Research progress in the role of FBXW7 in drug resistance against non-small cell lung cancer

Abstract

Non-small cell lung cancer (NSCLC) is one of the most common malignant tumors in the world. NSCLC shows serious effect on prognosis for drug resistance, and it is necessary to study the molecular mechanism for drug resistance in NSCLC. Ubiquitin-proteasome system (UPS) can regulate some important cellular processes by degrading short-term protein, and the abnormal expression is closely related to the occurrence, development and prognosis of tumor. The F-box family protein is an important component of the ubiquitin proteasome, such as cycle regulation, transcriptional regulation, signal transduction, apoptosis and differentiation. F-box and WD-40 domain protein 7 (FBXW7) is just the classic protein components among F-box family protein. Studies have shown that FBXW7 is related to drug resistance in NSCLC. The main mechanism is that FBXW7 mutation leads to drug resistance by reducing ubiquitination and degradation of its downstream proteins, including Snail protein, myeloid cell leukemia sequence 1 (MCL-1), mammalian target of rapamycin (mTOR), and coiled-coil-domain containing 6 (CCDC6). Rapamycin, histone deacetylase inhibitor MS-275, and rabdosia are effective in drug-resistant NSCLC patients with FBXW7 mutation.