5-Fluorouracil (5-FU) resistance and the new strategy to enhance the sensitivity against cancer: Implication of DNA repair inhibition - 19/03/21
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Graphical abstract |
Highlights |
• | Primary cause of 5-FU resistance has been attributed to presence of cancer stem like cells (CSCs) within the cancer cells niche. |
• | 5-FU in combination with other therapeutic agents are known to increase the drug response rates. |
• | Novel agent which will inhibit DNA repair and increase DNA damage simultaneously can lead to CSCs death and increase the 5 FU sensitivity. |
• | Targeted therapy using Nanoparticles (NPs) and down regulation of MDR proteins using drug reversal agent or MDR modulators improves 5-FU therapy. |
Abstract |
5-Fluorouracil (5-FU) has been an important anti-cancer drug to date. With an increase in the knowledge of its mechanism of action, various treatment modalities have been developed over the past few decades to increase its anti-cancer activity. But drug resistance has greatly affected the clinical use of 5-FU. Overcoming this chemoresistance is a challenge due to the presence of cancer stem cells like cells, cancer recurrence, metastasis, and angiogenesis. In this review, we have systematically discussed the mechanism of 5-FU resistance and advent strategies to increase the sensitivity of 5-FU therapy including resistance reversal. Special emphasis has been given to the cancer stem cells (CSCs) mediated 5-FU chemoresistance and its reversal process by different approaches including the DNA repair inhibition process.
Le texte complet de cet article est disponible en PDF.Abbreviations : 5-FU, CSCs, TS, TME, ABC, MDR, NPs, FBAL, FUPA, DPD, CH2THF, CRC, CC, MTX, LV, FdUMP, FdUDP, FdUTP, dTMP, MTHFR, OPR, RNR, PRPP, TK, TP, UK, UP, CDA, CES, CYP2A6, DHP, BUP-1, TPI, VNTR, 5’UTR, SNP, OS, DFS, hENT1, PKM1, BHB, EMT, OCR, ECAR, RanBPM, EIF5A2, TFAP2C, GPC4, PRC1, KAP1, NRF2, KCTD12, ET-1, β-arr1, AQP1, APCA, EC, HMVEC, NgBR, NSCLC, MKNK1, MDSCs, HR, NHEJ, BER, APC, DRI, UDG, FANCJ, 4-AAQB, NQC, TTR, APN, BCNU, MAP2K1, MSNs, PARP, CICs, ESCC
Keywords : 5-FU resistance, Cancer stemness, Angiogenesis, DNA repair, MDR modulators, Combination therapy
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