人乳头瘤病毒E6基因突变对子宫颈瘤脑源性神经营养因子调控和细胞增殖的影响:分子机制的见解

IF 2.8 4区 医学 Q3 BIOTECHNOLOGY & APPLIED MICROBIOLOGY
OncoTargets and therapy Pub Date : 2025-09-22 eCollection Date: 2025-01-01 DOI:10.2147/OTT.S488976
Ling Wei, Qian Yu, Su-Ning Chen
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引用次数: 0

摘要

目的:探讨人乳头瘤病毒E6 (HPV16 E6)基因突变通过调节脑源性神经营养因子(BDNF)对宫颈癌和宫颈上皮内瘤变I级(CIN I)细胞增殖的影响及其机制。方法:采用Real-time PCR检测宫颈癌及CIN组织中HPV16 E6 T350G、BDNF、p53 mRNA水平。构建慢病毒载体(pLV5-HPV16 E6 T350G和pLV5-vector)并转染人宫颈上皮细胞。Real-time PCR验证了HPV16 E6 T350G感染成功,并评估了HPV16 E6 T350G诱导的mRNA变化。Western Blot检测BDNF蛋白水平和PI3K/AKT磷酸化水平。用MTT法评估细胞增殖,这是一种评估体外细胞活力的标准方法。结果:与CIN宫颈组织比较,宫颈癌组织中HPV16 E6 T350G、BDNF mRNA表达阳性,p53 mRNA表达阴性;HPV16 E6 T350G在人宫颈上皮细胞中过表达上调BDNF mRNA和蛋白表达,激活其下游信号通路PI3K/AKT,降低p53蛋白表达;过表达HPV16 E6 T350G可增强人宫颈上皮细胞的增殖能力。结论:HPV16 E6 T350G过表达可促进宫颈癌细胞增殖能力,其机制可能是上调BDNF表达,促进PI3K/AKT信号通路激活,降低p53表达。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Influence of Human Papillomavirus E6 Gene Mutation on Brain-Derived Neurotrophic Factor Regulation and Cell Proliferation in Cervical Neoplasia: Insights Into Molecular Mechanisms.

Objective: To investigate the effects and mechanisms of human papillomavirus E6 (HPV16 E6) gene mutation on cervical cancer and cervical intraepithelial neoplasia grade I (CIN I) cell proliferation by regulating brain-derived neurotrophic factor (BDNF).

Methods: Real-time PCR was employed to measure mRNA levels of HPV16 E6 T350G, BDNF, and p53 in cervical cancer and CIN I tissues. Lentiviral vectors (pLV5-HPV16 E6 T350G and pLV5-vector) were constructed and transfected into human cervical epithelial cells. Real-time PCR validated successful infection and assessed mRNA changes induced by HPV16 E6 T350G. Western Blot was used to detect BDNF protein levels and PI3K/AKT phosphorylation. Cell proliferation was evaluated with the MTT assay, a standard method for assessing cell viability in vitro.

Results: Compared with CIN I cervical tissue, HPV16 E6 T350G and BDNF mRNA expression levels were positive in cervical cancer tissue, while p53 mRNA expression was negative; overexpression of HPV16 E6 T350G in human cervical epithelial cells upregulated BDNF mRNA and protein expression and activated its downstream signaling pathway PI3K/AKT, while reducing p53 protein expression; overexpression of HPV16 E6 T350G enhanced the proliferation ability of human cervical epithelial cells.

Conclusion: Overexpression of HPV16 E6 T350G can promote the proliferation ability of cervical cancer cells, possibly by upregulating BDNF expression to promote activation of the PI3K/AKT signaling pathway and decrease p53 expression.

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来源期刊
OncoTargets and therapy
OncoTargets and therapy BIOTECHNOLOGY & APPLIED MICROBIOLOGY-ONCOLOGY
CiteScore
9.70
自引率
0.00%
发文量
221
审稿时长
1 months
期刊介绍: OncoTargets and Therapy is an international, peer-reviewed journal focusing on molecular aspects of cancer research, that is, the molecular diagnosis of and targeted molecular or precision therapy for all types of cancer. The journal is characterized by the rapid reporting of high-quality original research, basic science, reviews and evaluations, expert opinion and commentary that shed novel insight on a cancer or cancer subtype. Specific topics covered by the journal include: -Novel therapeutic targets and innovative agents -Novel therapeutic regimens for improved benefit and/or decreased side effects -Early stage clinical trials Further considerations when submitting to OncoTargets and Therapy: -Studies containing in vivo animal model data will be considered favorably. -Tissue microarray analyses will not be considered except in cases where they are supported by comprehensive biological studies involving multiple cell lines. -Biomarker association studies will be considered only when validated by comprehensive in vitro data and analysis of human tissue samples. -Studies utilizing publicly available data (e.g. GWAS/TCGA/GEO etc.) should add to the body of knowledge about a specific disease or relevant phenotype and must be validated using the authors’ own data through replication in an independent sample set and functional follow-up. -Bioinformatics studies must be validated using the authors’ own data through replication in an independent sample set and functional follow-up. -Single nucleotide polymorphism (SNP) studies will not be considered.
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