Abstract：Objective: To investigate the expression profile of long non-coding RNA (lncRNA) LINC00511 in cervical cancer induced by high-risk human papillomavirus (HPV) and deeply analyze its molecular mechanism of promoting cervical cancer progression by regulating Phosphoglycerate Kinase 1 (PGK1), as well as evaluate the feasibility of LINC00511 as a potential therapeutic target. Methods: A mouse model of cervical cancer infected with high-risk HPV16 was established, and the experimental animals were divided into a control group and a LINC00511 knockdown group (si-LINC00511 group). qRT-PCR was used to detect the mRNA expression levels of LINC00511 and PGK1 in mouse tumor tissues, and Western blot was performed to detect the protein expression and phosphorylation level of PGK1. Immunohistochemical analysis was used to examine the expression of PGK1 and the proliferation marker Ki-67 in tumor tissues. Tumor volume and weight were measured, and tumor cell apoptosis was evaluated. The target regulatory relationship between LINC00511 and PGK1 was verified. Results: The expression level of LINC00511 in cervical cancer tissues of HPV16-infected mice was significantly higher than that in the normal control group (P<0.001). The mRNA and protein expression levels of PGK1 were significantly upregulated (P<0.01). In the tumor tissues of LINC00511-knockdown mice, the mRNA and protein expression levels of PGK1 were significantly downregulated (P<0.01), and the phosphorylation level of PGK1 was also significantly reduced, indicating that LINC00511 positively regulates PGK1 expression and activity. The tumor volume in the si-LINC00511 group was 562.3±43.5mm3, compared with 825.1±67.2 mm3 in the control group (P<0.001). The tumor weight was 0.48±0.05 g in the si-LINC00511 group and 0.79±0.06 g in the control group (P<0.001). Immunohistochemical analysis showed that the proportion of Ki-67-positive cells in the tumor tissues of LINC00511-knockdown mice was significantly reduced (P<0.01), indicating that tumor cell proliferation was inhibited. TUNEL assay showed a significant increase in the proportion of apoptotic positive cells (P<0.01), suggesting that LINC00511 knockdown promotes tumor cell apoptosis. Dual-luciferase reporter gene assay showed that LINC00511 positively regulates PGK1 expression by binding to the 3'UTR of PGK1 mRNA. Conclusion: LINC00511 is significantly overexpressed in cervical cancer associated with high-risk HPV16 infection and promotes tumor cell proliferation while inhibiting apoptosis by upregulating PGK1 expression. Knockdown of LINC00511 effectively reduces PGK1 expression and slows tumor growth, suggesting that the LINC00511-PGK1 axis plays a crucial role in the development and progression of high-risk HPV-related cervical cancer.
王丽静, 田苗, 曹基婷, 焦雅坤, 赵思, 孙蕾, 曲姣. 高危HPV分型宫颈癌小鼠模型中LINC00511调控PGK1的机制研究[J]. 河北医学, 2025, 31(6): 1003-1010.
WANG Lijing, TIAN Miao, CAO Jiting, et al. Mechanistic Study of LINC00511 Regulating PGK1 in a Mouse Model of High-Risk HPV-Positive Cervical Cancer. HeBei Med, 2025, 31(6): 1003-1010.
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2025, Vol. 31 
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