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Lnc-GATS-3:3/MCM7 promotes the proliferation and invasion of cervical squamous cell carcinoma cells by regulating the CDK/Rb/E2F signaling pathway

ABSTRACT: This study investigated the role and mechanism of lnc-GATS-3:3/Mini-chromosome maintenance protein 7 (MCM7) in the proliferation, invasion, migration, and apoptosis of SiHa cervical cancer cells. Whole transcriptome sequencing was conducted on matched pairs of cervical cancer and normal tissue samples, followed by GO and KEGG enrichment analysis. The cis method was utilized to identify lncRNAs and mRNAs associated with the cell cycle. The expression levels of lnc-GATS-3:3 and MCM7 in cervical cancer and normal tissues were measured using qRT-PCR. Subsequently, the CCK-8, TUNEL, Transwell, Western Blot, and flow cytometry experiments were employed to assess the effects of lnc-GATS-3:3 silencing on cervical cancer cell proliferation, apoptosis, migration, and invasion. The impact of lnc-GATS-3:3 downregulation on MCM7 and the CDK/Rb/E2F signaling pathway was confirmed using qRT-PCR and WB analysis. Lastly, tumorigenesis experiments were performed to validate the altered tumor proliferation capacity following lnc-GATS-3:3 silencing. The expression of lnc-GATS-3:3 and MCM7 was significantly elevated in cervical cancer tissues (p < 0.05). Silencing of lnc-GATS-3:3 inhibited the proliferation, migration, and invasion of cervical cancer cells (p < 0.05), promoted cell apoptosis (p < 0.05), and suppressed the expression of MCM7, CDK-4, CDK-6, Rb, and Cyclin D1. Furthermore, silencing lnc-GATS-3:3 inhibited tumor growth in nude mice. In summary, our findings establish that the Lnc-GATS-3:3/MCM7 axis promotes the proliferation, invasion, and migration of cervical cancer cells while inhibiting apoptosis by modulating the CDK/Rb/E2F signaling pathway, thereby identifying it as a key player in cervical cancer progression.

ORGANISM(S): Homo sapiens

PROVIDER: GSE318000 | GEO | 2026/02/25

REPOSITORIES: GEO

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Lnc-GATS-3:3/MCM7 promotes the proliferation and invasion of cervical squamous cell carcinoma cells by regulating the CDK/Rb/E2F signaling pathway

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