ASPH (Aspartate beta-hydroxylase)

Clinical trials of Claudin 18.2-targeted therapies (e.g., Zolbetuximab) further expand personalized treatment options...Despite the abundance of research in this field, this paper prioritizes the analysis and discussion of prospective or high-quality retrospective studies that include explicit efficacy prediction endpoints (such as pCR, TRG, AUC) to ensure the reliability of the evidence presented. This review emphasizes that multi-omics integrated predictive models and the clinical translation of targeted therapies represent critical directions for future research, aiming to optimize the neoadjuvant treatment strategies for locally advanced gastric cancer.

ASPHD1 overexpression also upregulated neuronal differentiation-related genes, produced more negative resting membrane potentials on whole-cell patch-clamp recordings, enhanced depolarization-evoked Ca2+ transients on calcium imaging, and increased NeuN protein expression. Together, these findings identify ASPHD1 as a favorable prognostic biomarker in glioma and suggest that high ASPHD1 expression restrains glioma progression while promoting neuron-like differentiation of glioma cells.

These patients also showed heightened sensitivity to several chemotherapeutic and targeted agents, including Cisplatin and Crizotinib. Integrating single-cell sequencing, MR-based causality, clinical validation, and functional experiments, we identified ASPH and PTTG1 as key regulators of LUAD angiogenesis and immune evasion. These findings substantiate ASPH/PTTG1 as promising biomarkers and therapeutic targets, offering new insights into precision therapies integrating anti-angiogenic and immunomodulatory strategies.

Overexpression of ASPH reversed the inhibitory effects on cell growth and glycolysis caused by knockdown of HRASLS2 in pancreatic cancer cells. This investigation revealed a novel mechanism of HRASLS2 in promoting the growth and glycolysis of PAAD by upregulating ASPH protein and indicated that HRASLS2 may be a potential therapeutic strategy for PAAD.

Our single-cell analysis focused on palmitoylation reveals new dimensions of tumor diversity in LUAD and establishes a validated 12-gene risk signature. Functional studies highlight ASPH as a promising candidate for therapeutic targeting. These results deepen our understanding of palmitoylation-associated pathways and present a foundation for both outcome prediction and precision-based treatment strategies in LUAD.

ASPH inhibition did not reduce tumor growth or promote the anti-tumor effect of innate immunity stimulation with the synthetic oligonucleotide ODN1826, but it significantly enhanced tumor growth reduction induced by DNA vaccination...Different types of lymphoid and myeloid cells were likely involved in the activated immune response that was efficient against tumors with MHC-I downregulation, which are often resistant to T-cell-based therapies. Due to different types of activated immune cells, ASPH inhibition could improve immunotherapy for tumors with various MHC-I expression levels.

The TME of ICC was heterogeneous. ASPH markedly enhanced ICC invasion The ASPH inhibitor CEP significantly inhibits ICC progression and may serve as a targeted therapeutic drug for ICC. Tumor cells in N1 lymph nodes demonstrate high expression of tumor-specific MHC-II molecules, but silencing of co-stimulatory factors such as CD80/CD86 induces CD4+ T cells into an anergic state. Our study indicated that ASPH and MHC-II may serve as novel therapeutic targets for ICC.

Three selected oligomers, AP-CEC 1, AP-CEC 2, and AP-CEC 3, showing Kd values of 43.09 nM, 34.85 nM, and 35.92 nM, respectively, were achieved based on the affinity assessment of the ASPH-expressing cells. Our research suggested that CEC hybrid-SELEX could help recognize which oligomers from CE-SELEX are more capable of binding native ASPH in vivo.

These data validate ASPH as a biomarker in CS and as a factor in the metastatic phenotype. Systemic treatment with an SMI directed against ASPH inhibits tumor progression in a preclinical model, suggesting that ASPH-targeted therapy may be a new treatment strategy for chondrosarcoma expressing ASPH.

Furthermore, ASPH contributes to heightened tumor drug metabolism, hence raising the IC50 values for gemcitabine and paclitaxel. ASPH plays a role in promoting the development of gallbladder cancer and resistance to chemotherapeutic agents, rendering it a promising target for therapeutic interventions. Active therapeutic compounds targeted on ASPH can be identified among the active ingredients present in traditional Chinese medicine.

The study confirms that nsEP is more effective than µsEP in disrupting cancer cell viability, enhancing oxidative stress, and triggering immune responses, likely through HSP overexpression and ROS generation. nsEP also appears to reduce CSC viability, offering a promising therapeutic approach. However, preserving CD133 expression in the presence of calcium suggests complex interactions that require further investigation. These findings highlight the potential of nsCaEP as an innovative strategy for targeting both cancer cells and CSCs, potentially improving treatment outcomes in colorectal cancer. Further studies are needed to explore the exact cell death mechanisms and optimize protocols for clinical applications.