Long non-coding RNA signature in colorectal cancer: research progression and clinical application - Cancer Cell International

France Nouvelles Nouvelles

Long non-coding RNA signature in colorectal cancer: research progression and clinical application - Cancer Cell International
France Dernières Nouvelles,France Actualités
  • 📰 BioMedCentral
  • ⏱ Reading Time:
  • 26 sec. here
  • 2 min. at publisher
  • 📊 Quality Score:
  • News: 14%
  • Publisher: 71%

A Review published in Cancer Cell International discusses the role of long non-coding RNAs in colorectal cancer, their value in tumor diagnosis, their role in treatment response and prognosis prediction, and the signaling pathways they are associated with.

]. In one study, LINC01559 was found to be downregulated in CRC compared to normal tissues and lower expression of LINC01559 in CRC patients indicated a poor prognosis; this study revealed the mechanism as negative regulation of the LINC01559/miR-106b-5p/PTEN axis in CRC progression and disclosed a new mechanism of METTL3-mediated m6A modification on LINC01559 [EMT is one of the important mechanisms of CRC metastasis.

found that the expression of lncRNA SATB2-AS1 in CRC tissues was significantly lower than in normal tissues, and its expression was related to tumor staging and prognosis [cell proliferation, invasion and migration in vivo and in vitroAnother study showed that SATB2-AS1 could inhibit metastasis of CRC cells and regulates Th1-type chemokine expression and immune cell density in CRC tissues; SATB2-AS1 could directly bind to WDR5 and GADD45A, and mediate the deposition of H3K4me3 in the SATB2...

Nous avons résumé cette actualité afin que vous puissiez la lire rapidement. Si l'actualité vous intéresse, vous pouvez lire le texte intégral ici. Lire la suite:

BioMedCentral /  🏆 22. in UK

France Dernières Nouvelles, France Actualités

Similar News:Vous pouvez également lire des articles d'actualité similaires à celui-ci que nous avons collectés auprès d'autres sources d'information.

Development and validation of a protocol for characterizing lipid nanoparticles for RNA deliveryDevelopment and validation of a protocol for characterizing lipid nanoparticles for RNA deliveryThis app note looks at how to meet regulatory needs in the characterization of lipid nanoparticles for RNA delivery.
Lire la suite »

The rise in interracial relationships is changing who is affected by sickle cellThe rise in interracial relationships is changing who is affected by sickle cellThe absence of a consideration of modern-day shifts in society could lead to missed diagnoses and exclusion from testing and screening programs ✒️ DrYemisiBokinni for ipaperviews
Lire la suite »

Targeting the overexpressed mitochondrial protein VDAC1 in a mouse model of Alzheimer’s disease protects against mitochondrial dysfunction and mitigates brain pathology - Translational NeurodegenerationTargeting the overexpressed mitochondrial protein VDAC1 in a mouse model of Alzheimer’s disease protects against mitochondrial dysfunction and mitigates brain pathology - Translational NeurodegenerationBackground Alzheimer's disease (AD) exhibits mitochondrial dysfunctions associated with dysregulated metabolism, brain inflammation, synaptic loss, and neuronal cell death. As a key protein serving as the mitochondrial gatekeeper, the voltage-dependent anion channel-1 (VDAC1) that controls metabolism and Ca2+ homeostasis is positioned at a convergence point for various cell survival and death signals. Here, we targeted VDAC1 with VBIT-4, a newly developed inhibitor of VDAC1 that prevents its pro-apoptotic activity, and mitochondria dysfunction. Methods To address the multiple pathways involved in AD, neuronal cultures and a 5 × FAD mouse model of AD were treated with VBIT-4. We addressed multiple topics related to the disease and its molecular mechanisms using immunoblotting, immunofluorescence, q-RT-PCR, 3-D structural analysis and several behavioral tests. Results In neuronal cultures, amyloid-beta (Aβ)-induced VDAC1 and p53 overexpression and apoptotic cell death were prevented by VBIT-4. Using an AD-like 5 × FAD mouse model, we showed that VDAC1 was overexpressed in neurons surrounding Aβ plaques, but not in astrocytes and microglia, and this was associated with neuronal cell death. VBIT-4 prevented the associated pathophysiological changes including neuronal cell death, neuroinflammation, and neuro-metabolic dysfunctions. VBIT-4 also switched astrocytes and microglia from being pro-inflammatory/neurotoxic to neuroprotective phenotype. Moreover, VBIT-4 prevented cognitive decline in the 5 × FAD mice as evaluated using several behavioral assessments of cognitive function. Interestingly, VBIT-4 protected against AD pathology, with no significant change in phosphorylated Tau and only a slight decrease in Aβ-plaque load. Conclusions The study suggests that mitochondrial dysfunction with its gatekeeper VDAC1 is a promising target for AD therapeutic intervention, and VBIT-4 is a promising drug candidate for AD treatment.
Lire la suite »

Characterization of retrovirus-based vectors used in gene and cell therapiesCharacterization of retrovirus-based vectors used in gene and cell therapiesComprehensive and reliable characterization, along with accurate quantitation, are essential for ensuring the quality and efficacy of retrovirus-based vectors used in novel gene and cell therapies.
Lire la suite »

Novel metabolic pathway that makes immunology more efficient revealedNovel metabolic pathway that makes immunology more efficient revealedThe metabolic pathways that produce a specific type of T cell are distinct from previously assumed, according to findings from UMich. Read more from the research below!👇 metabolomics science cells
Lire la suite »



Render Time: 2025-02-27 20:14:34