQGAP1-CARM1 axis promotes renal cell carcinoma progression through glycolytic reprogramming. Cell Death Dis (2026). https://doi.org/10.1038/s41419-026-08661-w

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  • Received: 15 October 2025

  • Revised: 16 February 2026

  • Accepted: 11 March 2026

  • Published: 27 March 2026

  • DOI: https://doi.org/10.1038/s41419-026-08661-w

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