{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMicroRNA MIR4723 has emerged as an important tumor suppressor in prostate cancer by directly regulating key oncogenic signaling proteins. In prostate cancer clinical specimens, MIR4723 expression is significantly reduced, a decline that correlates with poor patient survival. Functional assays in prostate cancer cell lines reveal that restoring MIR4723 levels leads to decreased cell growth, clonogenicity, invasion, and migration, as well as a marked induction of apoptosis. Mechanistically, MIR4723 targets critical proteins including Abl1 and Abl2 kinases, integrin alpha 3, and methyl-CpG binding protein; notably, Abl kinase expression is inversely correlated with MIR4723 levels. These data suggest that MIR4723 plays a central role in mediating prostate carcinogenesis and may serve as a valuable diagnostic, prognostic, and therapeutic target."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn triple-negative breast cancer, MIR4723 is also implicated in tumor biology as a downstream effector of the oncogene c-myc. High-throughput sequencing and qRT-PCR analyses demonstrate that c-myc knockdown in MDA-MB-231 cells results in a significant reduction in MIR4723 levels. Bioinformatic predictions further suggest that MIR4723 targets genes such as TRAF4, which are associated with cancer pathways and metastasis. These findings indicate that MIR4723, through its c-myc–mediated regulation, may influence tumor progression and metastasis in aggressive breast cancer subtypes."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Sumit Arora, Sharanjot Saini, Shinichiro Fukuhara, et al. "}, {"type": "b", "children": [{"type": "t", "text": "MicroRNA-4723 inhibits prostate cancer growth through inactivation of the Abelson family of nonreceptor protein tyrosine kinases."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "PLoS One (2013)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1371/journal.pone.0078023"}], "href": "https://doi.org/10.1371/journal.pone.0078023"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "24223753"}], "href": "https://pubmed.ncbi.nlm.nih.gov/24223753"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Xi-Xin Jin, Chao Gao, Wen-Xin Wei, et al. "}, {"type": "b", "children": [{"type": "t", "text": "The role of microRNA-4723-5p regulated by c-myc in triple-negative breast cancer."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Bioengineered (2022)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1080/21655979.2022.2056824"}], "href": "https://doi.org/10.1080/21655979.2022.2056824"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "35382692"}], "href": "https://pubmed.ncbi.nlm.nih.gov/35382692"}]}]}]}