MYO3B promotes cancer progression in endometrial cancer by mediating the calcium ion-RhoA/ROCK1 signaling pathway
- J Cancer Res Clin Oncol. 2024 Sep 19;150(9):424. doi: 10.1007/s00432-024-05940-x.
- 1. Department of Gynecology, First Hospital of Shanxi Medical University, No.85, Jiefang South Road, Yingze District, Taiyuan, Shanxi Province, 030001, China.
- 2. Department of Basic Medicine, Shanxi Medical University, No.56, Xinjian South Road, Yingze District, Taiyuan, Shanxi Province, 030001, China. [email protected].
- 3. Department of Urology, First Hospital of Shanxi Medical University, Taiyuan, 030001, China.
- 4. Shanxi Inspection and Testing Center, Taiyuan, 030001, China.
- 5. Department of Gynecology, First Hospital of Shanxi Medical University, No.85, Jiefang South Road, Yingze District, Taiyuan, Shanxi Province, 030001, China. [email protected].
Purpose: This study aimed to investigate the effect of MYO3B on endometrial Cancer (EC) proliferation and invasion.
Methods: The expression of MYO3B in EC tissues and cells was analyzed using TCGA database, immunohistochemical staining, Real-Time PCR, and western blot (WB). Cell proliferation was detected by CCK8, Annexin V-APC/PI flow cytometry was used to detect Apoptosis, intracellular calcium ion (CA2+) was detected by flow cytometry with Fluo-4 AM fluorescent probe, cell migration by scratch assay, and cell invasion by Transwell assay, and the expression of proteins related to CA2+ homeostasis and RhoA/ROCK1 signaling pathway was detected by WB and immunofluorescence staining.
Results: The expression of MYO3B was an influential factor in EC recurrence, and the expression of MYO3B was significantly up-regulated in EC tissues and cells, but down-regulated in KLE cells, and MYO3B knockdown inhibited the proliferation, migration, and invasion ability of EC cells and promoted Apoptosis, suggesting that MYO3B plays a tumor-promoting role in EC. Furthermore, MYO3B knockdown decreased CA2+ concentration in EC cells and the RhoA/ROCK1 signaling pathway was inhibited, and the effect of MYO3B knockdown on RhoA/ROCK1 signaling was reversed by treatment with the Calmodulin agonist CALP-2, and the effects of MYO3B knockdown on cell proliferation, migration, and invasion were reversed after treatment with the RhoA agonist U-46,619.
Conclusion: MYO3B promotes the proliferation and migration of endometrial Cancer cells via CA2+-RhoA/ROCK1 signaling pathway. High expression of MYO3B may be a biomarker for EC metastasis.
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Cat. No.Product NameDescriptionTargetResearch Area
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target: Prostaglandin ReceptorResearch Areas: Cardiovascular Disease
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Research Areas: Cancer