TUBA1B (Tubulin Alpha 1b)

Meanwhile, significant co-localization of TUBA1B with CD8+ T cells was observed in OC tissues from the mice model. This study is the first to delineate the role of aggrephagy regulators-mediated intercellular communication of the TME in regulating OC growth and antitumor immunomodulation.

Notably, post-surgical declines in KIAA1841 and TUBA1B levels were observed. Our findings highlight the clinical relevance of metabolic syndrome-related genes in HCC, linking them to prognosis, tumor microenvironment remodeling, cancer stemness, and immunotherapy response.

Both sets showed a promising clinical prediction value. In sum, this study preliminarily revealed the landscape of the TME in HR-NB at a single-cell level; several TME cell clusters that could inhibit immune activities or promote tumor progression in HR-NB were determined, thereby providing novel immunotherapeutic targets and an immune-related prognostic signature for HR-NB and promoting the development of immunotherapy of HR-NB.

We further devised a simply digital PCR method for feasible quantifying the 7-gene signature, which still significantly differentiated the survival of MM patients and possesses considerable clinical application value. Overall, this integrated risk-scoring model derived from scRNA-seq data was significantly associated with a more advanced stage of myeloma patients, facilitating guided risk-adapted treatment strategies for such ultra-high-risk patients.

Our study identified a two-gene prognostic signature based on NK cell markers and highlighted their role in the TME, which may offer novel insights in immunotherapy strategies. Additionally, we developed an accurate and reliable prognostic model, combining clinical factors to aid clinicians in decision-making.

TUBA1B was shown to influence glioma cell proliferation, migration, invasion, and autophagy, impacting tumor progression and treatment response through intercellular communication and metabolic pathways. The study demonstrates that high TUBA1B expression is closely associated with glioma malignancy and poor prognosis, making it a potential therapeutic target.

Elevated TUBA1B levels are associated with an immunosuppressive tumor microenvironment, impacting cancer progression and treatment outcomes. Targeting TUBA1B may offer promising therapeutic avenues for enhancing cancer treatment, offering new perspectives for innovative anti-tumor strategies with high clinical impact.

Subsequently, the direct interaction between AA and TUBA1B was verified by surface plasmon resonance, pull-down and cellular thermal shift experiments, drug affinity responsive target stability assay, and molecular docking. This research will offer fresh perspectives on how AA prevents liver cancer at the molecular level.

Cases with both high-risk features had significantly poorer survival. This study expands the literature database of GLI1-altered mesenchymal tumors and identifies features which can be used for risk stratification.

This study marks an initial foray into understanding how AA-associated processes may potentiate the TME and weaken immune function. Our findings provide insights into the complex dynamics of the TME and highlight potential targets for therapeutic intervention, suggesting a key role for AA in the advancement of colorectal cancer.

Our study establishes a precise single-cell atlas of breast cancer TAMs, shedding light on their multifaceted roles in tumor biology and providing resources for targeting TAMs in breast cancer immunotherapy.

In summary, the findings of this novel study indicated that EGCG promotes apoptosis of MM cells, both via activation of the ER stress pathway and disruption of cytoskeletal integrity. These findings highlight the multi-faceted anti-tumor effects of EGCG and its potential clinical application in MM treatment.