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MZF1 Transcriptionally Activated MicroRNA-328-3p Suppresses the Malignancy of Stomach Adenocarcinoma via Inhibiting CD44
MicroRNA-328-3p (miR-328-3p) plays a critical role in mediating the progression of multiple types of cancers. To date, no study has concentrated on the molecular mechanism of miR-328-3p in mediating stomach adenocarcinoma (STAD). In this study, it was found that miR-328-3p was downregulated in STAD,...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9167131/ https://www.ncbi.nlm.nih.gov/pubmed/35669102 http://dx.doi.org/10.1155/2022/5819295 |
Sumario: | MicroRNA-328-3p (miR-328-3p) plays a critical role in mediating the progression of multiple types of cancers. To date, no study has concentrated on the molecular mechanism of miR-328-3p in mediating stomach adenocarcinoma (STAD). In this study, it was found that miR-328-3p was downregulated in STAD, and inhibition of miR-328-3p significantly promoted the growth, migration, invasion, and stemness of STAD cells, while miR-328-3p overexpression exerted reverse effects. Through bioinformatics analysis, it was uncovered that a cluster of differentiation 44 (CD44) was upregulated in STAD and closely associated with the prognosis of STAD patients. Mechanistically, we identified CD44 as the target gene of miR-328-3p. Notably, knockdown of CD44 abolished the promoting function of miR-328-3p inhibitor in the development of STAD. Moreover, myeloid zinc finger protein 1 (MZF1) was confirmed as an upstream transcription factor for miR-328-3p, which is involved in enhancing miR-328-3p expression. In addition, the role of MZF1 downregulation in the malignant traits of STAD cells was blocked by miR-328-3p overexpression. More importantly, upregulation of miR-328-3p efficiently suppressed STAD tumor growth in vivo. Collectively, our findings illustrated that MZF1-mediated miR-328-3p acted as a cancer suppressor in STAD progression via regulation of CD44, which suggested the possibility of the MZF1/miR-328-3p/CD44 axis as a novel promising therapeutic candidate for STAD. |
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