ArticleHuman cell2022
Circular RNA circ-PLCD1 functions as a tumor suppressor in non-small cell lung cancer by inactivation of PI3K/AKT signaling pathway.
Article in Human cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
The trial behind it
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
8 citing papers in PubMed, 14 citations in OpenAlex.
- Metabolic reprogramming and lung cancer focused on roles, mechanism, and clinical prospects of circRNAs: a narrative review.Frontiers in oncology · 2026Review
- Review
- Circular RNA ATP9A Stimulates Non-small Cell Lung Cancer Progression via MicroRNA-582-3p/Ribosomal Protein Large P0 Axis and Activating Phosphatidylinositol 3-Kinase/Protein Kinase B Signaling Pathway.Applied biochemistry and biotechnology · 2025Article
- Non-coding RNAs and regulation of the PI3K signaling pathway in lung cancer: Recent insights and potential clinical applications.Non-coding RNA research · 2025Review
- Review
- Circ_0087378 intensifies the malignant behavior of non-small cell lung cancer cellsTranslational lung cancer research · 2023Article
- Review
- Circular RNAs Involved in the Regulation of the Age-Related Pathways.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Circular RNAs (circRNAs) are emerging as crucial regulators in tumorigenesis and aggressive progression. However, their biological roles in non-small cell lung cancer (NSCLC) remain largely unknown. Here, by performing circRNA high throughput sequencing in 4 paired NSCLC and normal tissues, we found a NSCLC-associated circRNA, circ-PLCD1, which was evidently downregulated in NSCLC tissues and cell lines. Circ-PLCD1 was transcriptionally activated by tumor-inhibiting protein p53, and exogenous expression of circ-PLCD1 inhibited NSCLC cell proliferation, invasion and induced apoptosis. Mechanistically, circ-PLCD1 acted as a competitive endogenous RNA (ceRNA) to sponge miR-375 and miR-1179 and elevate PTEN, a well-known inhibitor of oncogenic PI3K/AKT signaling, thereby repressing NSCLC tumorigenesis. Importantly, we also identified this ceRNA regulatory axis of circ-PLCD1/miR-375/miR-1179/PTEN in vivo by establishing a xenograft tumor model. Clinically, NSCLC patients with low circ-PLCD1 expression had larger tumor size, later clinical stage and shorter survival time than those with high circ-PLCD1 expression. Altogether, our findings reveal the important tumor suppressive role of circ-PLCD1 in NSCLC, reactivation of this circRNA may be considered as a novel therapeutic avenue for patient with NSCLC.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.