KIF26B (Kinesin Family Member 26B)

IL-6 also recruited DLAT to acetylate NSUN2 at K229 site and increased association affinity between NSUN2 and KIF26B. Together, these established a KIF26B/NSUN2/m5C/IL-6 positive feedback loop, suggesting that targeting KIF26B may be a promising therapeutic strategy for BCa.

Knockdown of kif26b blocks the proliferation, metastasis, and cisplatin resistance of bladder cancer cells...Additionally, phosphorylation of tyrosine 78 in TRAF2 is essential for its binding to KIF26B in response to Wnt3a signaling. Furthermore, a KIF26B/TRAF2/PD-L1 axis is identified in bladder cancer, and combined therapy of anti-B7-H3 antibody with kif26b knockdown yields superior anti-tumor effects.

AC105118.1 facilitates glycolysis and increases CRC cells' resistance to oxaliplatin by targeting the miR-378a-3p/KIF26B axis. The present work shed new insights into the function and mechanism of AC105118.1 in molecular function and suggested that the AC105118.1/miR-378a-3p/KIF26B axis is a promising target for intervening CRC oxaliplatin resistance.

The analyses of genetic status of patients with 25-genes model might improve the ability to predict the prognosis of patients with OC and help to select patients suit able to therapies. Immune-related gene GBP1P1 might serve as prognostic biomarker for OC.

Our findings suggest that KIF26B may play a role in the pathogenesis and progression of OSCC as an oncogene. This study establishes a foundation for the identification of potential therapeutic targets for OSCC.

KIF26B regulated M2 polarization of macrophage through activating CAFs, regulating the occurrence and metastasis of GC.

This study constructed a new cuproptosis-related gene signature that has a good prognostic capacity in assessing the outcome of OC patients. This study enhances our understanding of cuproptosis associated with ovarian cancer aggressiveness, cross-talk with immunocytes, and serves as a novel chemotherapy strategy.

The local infection or inflammation of ovarian may affect the immunity of OV. KIF26B and CREB3L1 are expected to be potential targets for the immunotherapy of OV.

For example, in basal-like breast cancer, we found four oncogenes (COPZ2, SF3B4, KRTCAP2 and POLR2J) and nine tumor suppressor genes (KIR2DL4, KIF26B, ARL15, ARHGAP25, EMCN, GMFG, TPK1, NR5A2 and TEK) containing a driver mutation in their promoter region, possibly explaining their deregulation. Moonlight2R is available at https://github.com/ELELAB/Moonlight2R.