A team from Universidad Andrés Bello (UNAB) used CRISPR to remove a tiny fragment of MALAT1 RNA, a molecule that plays a key role in gastric and breast cancer. By doing so, the researchers managed to...

Read the full paper: Combination of Astragaloside IV and Tetramethylpyrazine Promotes Angiogenesis via the MALAT1–CXCL12/CXCR4 Axis in Brain Endothelial Cells After Ischemic Injury

Regulation of the 3′-end processing of lncRNA MALAT1 has remained unknown. Here, the authors identified a previously unrecognized RNase MRP and P control (RMPPc) pathway that controls posttranscriptional processing of MALAT1 and over 90% of the total RNA content in human cells.

Although abundance of the metastasis-associated long non-coding RNA MALAT1 depends on the maturation of its triple-helix-containing 3′ end via non-canonical processing, the control of this step has remained unknown. Using iterative genome-wide screening, we identified TRNAU1AP and PRPF39 that together control the 3′-end processing of MALAT1, enabling a reduction in its levels. We further show that these factors form part of a previously unrecognized RNase MRP and P control (RMPPc) pathway that, in addition to MALAT1, establishes integrated control over the processing of MEN-β, internal transcribed spacers in pre-rRNA, and 5′-leader sequences in pre-tRNA, thereby impacting fundamental processes prerequisite for translation. We demonstrate that this far-reaching impact is achieved through a single control point: inclusion of the initiating ATG-containing exon 2 in RPP14, an essential component of both RNase MRP and RNase P, thereby controlling both catalytic RNAs—MRP RNA and H1 RNA. Fina

scQCenrich integrates canonical, nuclear-enrichment, and stress-related metrics to improve quality control in single-cell RNA sequencing while preserving biologically coherent cell populations.

Measuring urinary cell-derived lncRNA MALAT1 could improve the ability to differentiate between diabetic and nondiabetic kidney disease in people with type 2 diabetes.

Read the full paper: Evaluating Malat1-derived 3’end sequences for functional transgene expression in human cells using synthetic mRNA delivery

Read the full paper: Deletion of the MALAT1 RNA 3’ end Promotes Transcript Decay, TALAM1 downregulation, and Inhibits Proliferation in Gastric and Breast Cancer Cells

The tumor cells exhibited strong positivity for CD163 (a), approximately 40% positivity for Cyclin D1 (b), and a Ki-67 proliferation index of approximately 40% in hotspot regions (h). Staining results were negative for ERG (c), WT1 (d), MPO (e), NKX2.2 (f), and CD117 (g).