ASPM (Assembly Factor For Spindle Microtubules)

Targeting ASPM may represent a promising therapeutic strategy to overcome EGFR-TKI resistance, enhance osimertinib efficacy, and expand treatment options for refractory NSCLC patients. These findings provide a foundation for developing ASPM-directed therapies in precision oncology.

We further found, with bioinformatics analysis, amino acid sequence 963-1263 of ASPM as a potential new drug target for overcoming RT resistance and identified 9 drug pockets within this domain for clinical translation. Our findings suggest that ASPM is a key regulator with an important role in promoting RT resistance in non-small cell lung cancer, and that suppressing or blocking its expression could be worth exploring as therapy for a variety of RT-resistant cancers.

Further, in vitro experiments were conducted to evaluate the effects of ASPM overexpression on cell proliferation and sensitivity to cisplatin...ASPM exhibits a dual role in LUAD prognosis, acting as a marker for improved chemotherapy outcomes while promoting tumor proliferation. These findings underscore ASPM's potential as a therapeutic target and predictive marker for personalized treatment in LUAD.

Collectively, we demonstrate that LLPS and transcriptional regulation form an oncogenic double positive feedback loop between ASPM and FOXM1. This provides a rationale strategy to treat HCC by targeting this mechanism.

High ASPM expression predicts poor prognosis in BC. It may play a role in treatment resistance within a specific subgroup of patients. Further clinical trials are warranted to explore the potential of ASPM as a target for therapeutic interventions in cancer.

ASPM holds promise as a novel biomarker for refining current risk stratification and predicting prognosis in neuroblastoma. Elevated levels of ASPM, LDH, and GLZLM_ZLNU may be associated with poorer survival outcomes in neuroblastoma patients.

These findings suggest that ASPM promotes HCC stemness and progression through the Wnt/β-catenin pathway. Targeting ASPM or the Wnt/β-catenin pathway may be a promising strategy to prevent HCC chemoresistance and recurrence, ultimately improving patient prognosis.

Nrf2 drives EMT, CSCs characteristics and VM in HCC under hypoxia through the modulation of ASPM. Retinol metabolism pathway was dysregulated in HCC cells with ASPM overexpression. Nrf2/ASPM axis and related pathway provided potential therapeutic target for HCC.

Comparative Toxicogenomics Database analysis indicated that the core genes (CENPE, SPAG5, and ASPM) are associated with gastric tumors, gastric diseases, gastritis, gastric ulcers, tumors, inflammation, and necrosis. The SPAG5 and ASPM genes are overexpressed in gastric cancer tissues, and higher expression levels are associated with worse prognosis, may serve as potential prognostic markers.

TOP2A and MELK genes are highly expressed in psoriasis, and higher expression of TOP2A and MELK genes is associated with poorer prognosis.

Echoing these findings, NICD1 was found to be strongly co-expressed with ASPM-i1 in cancer cells in human HCC tissues (P < 0.001). In conclusion, our study identifies a novel Notch signaling regulatory mechanism mediated by protein-protein interaction between NICD1, FBXW7, and ASPM-i1 in HCC cells, representing a targetable vulnerability in human HCC.

ASPM promotes the migration, proliferation, and invasiveness of RCC cells, and the Wnt3a pathway may be implicated in this process. In conclusion, these results indicate that ASPM contributes to the cancer progression of RCC by targeting the Wnt3a signaling pathway.