BASP1 (Brain Abundant Membrane Attached Signal Protein 1)

Mechanistically, BASP1 positively regulates LIN7A expression through phosphorylation of AKT as well as by supressing microRNA hsa-mir-501-3p, which in turn induces β-catenin-mediated EMT in chemoresistant cells. Overall, our study demonstrates that BASP1 acts as a key regulator of EMT in cisplatin-resistant OSCC and represents a promising therapeutic target to overcome drug resistance in advanced stages of the disease.

Importantly, BASP1 expression from LNPs effectively suppressed SW480 proliferation. Overall, PP coated LNPs for oral administration can efficiently deliver nucleic acids into intestinal tumor cells, which may be suitable to interfere with the tumorigenic phenotype.

Our study identified that NSUN7 regulates key oncogenic pathways associated with tamoxifen resistance and metastasis. Its suppression enhanced tamoxifen sensitivity and reduced metastatic potential, collectively highlighting NSUN7 as a novel driver of tamoxifen resistance and a potent therapeutic target in estrogen receptor-positive breast cancer.

BASP1's role in GC progression and tumor microenvironment modulation via IL6, M2 macrophages, and PI3K/AKT has been elucidated. This provides a basis for new GC therapies targeting BASP1.

This study demonstrates that BASP1 promotes macrophage polarization by activating the EGFR/PI3K/AKT pathway, thereby facilitating tumor progression.

Our findings shed light on the proteomics of CSF from MMD patients, identifying potential novel biomarkers such as SLITRK1 and markers of preoperative cerebral infarction (BASP1, LDHA) and clinical outcome (CD9, EMILIN1). These markers have potential as new diagnostic and therapeutic targets for MMD.

Dysregulation of mitotic control may underlie latent metastatic competence in ccRCC. CDCA8 and TROAP emerge as candidate prognostic biomarkers, linking postoperative metastatic progression in an initially M0 cohort with survival in metastatic disease. These hypothesis-generating findings warrant validation in larger, prospective cohorts.

Concurrently, BASP1-AS1-mediated histone H3K14 lactylation transcriptionally upregulates both LDHA and PCBP2, generating a self-amplifying metabolic-epigenetic circuit. This axis critically suppresses ferroptosis and maintains chemoresistance, providing actionable targets for overcoming oxaliplatin resistance in GC.

qPCR confirmed that BASP1, FCGR1B, and FKBP11 were significantly upregulated in KIRC compared to adjacent normal tissues, whereas CCL8 showed no significant differential expression between KIRC and paracancerous tissues. Our study has the potential to assist clinicians assess KIRC prognosis and modify more appropriate personalized treatment for KIRC patients in a timely manner.

The STS molecular subtyping system based on multi-omics data effectively distinguishes patients with poor prognosis. The subtyping results are robust and reliable, providing new insights for the precise diagnosis and treatment of these patients.

Additionally, several de novo peptides with ALC > 90% were identified. In silico analyses, including prediction and molecular modeling, suggested antimicrobial activity for some of these peptides, paving the way for future studies with biotechnological and therapeutic interests.

The characteristics of the transcriptome in peripheral blood and single-cell transcriptome in the prefrontal cortex exhibit significant differences between male and female patients with AD, which providing a basis for future sex stratified treatment of AD.