ArticleDiscover oncology2024
POLQ knockdown inhibits proliferation, migration, and invasion by inducing cell cycle arrest in colorectal cancer.
Article in Discover oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
3 citing papers in PubMed.
- DNA polymerase theta (Polθ): a novel candidate for targeted cancer therapy.Cancer biology & therapy · 2026Review
- POLQ promotes tumor progression and immunosuppression via ATM‑P53 signaling in endometrial cancer.Oncology reports · 2026Article
- DNA Polymerase θ Drives Colorectal Cancer Progression through Wnt/β-Catenin Activation and Shows Potential Association with Immunosuppressive Microenvironment Remodeling.Oncology research · 2026Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
backgroundPolymerase θ (POLQ) is an error-prone translesion synthesis polymerase that participates in the repair of DNA double-strand breaks. Previous studies have reported that the level of POLQ expression is distinctly upregulated in colorectal cancer (CRC), but little attention has been given to its function and regulation of CRC progression. This study aimed to explore the specific function of POLQ in CRC.
methodsQuantitative real-time PCR and western blotting analysis were used to assess the transcription and translation levels of POLQ. Then, POLQ was stably silenced using small interfering RNA in SW480 and HCT116 cells. Afterwards, the function of POLQ in CRC cells was proven via Cell Counting Kit‑8, scratch wound healing, colony formation, and Boyden chamber assays. Furthermore, we investigated the effects of POLQ on the cell cycle signaling pathway that obtained from biological pathway enrichment analysis and further verified by activating the signaling pathway.
resultsThe results showed that POLQ was highly expressed in CRC tissues and cells and was associated with poor clinical outcomes of patients. Knockdown of POLQ significantly reduced the proliferation, migration and invasion of CRC cells. Additionally, POLQ knockdown markedly decreased the expression levels of MMP2 and MMP9, and blocked cell cycle progression by inhibiting the expression of G1/M and S/M phases proteins.
conclusionsPOLQ knockdown restrained the progression of CRC by blocking the cell cycle signaling pathway.
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