Mouse pre-microRNA Expression Construct mir-139
- Known as:
- Mouse pre-microRNA Expression Construct mir-139
- Catalog number:
- mmir-139-pa-1
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Sbi systeme bioscience
- Gene target:
- Mouse pre-microRNA Expression Construct mir-139
Related genes to: Mouse pre-microRNA Expression Construct mir-139
- Gene:
- MIR139 NIH gene
- Name:
- microRNA 139
- Previous symbol:
- MIRN139
- Synonyms:
- hsa-mir-139
- Chromosome:
- 11q13.4
- Locus Type:
- RNA, micro
- Date approved:
- 2004-04-23
- Date modifiied:
- 2019-01-31
Related products to: Mouse pre-microRNA Expression Construct mir-139
Related articles to: Mouse pre-microRNA Expression Construct mir-139
- Neoadjuvant chemotherapy (NAC) is the standard of care for locally advanced breast cancer, yet the molecular predictors of pathological response remain incompletely defined, particularly regarding microRNA (miRNA) dynamics. We investigated paired pre- and post-NAC miRNA expression profiles in relation to molecular subtype, residual cancer burden (RCB), and clinical timing parameters. Seven patients with invasive breast cancer (Luminal A = 3, Luminal B = 1, TNBC = 2, HER2+ = 1) who received NAC (AC-T or TCHP) were included in this pilot study. Small-RNA sequencing (NovaSeq X Plus, CeGaT GmbH, project S17293) was performed on 14 FFPE specimens (7 pre-NAC core needle biopsies, 7 post-NAC surgical specimens). Differential expression analysis used the paired Wilcoxon signed-rank test with Benjamini-Hochberg correction. Spearman correlations assessed associations between miRNA expression, RCB score, and clinical timing intervals. Candidate miRNAs were subsequently annotated using experimentally validated miRNA-target interactions. After filtering (≥ three counts in ≥ three samples), 759 miRNAs were analysed. No miRNA reached strict significance (adj < 0.05, |logFC| > 1.0) after multiple testing correction, consistent with the limited statistical power ( = 7). Under exploratory criteria ( < 0.10, |logFC| > 0.5), 156 candidate miRNAs were identified: 70 upregulated and 86 downregulated post-NAC. Leading candidates included hsa-miR-139-3p (+2.60), hsa-miR-139-5p (+2.36), and hsa-miR-1323 (+1.55) as upregulated, and hsa-miR-429 (-2.53), hsa-miR-141-3p (-1.79), and hsa-miR-1277-5p (-1.25) as downregulated post-NAC. The single patient achieving the lowest residual disease burden (P3, Luminal B, RCB-I, score 1.32) displayed a distinct pre-treatment miRNA profile, separating from all other pre-NAC specimens on principal component analysis and characterised by higher baseline hsa-miR-139-3p/-5p and lower baseline hsa-miR-429 and hsa-miR-141-3p expression, suggesting that baseline miRNA expression patterns may contribute to differential chemotherapy response. RCB score showed a non-significant positive trend with post-NAC Ki-67 (ρ = +0.71, = 0.07). This pilot study identifies NAC-modulated candidate miRNAs in breast cancer and establishes a paired FFPE-based small-RNA-sequencing workflow applicable in routine clinical settings. The distinct pre-treatment profile of the single best responder generates the testable hypothesis that baseline expression of tumour suppressor miRNAs of the miR-139 family, together with low miR-200-family expression, may track chemosensitivity. As no candidate reached statistical significance after multiple testing correction and none has been validated in an independent cohort or by an orthogonal method, all findings are exploratory and hypothesis-generating. The results support larger prospective validation studies examining miRNA signatures as predictive biomarkers of NAC response across breast cancer molecular subtypes. - Source: PubMed
Publication date: 2026/08/31
Komporaly Isabela AndaGheorghe Adelina SilvanaIovănescu Elena AdrianaGeorgescu BogdanStănculeanu Dana Lucia - MicroRNAs (miRNAs) are key post-transcriptional regulators of gene expression that modulate cancer-related processes, including cell growth, proliferation, differentiation, and invasion. While numerous oncogenic (oncomiRs) and tumor suppressor (TS) miRNAs have been characterized, structural features distinguishing these groups are not fully understood. This study investigates whether guanine (G) enrichment in precursor miRNA (pre-miRNA) terminal loop (TL) regions across the human miRNome is associated with tumor-suppressive activity in lung cancer. - Source: PubMed
Publication date: 2026/07/22
Cohen AmitBurgos-Aceves Mario AlbertoSmith Yoav - miR-139 acts as a tumor suppressor in breast cancer cells, yet its role within the tumor immune microenvironment (TIME) remains unclear. This study explores the dual functions of miR-139 in both tumor and immune cells, particularly its effect on CD8 T cell function and chemokine-mediated immune recruitment. Bioinformatics analysis using TCGA and GEO data identified miR-139 as differentially expressed in breast cancer. Using samples from 32 patients, we detected elevated miR-139 levels in tumor-infiltrating CD8 T cells compared with adjacent normal tissues. Further experiments confirmed that miR-139 directly targets CD28, leading to its downregulation. Concurrently, increased expression of exhaustion markers PD-1 and TIGIT was observed. Moreover, tumors with high miR-139 expression showed upregulation of T-cell-recruiting chemokines CX3CL1, CXCL12, and CXCL14. These results demonstrate that miR-139 promotes CD8 T cell exhaustion via suppression of CD28 and facilitates chemokine-mediated T cell recruitment, highlighting its immunosuppressive role in breast cancer. - Source: PubMed
Publication date: 2026/06/23
Chen JianrongZhang HaiyongLv YantingLi XiufangHu Mengjun - Non-small cell lung cancer (NSCLC) remains a significant global health challenge, making the exploration of potential therapeutic targets critically important. In this study, we discovered that ZNF200 is highly expressed in NSCLC tissues and plays an oncogenic role by promoting cell proliferation and metastasis both in vitro and in vivo. Mechanistically, ZNF200 recruits DDX17 to the promoter region of RBPJ to upregulate the expression of RBPJ and activate the Notch signaling pathway. ZNF200 and DDX17 increase H3K4me3 enrichment at the RBPJ promoter. Furthermore, ZNF200 interacts with SETD1A to regulate H3K4me3 deposition, sustaining the transcriptional activity of the RBPJ promoter. Interestingly, DDX17 could maintain the protein stability of ZNF200 by inhibiting the ubiquitin-proteasome degradation pathway, which further increased the expression level of ZNF200 in the nucleus. Additionally, we revealed that miR-139 inhibits ZNF200 expression and that the introduction of miR-139 abrogates the increased cell proliferation and metastasis caused by ZNF200 over-expression. Overall, our work demonstrates the critical role and molecular mechanism of ZNF200 in regulating NSCLC development, highlighting the potential of targeting ZNF200 as an effective strategy in NSCLC treatment. - Source: PubMed
Publication date: 2026/06/24
Zhang YankeZhu HongbinWang XueqinDong WeiZhang MaoyuSong XinyueHan DanyeChai QianFeng XueyiWei XiaozhengChen HongyuLi YonghuaiZhao LeiDai Qian - Mechanisms regulating the transition between two consecutive reproductive cycles are complex and remain poorly understood, mostly because they involve a dialog between the ovary and the central nervous system that is difficult to disentangle. - Source: PubMed
Publication date: 2026/05/21
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