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ARTICLE

High Expression of KRT6A in Cervical Cancer and Its Promoting Effects on Cell Proliferation and Invasion

Min Ma1,2,3,#, Zhuxiu Wang4,#, Yan Cao4, Juanying Yang4, Zeliang Zhuang5, Linqian Shi4,*, Qian Gao4,*
1 Department of Obstetrics and Gynecology, Affiliated Hospital of Yangzhou University, Yangzhou University, Yangzhou, 225001, China
2 Department of Clinical Medicine, Yangzhou University Medical College, Yangzhou University, Yangzhou, 225009, China
3 Jiangsu Key Laboratory of Non-Coding RNA Basic and Clinical Transformation, Yangzhou University, Yangzhou, 225009, China
4 Department of Obstetrics and Gynecology, Yixing Hospital of Chinese Traditional Medicine Affiliated to Yangzhou University Medical College, Yangzhou University, Yixing, 214200, China
5 Department of Pathology, Yixing People’s Hospital, Yixing, 214200, China
* Corresponding Author: Linqian Shi. Email: email; Qian Gao. Email: email
# These authors contributed equally to this work

BIOCELL https://doi.org/10.32604/biocell.2025.071255

Received 03 August 2025; Accepted 20 October 2025; Published online 21 November 2025

Abstract

Objectives: Keratin 6A (KRT6A) has been implicated in the progression of multiple malignancies; however, its expression pattern and biological role in cervical cancer (CC) have not been elucidated. This study aims to investigate KRT6A expression in CC tissues and evaluate its effects on cellular proliferation, migration, and invasion, thereby assessing its potential as a biomarker and therapeutic target. Methods: Differentially expressed genes were screened from the Gene Expression Omnibus (GEO) dataset (GSE9750) using the thresholds |log2FC| > 2 and false discovery rate (FDR) < 0.05. Immunohistochemistry was performed to evaluate KRT6A protein expression in tumor tissues. Stable KRT6A knockdown was established in CC cell lines to assess proliferation, colony formation, migration, and invasion in vitro. A nude-mouse xenograft model was used to evaluate tumor growth in vivo. Results: KRT6A expression was significantly increased in CC tissues relative to adjacent non-tumor tissues (p = 0.019). Patients with KRT6A-positive tumors had a significantly lower 3-year progression-free survival (PFS) rate than those with KRT6A-negative tumors (45.16% vs. 78.57%; p = 0.009). KRT6A was identified as an independent prognostic indicator for CC (p = 0.044). In vitro, KRT6A silencing significantly reduced colony formation, proliferation, migration, and invasion in SiHa and HeLa cells in comparison to controls (p < 0.05). In vivo, tumors in the KRT6A knockdown group were significantly smaller, with reduced expression of both KRT6A and Ki-67 in tumor tissues (p < 0.05). Conclusion: KRT6A is overexpressed in CC and associates with adverse clinicopathological features and poor PFS. Knockdown of KRT6A suppresses cell proliferation, migration, and invasion, indicating that KRT6A may represent a promising prognostic biomarker and potential target for treating CC.

Keywords

Cervical cancer; KRT6A; cell proliferation assay; prognostic biomarker

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