LncRNA KIAA0125 promotes the proliferation of Kasumi-1 cells through the miR-4640-5p/KCNQ1 axis with associated changes in the Wnt/β-catenin signaling pathway
5 affiliations
- 1Department of Clinical Biochemistry, School of Clinical Laboratory Science, Guizhou Medical University
- 2Center for Clinical Laboratories, The Affiliated Hospital of Guizhou Medical University
- 3Department of Hematology, Affiliated Hospital of Guizhou Medical University
- 4Affiliated Stomatology Hospital of Guizhou Medical University
- 5Department of Hematology, Guizhou Provincial People’s Hospital
Abstract
To investigate the effects of the long non-coding RNA (lncRNA) KIAA0125 on the proliferation and apoptosis of the human acute myeloid leukemia subtype M2 (M2-AML) cell line Kasumi-1. Recombinant lentivirus technology and CRISPR/Cas9-SAM technology were used to construct Kasumi-1 cells with downregulated or overexpressed lncKIAA0125, respectively. The cell proliferation rate of each group was determined using the cell counting kit-8 (CCK-8) assay, and the apoptosis rate was determined via flow cytometry. The binding between miR-4640-5p and lncKIAA0125, and between miR-4640-5p and KCNQ1, was subsequently verified using RIP and dual-luciferase assays. Western blotting was used to detect proteins related to the Wnt/β-catenin signaling pathway in each group, and rescue experiments were performed to confirm the role of the lncKIAA0125/miR-4640-5p/KCNQ1 axis in Kasumi-1 cells. Finally, a subcutaneous xenograft tumor model was established to verify the effect of lncKIAA0125 on the growth of Kasumi-1 cells in vivo. Downregulation of lncKIAA0125 inhibited Kasumi-1 cell proliferation and promoted apoptosis, whereas upregulation of lncKIAA0125 had the opposite effect on cell proliferation. RIP and dual-luciferase assays confirmed that lncKIAA0125 directly bound to miR-4640-5p and that miR-4640-5p also bound to KCNQ1. Moreover, downregulation of lncKIAA0125 inhibited KCNQ1 expression at both the mRNA and protein levels and reduced signaling related to the Wnt/β-catenin pathway. Conversely, upregulation of lncKIAA0125 produced the opposite effects. Finally, in vivo findings demonstrated that downregulating lncKIAA0125 expression suppressed the proliferation of Kasumi-1 cells in nude mice. lncKIAA0125 is highly expressed in AML cells and appears to promote the proliferation of Kasumi-1 cells via the miR-4640-5p/KCNQ1 axis and was associated with changes in the Wnt/β-catenin signaling pathway.
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BibTeX
@article{hu2026lncrna,
title = {{LncRNA KIAA0125 promotes the proliferation of Kasumi-1 cells through the miR-4640-5p/KCNQ1 axis with associated changes in the Wnt/β-catenin signaling pathway}},
author = {Huali Hu and Yuancheng Liu and Fahua Deng and Siqi Wang and Jianxia Xu and Jingxin Zhang and Yaming Zhang and Lianghong Wang and Pengxiang Guo and Tingting Lu and Hai Huang and Sixi Wei},
journal = {Scientific Reports},
year = {2026},
month = jul,
doi = {10.1038/s41598-026-62663-4},
url = {https://doi.org/10.1038/s41598-026-62663-4},
note = {CC BY},
}
RIS
TY - JOUR
TI - LncRNA KIAA0125 promotes the proliferation of Kasumi-1 cells through the miR-4640-5p/KCNQ1 axis with associated changes in the Wnt/β-catenin signaling pathway
AU - Huali Hu
AU - Yuancheng Liu
AU - Fahua Deng
AU - Siqi Wang
AU - Jianxia Xu
AU - Jingxin Zhang
AU - Yaming Zhang
AU - Lianghong Wang
AU - Pengxiang Guo
AU - Tingting Lu
AU - Hai Huang
AU - Sixi Wei
PY - 2026
DA - 2026/07/01
JO - Scientific Reports
DO - 10.1038/s41598-026-62663-4
UR - https://doi.org/10.1038/s41598-026-62663-4
AB - To investigate the effects of the long non-coding RNA (lncRNA) KIAA0125 on the proliferation and apoptosis of the human acute myeloid leukemia subtype M2 (M2-AML) cell line Kasumi-1. Recombinant lentivirus technology and CRISPR/Cas9-SAM technology were used to construct Kasumi-1 cells with downregulated or overexpressed lncKIAA0125, respectively. The cell proliferation rate of each group was determined using the cell counting kit-8 (CCK-8) assay, and the apoptosis rate was determined via flow cytometry. The binding between miR-4640-5p and lncKIAA0125, and between miR-4640-5p and KCNQ1, was subsequently verified using RIP and dual-luciferase assays. Western blotting was used to detect proteins related to the Wnt/β-catenin signaling pathway in each group, and rescue experiments were performed to confirm the role of the lncKIAA0125/miR-4640-5p/KCNQ1 axis in Kasumi-1 cells. Finally, a subcutaneous xenograft tumor model was established to verify the effect of lncKIAA0125 on the growth of Kasumi-1 cells in vivo. Downregulation of lncKIAA0125 inhibited Kasumi-1 cell proliferation and promoted apoptosis, whereas upregulation of lncKIAA0125 had the opposite effect on cell proliferation. RIP and dual-luciferase assays confirmed that lncKIAA0125 directly bound to miR-4640-5p and that miR-4640-5p also bound to KCNQ1. Moreover, downregulation of lncKIAA0125 inhibited KCNQ1 expression at both the mRNA and protein levels and reduced signaling related to the Wnt/β-catenin pathway. Conversely, upregulation of lncKIAA0125 produced the opposite effects. Finally, in vivo findings demonstrated that downregulating lncKIAA0125 expression suppressed the proliferation of Kasumi-1 cells in nude mice. lncKIAA0125 is highly expressed in AML cells and appears to promote the proliferation of Kasumi-1 cells via the miR-4640-5p/KCNQ1 axis and was associated with changes in the Wnt/β-catenin signaling pathway.
SN - 2045-2322
ER -