ArticleIranian journal of biotechnology2025
CircFNIP1 Regulates Proliferation and Invasion in Lung Cancer Cells and Represents a Potential Therapeutic Target.
Article in Iranian journal of biotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Lung cancer (LC) remains the leading cause of cancer-related mortality. Circular RNAs (circRNAs) are emerging as important regulators in cancer biology. Objectives: This study investigated the functional role and therapeutic potential of circFNIP1 (hsa_circ_0073858) in LC. Materials and Methods: The expression of circFNIP1 in multiple lung cancer cell lines was quantified using quantitative real-time PCR, and its subcellular localization was determined by fluorescence in situ hybridization. To investigate function, circFNIP1 was silenced in PC-9 and SPC-A1 cells using siRNA-mediated knockdown. Cellular proliferation was measured by CCK-8 and colony formation assays, while apoptosis was evaluated via flow cytometry. Cell migration and invasion capacities were assessed using wound healing and transwell assays. In vivo tumorigenic potential was examined by establishing subcutaneous xenografts in nude mice, followed by intratumoral administration of antisense oligonucleotides targeting circFNIP1. Bioinformatics analyses, including interrogation of circRNA and miRNA databases and protein-protein interaction networks, were performed to predict circFNIP1-associated miRNAs and downstream targets. All experiments were conducted in triplicate, and statistical analyses were performed to determine significance. Results: CircFNIP1 was highly expressed in LC cells and localized to both the nucleus and cytoplasm. Knockdown of circFNIP1 significantly reduced proliferation, colony formation, migration, and invasion in vitro, and suppressed tumor growth in a mouse xenograft model. Bioinformatics predicted miR-1231 and miR-657 as key targets, with ICAM1 identified as a downstream effector of miR-657. Conclusions: CircFNIP1 functions as an oncogenic circRNA in LC and represents a promising target for RNA-based therapeutic strategies. These findings provide a basis for the development of circFNIP1-targeted interventions in LC management.
Indexed as
Identifiers
What OpenQuestion holds
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.