Kinesin family member 14 in digestive tract malignancies: Oncogenic mechanisms, clinical implications, and therapeutic prospects

Table 1 Mechanisms of Kinesin family member 14 in different cancer types

Cancer types	Related proteins, factors and signaling pathways	Related tumor cell proliferation, migration, apoptosis and so on	Representatives of relevant tumor resistance	Ref.
Endometrial cancer	After KIF14 was silenced, the expression of KI-67 protein decreased, while the expression levels of Bax and cleaved-caspase-3 increased	After KIF14 was silenced, the number of cervical cancer resistant cell lines Ishikawa/DDP increased and apoptosis decreased	Silencing KIF14 can inhibit the proliferation of Ishikawa/DDP resistant endometrial cancer cells, promote apoptosis and increase their sensitivity to cisplatin	[39]
Breast cancer	KIF14 high expression promotes AKT pathway phosphorylation	Promote MDA-MB-231 cell proliferation, migration and inhibition of apoptosis	KIF14 high expression increases docetaxel resistance in chemotherapy	[40]
Prostatic cancer	The high expression of KIF14 promotes the phosphorylation of downstream AKT pathway	To be verified	The high expression of KIF14 promoted the drug resistance of DU145/DTX50 and PC-3/DTX30 cells to cabazitaxel-doxorubicin	[41]
Lung cancer	Recruit the adhesion molecules CDH11 and MCAM to the cell membrane	Promote the adhesion, migration, and invasion of CL1-5 and A549 cells	To be verified	[42]
Glioblastoma human	Silencing KIF14 inhibited AKT phosphorylation (S473 and T308 sites) and increased the expression of apoptotic proteins caspase-3 and PARP	Silence KIF14 inhibited the proliferation and migration of U251 glioblastoma cells and promoted apoptosis	To be verified	[43]

KIF14: Kinesin family member 14.