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Lncrna Flvcr1-As1 Sponges Mir-381-3P and Promotes Wnt Signaling Pathway Resulting in Colorectal Cancer Progression Publisher



Ahmadi Beni F1, 2 ; Abdolvand M3 ; Poorbafrani F4 ; Salehi M1, 3 ; Dehghanian F5 ; Kazemi M1, 2
Authors
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Authors Affiliations
  1. 1. Department of Genetics and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
  2. 2. Reproductive Sciences and Sexual Health Research Center, Isfahan University of Medical Sciences, Isfahan, Iran
  3. 3. Cellular, Molecular and Genetics Research Center, Isfahan University of Medical Sciences, Isfahan, Iran
  4. 4. Department of Clinical Nutrition, School of Nutrition and Food Science, Food Security Research Center, Isfahan University of Medical Sciences, Isfahan, Iran
  5. 5. Department of Cell and Molecular Biology and Microbiology, Faculty of Biological Science and Technology, University of Isfahan, HezarJarib Street, Isfahan, 81746-73441, Iran

Source: Egyptian Journal of Medical Human Genetics Published:2025


Abstract

Background: Colorectal cancer (CRC) is the third most frequent cancer and the second deadliest cancer, worldwide. Long noncoding RNAs (lncRNAs) have been introduced as crucial regulators of CRC. lncRNA feline leukemia virus subgroup C receptor 1 antisense RNA 1 (FLVCR1‑AS1) is suggested to play a significant role in the tumorigenesis of several cancers. The Wnt signaling pathway is the most deregulated pathway in CRC. Objective: The present study aimed to investigate the underlying mechanism of function of FLVCR1-AS1 in CRC through FLVCR1-AS1/miR-381-3p/CTNNB1, LRP6, and FZD3 axis. Methods: The expression levels of FLVCR1-AS1 were analyzed in colorectal cancer (CRC) tissues compared to adjacent normal tissues, as well as across various CRC cell lines. In HCT116 cells, FLVCR1-AS1 was knocked down, and the subsequent effects on the expression levels of FLVCR1-AS1, miR-381-3p, and three genes were measured using real-time PCR. Proliferation differences were assessed through an MTT assay, while cell death was evaluated using flow cytometry. Results: The results confirmed that FLVCR1-AS1 was upregulated in CRC tissues compared to adjacent normal tissues. RT-qPCR validated that FLVCR1-AS1 has the most level of expression in HT29, HCT116, SW480, and Caco2; respectively. Knockdown of FLVCR1‑AS1 was significantly followed by attenuated viability of HCT116 cells; while resulted in enhancement of apoptosis and necrosis. Conclusion: These findings support the idea that FLVCR1-AS1 may act as an oncogene in CRC, and targeting FLVCR1-AS1/miR-381-3p/CTNNB1, LRP6, and FZD3 axis may be introduced as a novel target for CRC therapy and diagnosis in the future. © The Author(s) 2025.
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