PLXNA1 (Plexin A1)

Structural studies revealed that this bsAb binds to PLXNA1/NRP2 at sites distinct from the SEMA3F-binding site, but in a manner that allows proper spacing for receptor complex formation and flexibility of conformational changes for signalling. This study demonstrates the potential of these receptors as targets for agonistic bsAbs development and provides the groundwork for further exploration in tumour models.

Data mining revealed the crucial roles of the Plexin family in COAD, especially in clinical indicators, immune infiltration, and prognosis of COAD patients. PLXND1, as an independent prognostic biomarker, enabled COAD cell invasion, metastasis and EMT by binding and modulating Notch3 signaling.

PLXNA1 plays a crucial role in transcriptional regulation and cancer pathways in EC. The expression of PLXNA1 was elevated in patients with EC and might play a key role in EC by regulating the transcriptional process and carcinogenic pathways.

Notably, NSUN2 was found to interact with PLXNA1 mRNA, and silencing NSUN2 in esophageal squamous cell carcinoma (ESCC) cells resulted in the downregulation of PLXNA1 expression through an m5C-mediated mechanism. Overall, our study provides valuable insights into the m5C profile and the relationship between the methylome and transcriptome in human tissues, highlighting the potential role of m5C modification as an epitranscriptomic biomarker.

FTX-101 enhanced the recruitment of oligodendrocytes and promoted myelination, addressing critical medical needs in demyelinating conditions. Specificity, solubility in water, and enduring stability render FTX-101 a highly promising candidate for a first-in-class therapeutic agent.

We found that boric acid activates apoptosis by triggering ROS formation at high doses and at the same time inhibits cell proliferation by increasing semaphorin signalling pathway expressions. Boric acid may act as an anti-cancer agent by activating different mechanisms in a dose-dependent manner.

Either inhibiting PLXNA1-NRP1 complex with an NRP1 inhibitor, EG01377, or targeting PLXNA1-mediated ENZR with AKT inhibitors, abolished the pro-resistance phenotype of PLXNA1. Taken together, combination of AKT inhibitor and AR inhibitors presents a promising therapeutic strategy for PCa, especially in advanced PCa patients exhibiting PLXNA1 overexpression.

Examining a clear cell renal cell carcinoma patient cohort, we find that SEMA3A expression is associated with reduced survival, and that T-cells appear trapped in SEMA3A rich regions. Our study establishes SEMA3A as an inhibitor of effector CD8+ T cell tumour infiltration, suggesting that blocking NRP1 could improve T cell function in tumours.

Overexpression of PlexinA1 enhanced Rac1 activation, ROS production, MICAL1 and Vimentin expressions, and favored cell migration. In conclusion, this study identified MICAL1 as an important facilitator of gastric cancer cell migration, at least in part, by affecting Vimentin expression and PlexinA1 promotes gastric cancer cell migration by binding to and suppressing MICAL1 degradation in a Rac1/ROS-dependent manner.

Our findings suggest that chronic stress plays an important role in GC progression and there is a potential for blocking the epinephrine-β2AR/PlexinA1 pathway in the treatment of GC.

Follow-up pathway and gene enrichment analyses demonstrated links between AAM-related proteins and obesity and diabetes, and between AAM and ANM-related proteins and various types of cancer. In conclusion, we identified proteomic signatures of reproductive ageing in women, highlighting biological processes at both ends of the reproductive lifespan.

PLXNA1 is highly expressed in HCC to promote tumor cell migration and proliferation and affect the patients' survival outcomes and immune microenvironment.