ArticleCytoJournal2024
Immunoglobulin superfamily member 1 upregulates myc proto-oncogene to accelerate invasion and metastasis of endometrial cancer: Molecular mechanisms and therapeutic prospects.
Article in CytoJournal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Endometrial cancer (EC) is a common gynecological malignancy, and its metastasis is one of the primary causes of treatment failure. Immunoglobulin superfamily member 1 (IGSF1), a membrane protein, has been associated with the aggressiveness and metastatic capability of various cancers. However, the role and mechanism of this protein in EC remains unclear. Therefore, this study aimed to explore the role of IGSF1 in EC and its possible mechanism. Material and Methods: In this study, IGSF1 expression was knocked down through small interfering RNA and short hairpin RNA techniques, and its levels were controlled through overexpression experiments to observe its effects on Ishikawa cells. Wound healing assays, Transwell migration and invasion assays, quantitative real-time polymerase chain reaction, Western blot, and immunofluorescence double labeling were performed to evaluate the ability of cells to migrate, invade, and express markers of the epithelium mesenchymal transition (EMT). In addition, we investigated the regulatory role of IGSF1 in Myc proto-oncogene (c-Myc) expression and its function in lung metastasis through animal models of lung metastasis. Results: The results indicate that IGSF1 knockdown inhibited EMT and greatly reduced the invasion ability of Ishikawa cells ( Conclusion: IGSF1 promotes EMT and metastasis in EC through the upregulation of the c-Myc expression. IGSF1 may serve as a potential therapeutic target for EC, and its inhibition can offer new strategies for mitigating the aggressiveness and metastatic potential of this malignancy.
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