铜死亡在口腔鳞状细胞癌治疗及预后中的研究进展

doi:10.13591/j.cnki.kqyx.2024.11.014

摘要/Abstract

摘要：

口腔鳞状细胞癌(oral squamous cell carcinoma,OSCC)是一种死亡率高的恶性肿瘤,其特点是诊断晚、复发转移率高、预后差。铜死亡(cuproptosis)作为一种新型的铜诱导细胞死亡的模式,激活相关通路能抑制癌细胞的生长和增殖,诱导癌细胞发生铜死亡为OSCC的治疗提供了新的见解。本综述旨在系统介绍铜死亡发生发展的机制以及铜死亡在OSCC治疗预后方面的研究进展,为临床治疗提供新的思路和方法。

关键词: 口腔鳞状细胞癌, 铜死亡, 铁氧还蛋白1, 蛋白质脂质, 铜螯合物, lncRNA, 三羧酸循环

Abstract:

Oral squamous cell carcinoma(OSCC)is a malignant tumor with a high mortality rate, which is characterized by late diagnosis, high recurrence and metastasis rates, and poor prognosis. Cuproptosis, as a novel mode of cupric induced cell death, can inhibit the growth and proliferation of cancer cells by activating related pathways, which provides a new insight into the treatment of OSCC. This review aims to systematically introduce the mechanism of cuproptosis occurrence and development, as well as the research progress of cuproptosis in the prognosis of OSCC treatment. It provides new ideas and methods for clinical treatment.

Key words: oral squamous cell carcinoma, cuproptosis, ferredoxin 1, protein lipids, copper chelates, lncRNA, tricarboxylic acid cycle

中图分类号:

R780.2

要甜, 马宇锋. 铜死亡在口腔鳞状细胞癌治疗及预后中的研究进展[J]. 口腔医学, 2024, 44(11): 871-875.

YAO Tian, MA Yufeng. Research progress of cuproptosis in the treatment and prognosis of oral squamous cell carcinoma[J]. Stomatology, 2024, 44(11): 871-875.

图/表 1

参考文献 45

[1]	Tsvetkov P, Detappe A, Cai K, et al. Mitochondrial metabolism promotes adaptation to proteotoxicstress[J]. Nat Chem Biol, 2019, 15(7): 681-689. doi: 10.1038/s41589-019-0291-9 pmid: 31133756
[2]	Li ZL, Cai H, Li ZQ, et al. A tumor cell membrane-coated self-amplified nanosystem as a nanovaccine to boost the therapeutic effect of anti-PD-L1 antibody[J]. Bioact Mater, 2022, 21: 299-312.
[3]	Del Re DP, Amgalan D, Linkermann A, et al. Fundamental mechanisms of regulated cell death and implications for heart disease[J]. Physiol Rev, 2019, 99(4): 1765-1817. doi: 10.1152/physrev.00022.2018 pmid: 31364924
[4]	Tang DL, Kang R, Berghe TV, et al. The molecular machinery of regulated cell death[J]. Cell Res, 2019, 29(5): 347-364. doi: 10.1038/s41422-019-0164-5 pmid: 30948788
[5]	Vitório JG, Duarte-Andrade FF, Dos Santos Fontes Pereira T, et al. Metabolic landscape of oral squamous cell carcinoma[J]. Metabolomics, 2020, 16(10): 105. doi: 10.1007/s11306-020-01727-6 pmid: 33000429
[6]	Ge EJ, Bush AI, Casini A, et al. Connecting copper and cancer: From transition metal signalling to metalloplasia[J]. Nat Rev Cancer, 2022, 22(2): 102-113.
[7]	Cobine PA, Brady DC. Cuproptosis: Cellular and molecular mechanisms underlying copper-induced cell death[J]. Mol Cell, 2022, 82(10): 1786-1787. doi: 10.1016/j.molcel.2022.05.001 pmid: 35594843
[8]	Tsvetkov P, Coy S, Petrova B, et al. Copper induces cell death by targeting lipoylated TCA cycle proteins[J]. Science, 2022, 375(6586): 1254-1261. doi: 10.1126/science.abf0529 pmid: 35298263
[9]	Tang DL, Chen X, Kroemer G. Cuproptosis: A copper-triggered modality of mitochondrial cell death[J]. Cell Res, 2022, 32(5): 417-418. doi: 10.1038/s41422-022-00653-7 pmid: 35354936
[10]	Duan WJ, He RR. Cuproptosis: Copper-induced regulated cell death[J]. Sci China Life Sci, 2022, 65(8): 1680-1682.
[11]	Zhao JN, Guo SC, Schrodi SJ, et al. Cuproptosis and cuproptosis-related genes in rheumatoid arthritis: Implication, prospects, and perspectives[J]. Front Immunol, 2022, 13: 930278.
[12]	黄本林, 付瑞, 王宁, 等. 铜死亡与肿瘤的关系研究进展[J]. 临床误诊误治, 2022, 35(11): 112-116.
[13]	Zanoni DK, Montero PH, Migliacci JC, et al. Survival outcomes after treatment of cancer of the oral cavity(1985—2015)[J]. Oral Oncol, 2019, 90: 115-121.
[14]	Parke SC, Langelier DM, Cheng JT, et al. State of rehabilitation research in the head and neck cancer population: Functional impact vs. impairment-focused outcomes[J]. Curr Oncol Rep, 2022, 24(4): 517-532. doi: 10.1007/s11912-022-01227-x pmid: 35182293
[15]	Sha SN, Si LY, Wu XR, et al. Prognostic analysis of cuproptosis-related gene in triple-negative breast cancer[J]. Front Immunol, 2022, 13: 922780.
[16]	Song Q, Zhou R, Shu FP, et al. Cuproptosis scoring system to predict the clinical outcome and immune response in bladder cancer[J]. Front Immunol, 2022, 13: 958368.
[17]	Shan JS, Geng R, Zhang Y, et al. Identification of cuproptosis-related subtypes, establishment of a prognostic model and tumor immune landscape in endometrial carcinoma[J]. Comput Biol Med, 2022, 149: 105988.
[18]	Li YQ. Copper homeostasis: Emerging target for cancer treatment[J]. IUBMB Life, 2020, 72(9): 1900-1908.
[19]	Babak MV, Ahn D. Modulation of intracellular copper levels as the mechanism of action of anticancer copper complexes: Clinical relevance[J]. Biomedicines, 2021, 9(8): 852.
[20]	Guo F, Yang Z, Kulbe H, et al. Inhibitory effect on ovarian cancer ALDH+ stem-like cells by Disulfiram and Copper treatment through ALDH and ROS modulation[J]. Biomed Pharmacother, 2019, 118: 109371.
[21]	Xiong K, Zhou Y, Karges J, et al. Autophagy-dependent apoptosis induced by apoferritin-Cu(Ⅱ) nanoparticles in multidrug-resistant colon cancer cells[J]. ACS Appl Mater Interfaces, 2021, 13(33): 38959-38968.
[22]	Machado JF, Sequeira D, Marques F, et al. New copper(I)complexes selective for prostate cancer cells[J]. Dalton Trans, 2020, 49(35): 12273-12286. doi: 10.1039/d0dt02157a pmid: 32839796
[23]	Chen SY, Chang YL, Liu ST, et al. Differential cytotoxicity mechanisms of copper complexed with disulfiram in oral cancer cells[J]. Int J Mol Sci, 2021, 22(7): 3711.
[24]	Kahlson MA, Dixon SJ. Copper-induced cell death[J]. Science, 2022, 375(6586): 1231-1232. doi: 10.1126/science.abo3959 pmid: 35298241
[25]	林锦贤, 王攀, 吴欣谋, 等. 铜稳态失调诱导调节性细胞死亡及其调控的研究进展[J]. 江苏大学学报(医学版), 2022, 32(4): 306-317.
[26]	Thongnuanjan P, Soodvilai S, Chatsudthipong V, et al. Fenofibrate reduces cisplatin-induced apoptosis of renal proximal tubular cells via inhibition of JNK and p38 pathways[J]. J ToxicolSci, 2016, 41(3): 339-349.
[27]	Ryumon S, Okui T, Kunisada Y, et al. Ammonium tetrathiomolybdate enhances the antitumor effect of cisplatin via the suppression of ATPase copper transporting beta in head and neck squamous cell carcinoma[J]. Oncol Rep, 2019, 42(6): 2611-2621. doi: 10.3892/or.2019.7367 pmid: 31638244
[28]	Xiong C, Ling H, Hao Q, et al. Cuproptosis: P53-regulated metabolic cell death?[J]. Cell Death Differ, 2023, 30(4): 876-884.
[29]	Suzuki S, Tanaka T, Poyurovsky MV, et al. Phosphate-activated glutaminase(GLS2), a p53-inducible regulator of glutamine metabolism and reactive oxygen species[J]. Proc Natl Acad Sci USA, 2010, 107(16): 7461-7466.
[30]	Tajan M, Hock AK, Blagih J, et al. A role for p53 in the adaptation to glutamine starvation through the expression of SLC1A3[J]. Cell Metab, 2018, 28(5): 721-736, e6. doi: S1550-4131(18)30448-0 pmid: 30122553
[31]	Chung CYS, Posimo JM, Lee SM, et al. Activity-based ratiometric FRET probe reveals oncogene-driven changes in labile copper pools induced by altered glutathione metabolism[J]. Proc Natl Acad Sci USA, 2019, 116(37): 18285-18294.
[32]	Jiang L, Kon N, Li TY, et al. Ferroptosis as a p53-mediated activity during tumour suppression[J]. Nature, 2015, 520(7545): 57-62.
[33]	Miller KD, Nogueira L, Mariotto AB, et al. Cancer treatment and survivorship statistics, 2019[J]. CA Cancer J Clin, 2019, 69(5): 363-385.
[34]	Bugshan A, Farooq I. Oral squamous cell carcinoma: Metastasis, potentially associated malignant disorders, etiology and recent advancements in diagnosis[J]. F1000 Research, 2020, 9: 229.
[35]	Wan LL, Gu DS, Li PZ. LncRNA SNHG16 promotes proliferation and migration in laryngeal squamous cell carcinoma via the miR-140-5p/NFAT5/Wnt/β-catenin pathway axis[J]. Pathol Res Pract, 2022, 229: 153727.
[36]	Yang LQ, Yu JL, Tao L, et al. Cuproptosis-related lncRNAs are biomarkers of prognosis and immune microenvironment in head and neck squamous cell carcinoma[J]. Front Genet, 2022, 13: 947551.
[37]	Zhou LQ, Shen JX, Zhou JY, et al. The prognostic value of m6A-related LncRNAs in patients with HNSCC: Bioinformatics analysis of TCGA database[J]. Sci Rep, 2022, 12(1): 579.
[38]	Li JF, Chen SY, Liao YX, et al. Arecoline is associated with inhibition of cuproptosis and proliferation of cancer-associated fibroblasts in oral squamous cell carcinoma: A potential mechanism for tumor metastasis[J]. Front Oncol, 2022, 12: 925743.
[39]	Roma-Rodrigues C, Mendes R, Baptista PV, et al. Targeting tumor microenvironment for cancer therapy[J]. Int J Mol Sci, 2019, 20(4): 840.
[40]	Pilankar A, Singhavi H, Raghuram GV, et al. A pro-oxidant combination of resveratrol and copper down-regulates hallmarks of cancer and immune checkpoints in patients with advanced oral cancer: Results of an exploratory study(RESCU 004)[J]. Front Oncol, 2022, 12: 1000957.
[41]	Pal K, Raghuram GV, Dsouza J, et al. A pro-oxidant combination of resveratrol and copper down-regulates multiple biological hallmarks of ageing and neurodegeneration in mice[J]. Sci Rep, 2022, 12(1): 17209. doi: 10.1038/s41598-022-21388-w pmid: 36241685
[42]	Gong J, Chehrazi-Raffle A, Reddi S, et al. Development of PD-1 and PD-L1 inhibitors as a form of cancer immunotherapy: A comprehensive review of registration trials and future considerations[J]. J Immunother Cancer, 2018, 6(1): 8. doi: 10.1186/s40425-018-0316-z pmid: 29357948
[43]	Li XG, Zhou WB, Zhu C, et al. Multi-omics analysis reveals prognostic and therapeutic value of cuproptosis-related lncRNAs in oral squamous cell carcinoma[J]. Front Genet, 2022, 13: 984911.
[44]	Patel SP, Kurzrock R. PD-L1 expression as a predictive biomarker in cancer immunotherapy[J]. Mol Cancer Ther, 2015, 14(4): 847-856. doi: 10.1158/1535-7163.MCT-14-0983 pmid: 25695955
[45]	Voli F, Valli E, Lerra L, et al. Intratumoral copper modulates PD-L1 expression and influences tumor immune evasion[J]. Cancer Res, 2020, 80(19): 4129-4144. doi: 10.1158/0008-5472.CAN-20-0471 pmid: 32816860