ArticleInternational journal of molecular sciences2025
Circ_RUSC2 Sequesters miR-661 and Elevates TUSC2 Expression to Suppress Colorectal Cancer Progression.
Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- m6A methylation of circKPNA2 promotes colorectal carcinogenesis by activating the RIN1-Ras pathway.Epigenetics · 2026Article
- Review
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDespite advancements in diagnostic efficiency, colorectal cancer (CRC) remains a leading cause of cancer-related mortality, with increasing incidence rates. Circular RNA (circRNA) is a closed-loop, generally stable noncoding RNA that functions as a sponge for microRNAs in CRC. The purpose of this study was to investigate the function and underlying mechanism of circ_RUSC2, a new circRNA, in CRC. The expression levels of circ_RUSC2, miR-661, and TUSC2 were assessed using qRT-PCR, Western blot, and immunohistochemistry. Functional assays, including CCK-8, Transwell, and scratch wound healing, were performed to evaluate cell proliferation, migration, and invasion. RNA pull-down and actinomycin D assays were used to study RNA interactions and stability. In both CRC cells and tissues, miR-661 was markedly elevated, while circ_RUSC2 expression was considerably reduced. Poor differentiation, distant metastases, lymph node metastases, and an advanced stage were all strongly correlated with either miR-661 overexpression or circ_RUSC2 downregulation. circ_RUSC2 was more stable compared to its linear RUSC2 mRNA. CRC cell invasion, migration, and proliferation were suppressed by circ_RUSC2 ectopic expression; this inhibitory effect was restored by a miR-661 mimic. Circ_RUSC2 served as miR-661's sponge. TUSC2 counteracted the effects of miR-661, which stimulated CRC cell proliferation, migration, and invasion. At the post-transcriptional level, miR-661 controlled the expression of TUSC2 in CRC cells. In comparison to the negative control, circ_RUSC2 expression was markedly reduced, and its half-life was shortened by methyltransferase-like 3 (METTL3) knockdown. Circ_RUSC2 is a stable cytoplasmic circRNA. Circ_RUSC2 inhibits CRC cell malignant phenotypes via the miR-661/TUSC2 axis. The onset and progression of CRC are linked to the downregulation of Circ_RUSC2. circ_RUSC2 might become more stable through N6-methyladenosine (m6A) methylation regulated by METTL3. According to our research, circ_RUSC2 might be a new biomarker and treatment target for CRC.
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