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已发表论文
长链非编码 RNA CKMT2-AS1 表达下调预示乳腺癌预后不良并促进其进展
Authors Xue D, Hou R, Xu H, Li X
Received 18 June 2025
Accepted for publication 11 November 2025
Published 26 December 2025 Volume 2025:17 Pages 1397—1411
DOI https://doi.org/10.2147/BCTT.S545732
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Professor Pranela Rameshwar
Dengfeng Xue,1,* Ruihong Hou,2,* Huijuan Xu,1 Xinzheng Li1
1Department of Breast Surgery, The Second Hospital of Shanxi Medical University, Taiyuan, Shanxi, People’s Republic of China; 2Department of Rheumatology, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Third Hospital of Shanxi Medical University, Tongji Shanxi Hospital, Taiyuan, Shanxi, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Xinzheng Li, Department of Breast Surgery, The Second Hospital of Shanxi Medical University, 382 Wuyi Road, Taiyuan, Shanxi, 030001, People’s Republic of China, Email Lixztaiyuan@163.com
Purpose: This research aimed to ascertain the clinical implications of lncRNA CKMT2-AS1 and its underlying molecular mechanism in patients with breast cancer.
Patients and Methods: CKMT2-AS1 expression were assessed in breast cancer. The prognostic implication of CKMT2-AS1 was evaluated using Cox regression analysis. Functional assays were conducted to explore the effects of CKMT2-AS1 on the cellular activities associated with breast cancer. Mechanistic investigations included dual-luciferase reporter assays, bioinformatics, and Western blot analyses to elucidate the molecular pathways involving CKMT2-AS1.
Results: The analysis revealed that CKMT2-AS1 was significantly reduced in breast cancer tissue specimens and cell lines (P< 0.05). Its expression was correlated with advanced stages of tumors (P=0.031) and the presence of lymph node metastasis (P=0.044). The upregulation of CKMT2-AS1 led to an obvious decline in cell proliferation, migration, and invasion, while also enhancing apoptosis in breast cancer cells (P< 0.05). Furthermore, mechanistic studies indicated that CKMT2-AS1 directly interacts with miR-106b-5p, a microRNA that is elevated in breast cancer, thereby influencing the expression of its target gene MECP2, which is recognized as a tumor suppressor.
Conclusion: CKMT2-AS1 exerts its tumor-suppressing function in breast cancer via sequestering miR-106b-5p and modulating MECP2 expression. Its decreased levels are linked to the unfavorable prognosis, positioning CKMT2-AS1 as a prospective indicator for prognosticating breast cancer.
Keywords: CKMT2-AS1, breast cancer, cell activity, prognosis, miR-106b-5p, MECP2
1Department of Breast Surgery, The Second Hospital of Shanxi Medical University, Taiyuan, Shanxi, People’s Republic of China; 2Department of Rheumatology, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Third Hospital of Shanxi Medical University, Tongji Shanxi Hospital, Taiyuan, Shanxi, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Xinzheng Li, Department of Breast Surgery, The Second Hospital of Shanxi Medical University, 382 Wuyi Road, Taiyuan, Shanxi, 030001, People’s Republic of China, Email Lixztaiyuan@163.com
Purpose: This research aimed to ascertain the clinical implications of lncRNA CKMT2-AS1 and its underlying molecular mechanism in patients with breast cancer.
Patients and Methods: CKMT2-AS1 expression were assessed in breast cancer. The prognostic implication of CKMT2-AS1 was evaluated using Cox regression analysis. Functional assays were conducted to explore the effects of CKMT2-AS1 on the cellular activities associated with breast cancer. Mechanistic investigations included dual-luciferase reporter assays, bioinformatics, and Western blot analyses to elucidate the molecular pathways involving CKMT2-AS1.
Results: The analysis revealed that CKMT2-AS1 was significantly reduced in breast cancer tissue specimens and cell lines (P< 0.05). Its expression was correlated with advanced stages of tumors (P=0.031) and the presence of lymph node metastasis (P=0.044). The upregulation of CKMT2-AS1 led to an obvious decline in cell proliferation, migration, and invasion, while also enhancing apoptosis in breast cancer cells (P< 0.05). Furthermore, mechanistic studies indicated that CKMT2-AS1 directly interacts with miR-106b-5p, a microRNA that is elevated in breast cancer, thereby influencing the expression of its target gene MECP2, which is recognized as a tumor suppressor.
Conclusion: CKMT2-AS1 exerts its tumor-suppressing function in breast cancer via sequestering miR-106b-5p and modulating MECP2 expression. Its decreased levels are linked to the unfavorable prognosis, positioning CKMT2-AS1 as a prospective indicator for prognosticating breast cancer.
Keywords: CKMT2-AS1, breast cancer, cell activity, prognosis, miR-106b-5p, MECP2