NTN1 (Netrin 1)

Netrin-1 expression was not associated with neoadjuvant treatment response in HER2-positive breast cancer. Nevertheless, considering its biological role and therapeutic relevance in multiple malignancies, further studies are warranted to clarify the predictive and therapeutic potential of Netrin-1.

Additional treatment with recombinant netrin-1 or netrin-4 induced fast-type MyHC mRNA expression; however, this effect was suppressed by UNC5A knockdown. These findings revealed that UNC5A is involved in fast-twitch myotube formation via netrin ligands, highlighting an autonomous fast-type myofiber commitment system within myoblasts.

In addition, sh-METTL3 downregulated the mRNA/protein levels of METTL3 and Netrin-1. AS regulates the H3K18la/METTL3/m~6A axis to inhibit the m~6A methylation of Netrin-1, reduce inflammatory cytokine secretion, and down-regulate fibrosis-related gene expression, thereby alleviating synovial fibrosis in KOA.

These data suggest that the netrin-1/NEO1 axis is a key regulator of PDAC progression, directly influencing cancer cell stemness and EMT, while indirectly promoting tumor growth through nerves. Inhibiting the netrin-1 pathway could represent a potential therapeutic approach for PDAC.

Draxin also supports long-range commissural guidance, but mutations in its binding site cause stronger defects. These results underscore how DCC's distinct modules drive specific developmental responses.

Machine learning combined with PPI network analysis identified NTN1 and CX3CL1 as key regulatory targets of SPP1, which may be associated with the occurrence and development of lung cancer. SPP1 may promote LUSC progression by mediating M2 macrophage polarization through suppressing NTN1 or activating CX3CL1, suggesting its potential as a prognostic biomarker and therapeutic target for high-risk male smokers.

The impact of Necrostatin-1s (Nec-1s) and cytarabine on neuronal degeneration was evaluated, along with a comparison of the effects of tamoxifen dissolved in different plant oils on lineage tracing in Sox10/iCreERT2; tdTomato mice, as well as on neuronal degeneration in NTN-1 cKO mice. These results suggest that, under pathological conditions, Cre recombinase can transfer from oligodendroglia to neurons, a process triggered by neuronal stress. This highlights the need for careful consideration in using Cre-loxP lineage tracing and gene-editing methods involving oligodendrocyte lineage cells and neurons.

These findings suggest that Netrin-1 protects dopaminergic neurons by regulating neuroinflammation, preserving DRD2 signaling, and inhibiting phosphorylation of GSK3β at Tyr216, thereby offering potential as a therapeutic agent for dopaminergic neurodegeneration.

Clinically, netrin-1 expression associated with poor survival and high CD133 expression in patients with CRC. Taken together, these results suggest that netrin-1 blockade could be a compelling therapeutic strategy to improve the poor outcomes and trigger cancer stemness inhibition in CRC treatment.

Silencing of LINC00592 impeded the ability of LUAD cells to migrate, invade, and form colonies, due to its ability to regulate the expression of NTN1, an important adhesion-related molecule. LINC00592 is a prognostic marker in LUAD patients and may represent a promising target for therapeutic intervention in this type of cancer.

We examined the effect of netrin on cell viability using DCC knockdown and NP137, a netrin-inhibiting antibody...TCGA analysis showed a negative correlation between NTN3 expression and survival. In conclusion, our data suggest that NTN-3, NTN-1, and DCC have interdependent oncogenic roles in PNENs, which can be reversed by blocking NTN binding to DCC.

The editors and Scientific Publishing Committee are in communication with the authors regarding the integrity of the image data, and Loma Linda University has confirmed the concerns are being reviewed. While we await the outcome of this review, we are publishing this Expression of Concern to indicate that the data and statements in the article may not be reliable.