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miR-944 inhibits malignant progression of bladder cancer through ATIC/AKT/FOXO3 A axis mediated by SHMT1
Zhiming Liu1, Zhao Chen1, Haibei Yang1
1Department of Urology, Qujing No.1 Hospital, No.1 Yuanlin Road, Qilin District, Qujing, 655000, Yunnan, China.
Abstract:
To investigate the role of miR-944 in the progression of bladder cancer (BC) and explore its potential as a therapeutic target. In this study, we collected 12 pairs of BC tissues and paracancerous tissues and subcutaneously injected T24 cells into BALB/c nude mice at 1 × 106/mouse to establish the BC animal model for experimental investigation. RT-qPCR and western blot were used to detect the expression of related genes and proteins, and the malignant progression of T24 cells and BC was detected by CCK-8, Transwell, scratch wound, and immunohistochemistry. This study found that miR-944 expression was low in BC clinical samples and cell lines. Overexpression of miR-944 inhibited the proliferation, migration, and invasion of BC cells and inhibited BC tumor growth in vivo. Mechanistically, overexpression of miR-944 downregulated ATIC by inhibiting SHMT1, thereby activating the AKT/FOXO3A signaling pathway and promoting the expression of autophagy-related proteins LC3II/I and Beclin1. At the same time, it can inhibit the expression of epithelial-mesenchymal transition (EMT)-related proteins vimentin, fibronectin, and N-cadherin, ultimately inhibiting the proliferation, migration, and invasion of BC cells, and increasing the apoptosis level of BC cells to improve the development of BC. Our study confirmed that the upregulation of miR-944 may become a new target for the treatment of BC.
Insights
Upregulating miR-944, a microRNA, can suppress bladder cancer (BC) progression by inhibiting cell proliferation, migration, and invasion. This finding suggests miR-944 as a potential therapeutic target for treating BC.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Bladder cancer (BC) remains a significant health concern with limited therapeutic options.
- Understanding the molecular mechanisms driving BC progression is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the role of miR-944 in bladder cancer (BC) progression.
- To explore the potential of miR-944 as a therapeutic target for BC.
Main Methods:
- Analysis of miR-944 expression in BC tissues and cell lines using RT-qPCR.
- In vitro assays (CCK-8, Transwell, scratch wound) to assess BC cell proliferation, migration, and invasion.
- In vivo study using a BC mouse model to evaluate tumor growth.
- Western blot analysis to detect protein expression related to signaling pathways and epithelial-mesenchymal transition (EMT).
Main Results:
- miR-944 expression was significantly downregulated in BC clinical samples and cell lines.
- Overexpression of miR-944 inhibited BC cell proliferation, migration, and invasion in vitro.
- miR-944 overexpression suppressed BC tumor growth in vivo.
- Mechanistically, miR-944 targets ATIC by inhibiting SHMT1, activating the AKT/FOXO3A pathway, modulating autophagy proteins (LC3II/I, Beclin1), and inhibiting EMT markers (vimentin, fibronectin, N-cadherin).
Conclusions:
- Upregulation of miR-944 demonstrates potent anti-tumor effects in bladder cancer.
- miR-944 acts by regulating key signaling pathways and cellular processes involved in BC progression.
- miR-944 represents a promising novel therapeutic target for bladder cancer treatment.
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