Show pageBacklinksCite current pageExport to PDFBack to top This page is read only. You can view the source, but not change it. Ask your administrator if you think this is wrong. ====== miR 144 ====== The [[transferrin]] receptor is a [[membrane glycoprotein]] whose only clearly defined function is to mediate cellular uptake of [[iron]] from a plasma glycoprotein, transferrin. Glioblastoma (Glioblastoma) remains the most common and malignant tumor of the human central nervous system. Increasing evidence has highlighted that tumor cells with high [[transferrin receptor]] (TFRC) expression show advantages in growth. [[Long non-coding RNA]]s ([[lncRNA]]s) are related to [[glioma progression]] by mediating [[microRNA]]s [[(MicroRNA]]s). However, the underlying mechanism among TFRC, MicroRNA and lncRNA in Glioblastoma is limited. Ma et al. identified a new lncRNA-induced signaling mechanism that regulates the [[transferrin receptor]] (TFRC) levels in Glioblastoma (Glioblastoma). The TFRC level was higher in [[glioma cell line]]s, and elevated TFRC expression promoted the proliferation and survival of [[glioma cell]]s. Further study showed that hsa-[[miR 144]]a-3p bound to the 3'-UTR of TFRC mRNA and inhibited its expression, preventing the malignant properties of glioma cells, such as [[proliferation]] and [[survival]]. They also found that the lncRNA RP1-86C11.7 sponges hsa-miR-144-3p to suppress its protective role in [[glioma]]. RP1-86C11.7 overexpression in glioma cells elevated TFRC expression, increased the intracellular free [[iron]] level, and deteriorated [[oncogenicity]], with a significant reduction in hsa-miR-144-3p. By contrast, silencing RP1-86C11.7 upregulated the hsa-miR-144-3p level, resulting in decreased TFRC expression and repressed glioma progression. However, the effect of silencing RP1-86C11.7 was reversed with simultaneous hsa-miR-144-3p inhibitor treatment: the TFRC level, intracellular iron level and proliferation in glioma cells increased. Mechanistically, this data indicated that RP1-86C11.7 exacerbates the malignant behavior of glioma through the hsa-[[miR]]-144-3p/TFRC axis. RP1-86C11.7 may be a potential [[biomarker]] or target to treat glioma in the future ((Ma Q, Wang X, Li J. [[LncRNA RP1-86C11.7]] exacerbates the [[glioma progression]] and [[oncogenicity]] by [[hsa-miR-144]]-3p/TFRC signaling. Transl Oncol. 2021 Sep 24;14(12):101215. doi: 10.1016/j.tranon.2021.101215. Epub ahead of print. PMID: 34571345.)). ---- Thirteen MicroRNAs including miR-125b-1 were downregulated, while only 4 MicroRNAs including miR-144 were upregulated in Gli1 high expression group. In summary, our study presents a subset of MicroRNAs which target the Hh signaling pathway in Glioblastomas, and throws some light on the aberrant activation mechanism ((Gu W, Shou J, Gu S, Sun B, Che X. Identifying hedgehog signaling specific microRNAs in glioblastomas. Int J Med Sci. 2014 Mar 21;11(5):488-93. doi: 10.7150/ijms.6764. PMID: 24688313; PMCID: PMC3970102.)) mir_144.txt Last modified: 2024/06/07 02:55by 127.0.0.1