Furthermore, we propose that targeting FBPs might be a promising strategy to overcome drug resistance and achieve better treatment outcome in cancer patients. Therefore, in this review, we describe the functions of FBPs that are involved in drug resistance and discuss how FBPs contribute to the development of cancer drug resistance. Recently, F-box protein (FBPs), key subunits in Skp1-Cullin1-F-box protein (SCF) E3 ligase complexes, have been found to play critical roles in carcinogenesis, tumor progression, and drug resistance through degradation of their downstream substrates. Although increased evidence has revealed that reduced drug uptake, increased drug efflux, drug target protein alterations, drug sequestration in organelles, enhanced drug metabolism, impaired DNA repair systems, and anti-apoptotic mechanisms, are critically involved in drug resistance, the detailed resistance mechanisms have not been fully elucidated in distinct cancers. Thus, overcoming drug resistance is pivotal to achieve enhanced therapy efficacy in various cancers. However, the frequent emergence of chemoresistance compromises chemotherapy efficacy leading to poor prognosis. Chemotherapy continues to be a major treatment strategy for various human malignancies.
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