C21orf2 as a potential regulator of JAK2/STAT3 signaling in prostate cancer cell proliferation and apoptosis - an exploratory study

Sep 23, 2026

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Prostate cancer is a major global health concern with rapidly increasing incidence, making identification of key molecular regulators essential for early diagnosis and targeted therapy. This exploratory study investigates how chromosome 21 open reading frame 2 (C21orf2) modulates prostate cancer cell proliferation and apoptosis through the JAK2/STAT3 signaling pathway. Functional assays test proliferation, migration, invasion, and apoptosis, while JAK2/STAT3 protein activity and gene expression are evaluated in vitro and validated in vivo.

LanguageEnglish

CategoryHealthcare

FormatPDF

Pages14

Reading Time35 min

AccessFree to download

Background

Materials and methods

Bioinformatics analysis

Results

Conclusions

Jiang et al. BMC Cancer (2026) 26:305 BMC Cancer [https://doi.org/10.1186/s12885-026-15637-8](https://doi.org/10.1186/s12885-026-15637-8) RESEARCH Open Access C21orf2 as a potential regulator of JAK2/STAT3 signaling in prostate cancer cell proliferation and apoptosis: an exploratory study ShiHao Jiang 1†, Shuai Su 1† and Del in Wang 1* Abstract Background Prostate cancer (PCa) is a major health concern for men worldwide, and its incidence is rising rapidly, so identifying key molecules that regulate the malignant biological behavior of PCa is crucial for early diagnosis and targeted therapy. This study aimed to elucidate the regulatory role of chromosome 21 open reading frame 2 (C21orf2) in the biological functions of prostate cancer cells and further explore the molecular mechanisms by which C21orf2 regulates cell proliferation and apoptosis via the JAK2/STAT3 signaling pathway. Materials and methods In vitro, C21orf2’s effects on cell proliferation, migration, invasion, and apoptosis were tested using CCK-8, scratch assays, Transwell assays, TUNEL staining, and electron microscopy. Western blotting assessed the impact of C21orf2 on JAK2/STAT3 proteins and related markers. Co-immunoprecipitation and immunofluorescence explored interactions with downstream targets. In vivo, a subcutaneous xenograft model in nude mice validated C21orf2’s role in tumor growth and apoptosis. Results C21orf2 was upregulated in prostate cancer tissues and regulated the malignant biological behavior of prostate cancer cells, and C21orf2 showed a negative correlation with KCTD5 . High expression of C21orf2 promoted the activation of the JAK2/STAT3 signaling pathway and upregulated its downstream target genes, including c-MYC, Cyclin A1, Bcl-2, and Cleaved caspase-3, thereby promoting cell proliferation and inhibiting apoptosis. Conclusions Our study indicates that C21orf2 is a potential biomarker for the diagnosis and treatment of prostate cancer and highlights its potential as a therapeutic target through the JAK2/STAT3 signaling pathway in prostate cancer. Keywords Prostate cancer, C21orf2, Proliferation, Apoptosis, JAK2/STAT3 signaling pathway †ShiHao Jiang and Shuai Su contributed equally to this work. *Correspondence: Delin Wang [202084@hospital.cqmu.edu.cn](202084@hospital.cqmu.edu.cn) 1Department of Urology, Molecular Medicine and Oncology Research Center, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China © The Author(s) 2026. Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit [http://creati](http://creati)[vecommons.org/l](vecommons.org/l)icenses/by-nc-nd/4.0/. Jiang et al. BMC Cancer (2026) 26:305 Background Prostate cancer (PCa) is one of the most common malignancies in men worldwide and poses a significant threat to male health [1]. According to the World Health Organization, PCa ranks second in the incidence of newly diagnosed cancers among men globally [2]. In Asia, particularly in China, although the incidence and mortality rates of prostate cancer are lower,

FAQs

What was the main objective of this exploratory study?

To clarify the regulatory role of C21orf2 in prostate cancer cell proliferation and apoptosis and to explore the molecular mechanism involving the JAK2/STAT3 signaling pathway.

How was C21orf2’s effect on prostate cancer cells evaluated?

In vitro assays assessed proliferation, migration, invasion, and apoptosis, including CCK-8, scratch assays, Transwell assays, TUNEL staining, and electron microscopy. Western blotting and interaction studies (co-immunoprecipitation and immunofluorescence) were used to examine JAK2/STAT3-related changes.

What conclusions were drawn about C21orf2 in prostate cancer?

C21orf2 was upregulated in prostate cancer tissues, promoted activation of the JAK2/STAT3 pathway, enhanced proliferation, and inhibited apoptosis, supporting its potential as a biomarker and therapeutic target.

Sep 23, 2026

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