CCHC zinc finger protein 10 (ZCCHC10) has been implicated in the progression of multiple malignancies, but its prognostic value and role in immune infiltration in breast cancer remain unclear. In this study, we systematically analyzed ZCCHC10 expression using public databases and validated the findings by immunohistochemistry. Associations with clinicopathological features and patient prognosis were assessed, and a prognostic nomogram was constructed. Co-expression networks and gene set enrichment analysis were used to explore functional pathways, while immune infiltration was evaluated and potential therapeutic agents were predicted. Functional assays, including proliferation and colony formation experiments, were performed to examine the biological role of ZCCHC10 in vitro. Our results demonstrated that ZCCHC10 was significantly upregulated in breast cancer and associated with poor prognosis and adverse clinicopathological characteristics. Enrichment analysis indicated involvement in immune-related pathways, and its expression correlated with immune cell infiltration and immunomodulators. Drug sensitivity prediction suggested Ipatasertib as a candidate targeted therapy requiring experimental verification. Knockdown of ZCCHC10 markedly inhibited breast cancer cell proliferation. Collectively, these findings suggest that ZCCHC10 serves as a prognostic biomarker and a key regulator of immune infiltration in breast cancer.
Miao Chen, Si-Qi Wang, Xiang Li et al.· Scientific Reports· 0 citations
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.
Huali Hu, Yuancheng Liu, Fahua Deng et al.· Scientific Reports· 0 citations
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