Roles of kinesin superfamily proteins in colorectal cancer carcinogenesis (Review)

Abstract

Colorectal cancer (CRC), a commonly occurring carcinoma, now ranks the second in terms of cancer‑associated deaths around the world. Among the numerous factors that contribute to CRC tumor progression, a class of motor proteins known as the kinesins has been found to play a vital role. Kinesins are responsible for the intracellular trafficking of functional proteins, organelles and biomacromolecules along microtubules. Dysregulation of kinesins has been revealed to influence the cell cycle to cause abnormal cell growth and affect cell adhesion to promote epithelial‑mesenchymal transition in breast, bladder, ovarian and prostate cancer. Studies on the function of kinesins in CRC have also been performed, although, to the best of our knowledge, little is known about the underlying mechanisms of kinesins in CRC progression. The present review outlines the roles played by different kinesins in CRC carcinogenesis, mainly discussing the most studied subfamilies (kinesin 3‑6, 8, 10, 11 and 13), This review aims to illustrate the functions of kinesins in CRC cell growth, cancer metastasis and chemoresistance to provide insights regarding kinesins as potential targets for determining CRC prognosis and selecting therapy.