Mouse pre-microRNA Expression Construct mir-301a
- Known as:
- Mouse pre-microRNA Expression Construct mir-301a
- Catalog number:
- mmir-301a-pa-1
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Sbi systeme bioscience
- Gene target:
- Mouse pre-microRNA Expression Construct mir-301a
Related genes to: Mouse pre-microRNA Expression Construct mir-301a
- Gene:
- MIR301A NIH gene
- Name:
- microRNA 301a
- Previous symbol:
- MIRN301, MIRN301A
- Synonyms:
- hsa-mir-301, hsa-mir-301a
- Chromosome:
- 17q22
- Locus Type:
- RNA, micro
- Date approved:
- 2004-04-23
- Date modifiied:
- 2019-01-30
Related products to: Mouse pre-microRNA Expression Construct mir-301a
Related articles to: Mouse pre-microRNA Expression Construct mir-301a
- Glioblastoma remains the most aggressive malignant brain tumor, with limited survival despite advances in surgery, radiotherapy, and chemotherapy. Current diagnostic modalities are insufficient for early detection and precise monitoring of disease progression, prompting interest in liquid biopsy-based biomarkers. Exosomal microRNAs (miRNAs) have been highlighted as significant biomarkers due to their stability and involvement in tumor progression. This narrative review evaluates current evidence regarding the diagnostic, prognostic, and therapeutic significance of exosomal and extracellular vesicle-associated miRNAs in brain tumors, particularly gliomas. Data were collected from PubMed and Google Scholar, and eight original articles published between 2016 and 2026 were included after careful screening. The findings demonstrated dysregulated expression of exosomal miRNAs, including miR-29b, miR-210, miR-301a, miR-454-3p, and miR-2276-5p, which were significantly associated with tumor grade, recurrence, survival, and treatment response. The majority of studies reported strong diagnostic performance, with receiver operating characteristic/area under the curve values ranging from 0.80 to 0.93, while mechanistic analyses implicated these miRNAs in oncogenic pathways, including PTEN/AKT signaling, hypoxia-mediated progression, autophagy regulation, and angiogenesis. Overall, exosomal miRNAs demonstrate considerable potential as noninvasive biomarkers for prognostication and therapeutic targeting, while their dynamic preoperative alterations further suggest utility in disease monitoring. - Source: PubMed
Publication date: 2026/07/06
Bashir Waleed QFatima AnamAli ShanzaAhmad ShahzebIsmail FizaYousaf Muhammad BilalSarwar AhsanNoor AhmadKhan Faiqa IMehmood Qadri Haseeb - - Source: PubMed
Publication date: 2026/06/17
Granda-Díaz RocíoManterola LoreaHermida-Prado FranciscoRodríguez RenéSantos LauraGarcía-de-la-Fuente VanessaFernández María TeresaCorte-Torres M DanielaRodrigo Juan PÁlvarez-Teijeiro SaúlLawrie Charles HGarcia-Pedrero Juana M - Pancreatic cancer stands out as a deadly disease because patients receive late diagnosis and struggle with ineffective treatments. Exosomal microRNAs (miRNAs) that exist inside lipid bilayers help tumors grow and spread while making cells resistant to treatment and enabling cell-to-cell communication. Their ability to stay stable in body fluids makes them good candidates for early disease detection and treatment prediction tests. Research shows that miR-21, miR-17-5p, and miR-155 exosomal miRNAs help pancreatic cancer progress but also provide new targets for medical treatment. This review consolidates current evidence on the diagnostic, prognostic, and therapeutic potential of exosomal miRNAs in pancreatic cancer, integrating mechanistic insights into key signaling pathways such as PTEN/PI3Kγ, KRAS/MAPK, and TGF-β. Compared with previous reports, this work provides a comparative framework linking disease-specific exomiR profiles to other cancers, highlighting miR-21, miR-17-5p, miR-155, and miR-301a as central modulators. We further discuss methodological challenges, translational opportunities, and future directions in developing exosome-based diagnostics and miRNA-loaded therapeutic platforms. Understanding exosomal miRNA networks can pave the way for precision detection and targeted therapy in pancreatic cancer. - Source: PubMed
Publication date: 2025/11/19
Mir RashidJan UlfatBarnawi JameelAlgehainy Naseh AJalal Mohammed MAltayar Malik AAlmotairi Reema MAlnour Tarig MsMustafa Syed KhalidAl-Otaibi Abdulaziz SAlthaqafy Adel DAlhathli Elham MAlrdahe SalmaMir Mohammad MuzaffarSageer Nada ZakiBabakr Abdullatif TahaKhan Afaq Ahmad - Therapeutic targeting of mutant KRAS pathways driving cancers is being actively investigated to identify feedback mechanisms responsible for the development of adaptive resistance to mutant KRAS inhibitors undergoing clinical trials. Here we report RASH3D19 as a mediator of RAS pathway activation through a positive feedback loop involving the KRAS-microRNA signalling axis. KRAS-induced miR-222 represses ETS1 expression and downstream transactivation of miR-301a leading to elevation of its target RASH3D19. RASH3D19 facilitates activation of RAS pathways by promoting dimerization and interaction of EGFR with the SOS2, GRB2, SHP2 and GAB1 complex. Genetic deletion of RASH3D19 in mutant KRAS-expressing cancer cells exhibits growth retardation in vitro, in vivo and sensitized pancreatic ductal adenocarcinoma and colorectal cancer cells, organoids and xenografts to mutant KRAS inhibitors, suppressing feedback reactivation of RAS pathways. Therapeutic targeting of RASH3D19 is expected to lead to tumour debulking and alleviating resistance to KRAS inhibitors in mutant KRAS-expressing cancers. - Source: PubMed
Publication date: 2025/12/01
Treekitkarnmongkol WarapenKatayama HiroshiSankaran DeivendranTai Mei-CheeRauth SanchitaChen HanxiaoNguyen TristianHara KiekoThege Fredrik IPonnusamy Moorthy PBatra Surinder KWang HuaminWistuba Ignacio ISchmittgen Thomas DHeymach John VKopetz ScottHu TonyYao WantongMaitra AnirbanSen Subrata - Gene pairing is a highly conserved and special mode of eukaryotic gene organization, and critically implicated in development and diseases including cancer. We previously found that PRR11 and SKA2 constitute a classic head-to-head gene pair. Here, we further demonstrate that PRR11, SKA2, and its intronic miR301a and miR454 constitute a more exquisite bidirectional transcription unit that are overexpressed in various types of cancers. Functional studies using lung cancer as a model system reveal that co-overexpression of PRR11, SKA2, miR301a and miR454 together remarkably accelerates cell growth, cell cycle progression and cell motility in lung cancer cells, and promotes tumor growth in mouse models in vivo, whereas CRISPRi-mediated repression of the entire transcription unit inhibits these malignant phenotypes. Mechanistically, the four component genes do not display any additive or synergistic effect, but rather compensate for each other for robustly sustained activation of PI3K-AKT pathway, with PRR11 interacting with GRB2, and SKA2 with EGFR. Notably, miR301a and miR454 exert their oncogenic functions at least partially via repressing PTEN translation. Moreover, the transcription unit presents as a prominent prognostic meta-marker for lung cancer. Collectively, these findings demonstrate the essential and coordinated roles of PRR11-SKA2-miR301a/454 bidirectional transcription unit in lung cancer progression, highlighting its potential diagnostic and therapeutic values in cancers. - Source: PubMed
Publication date: 2025/11/27
Liu TaoZuo XiaofengSun ShijieDu KailongTao ChuntaoXia XingYu LinliZhang ChunxueYang ZhengmeiWang YitaoYe JunhongBu Youquan