KIF15 (Kinesin Family Member 15)

KIF15 knockdown may promote dendritic cell infiltration and function, thereby inducing CD8+ T cell recruitment. In summary, the immune microenvironment-derived TMEscore represents an independent prognostic biomarker in breast cancer, while KIF15 emerges as a crucial molecular determinant of its immunosuppressive niche.

In vitro experiments revealed that TOP2A knockdown inhibited the viability, migration, and invasion of LUAD cells. These findings may be provided a theoretical foundation for the discovery of biomarkers for prognostic prediction and diagnosis in LUAD.

Notably, frequent phosphorylation of S146 across cancer types points to a potential tumor-specific regulatory role. Together, these findings provide the first systems-level insight into the role of MAST3 in cytoskeletal regulation and disease relevance.

Author J. Han and J. Huang did not indicate their agreement with the retraction. Authors X. Sun, G. Diao, R. Li and J. Guo did not respond to communications from the Publisher regarding the retraction.

The combination treatment had an IC₅₀ of 78 µg/mL in A549 LC cells and significantly reduced cell proliferation, migration, and TOP2A gene expression, as assessed by MTT assay, wound healing assay, and RT-PCR. The results corroborate the computational predictions and support the utility of EGCG and hesperetin in targeting LC at the cellular level.

The study highlights the potential diagnostic and prognostic value of mitochondrial fission-related genes, particularly MTFP2, in prostate cancer and underscores the importance of further investigating these pathways as therapeutic targets.

New directions toward inhibiting activity or reducing the levels of KIF15 promise to restrict tumor growth, offering new hope for cancer treatment. This combined understanding of KIF15 functions stresses its importance not only in the fundamental processes of cell division but also in the developing field of cancer treatment, highlighting the ongoing necessity for extensive research into creating effective treatments targeted against KIF15 in oncology.

[This retracts the article DOI: 10.1155/2020/6403012.].

All eight genes showed evidence of protein expression in prostate cancers or cell lines. These potentially druggable targets associated with prostate cancer cell line dependency and worse clinical outcomes have also demonstrated literature support as potential targets, supporting further research into their potential clinical relevance as therapeutic targets in prostate cancer.

These findings identified ATR-I as a promising therapeutic drug for overcoming enzalutamide resistance in CRPC patients and increased our understanding about its antitumor mechanisms.

The increased expression of KIF15 was found to be associated with the progression of NPC and play a role in the development of radioresistance in NPC. Inhibiting KIF15 was shown to impede tumor growth and improve the sensitivity of NPC to radiotherapy by triggering autophagy via the STAT3/ATG7 pathway.

The tumorigenic function of KIF15 in GBM was regulated by REST in vitro and in vivo and the combinational treatment of cell cycle inhibitor Palbociclib with P300 HAT inhibitor inhibited GBM xenografts survival more significantly. Our findings indicate that KIF15 promotes GBM progression under the synergistic transactivation of REST and P300. P300/REST/KIF15 signaling axis is expected to be served as a cascade of candidate therapeutic targets in anti-GBM.