Research Progress of Glycolytic Reprogramming in Oral Squamous Cell Carcinoma
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摘要: 口腔鳞状细胞癌(oral squamous cell carcinoma,OSCC)是口腔颌面部最常见的恶性肿瘤,发病率高且预后不佳。癌细胞通过糖酵解代谢重编程改变代谢方式,以支持其对ATP需求的增加。糖酵解重编程介导了包括口腔鳞状细胞癌在内的多系统肿瘤的发生发展,其中涉及多个信号通路和关键因子。总结OSCC中发生的糖酵解代谢改变、关键因子及临床诊治潜能,综述其在口腔鳞状细胞癌中的作用,以期为研究者提供新的研究方向和思路。Abstract: Oral squamous cell carcinoma (OSCC) is the most common malignant tumor in the oral and maxillofacial region with high incidence and poor prognosis. Cancer cells change their metabolism through glycolytic metabolic reprogramming to support their increased demand for ATP. Glycolytic reprogramming mediates the development of multisystem tumors, including oral squamous cell carcinoma, involving multiple signaling pathways and key factors. In this paper, the changes of glycolytic metabolism, key factors and potential clinical diagnostic and theraputic approches of OSCC are summarized, and the role of OSCC in oral squamous cell carcinoma is reviewed in order to provide new research directions and ideas.
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[1] Chi A C,Day T A,Neville B W. Oral cavity and oropharyngeal squamous cell carcinoma-an update[J]. CA:A Cancer Journal for Clinicians,2015,65(5):401-421. doi: 10.3322/caac.21293 [2] Romero-Garcia S,Lopez-Gonzalez J S,Báez-Viveros J L,et al. Tumor cell metabolism: an integral view[J]. Cancer Biol Ther,2011,12(11):939-948. doi: 10.4161/cbt.12.11.18140 [3] Warburg O,Posener K,Negelein E. On the metabolism of carcinoma cells[J]. Biochemische Zeitschrift,1924,152:309-344. [4] Wang Y,Xia Y,Lu Z. Metabolic features of cancer cells[J]. Cancer Communications (London,England),2018,38(1):65. doi: 10.1186/s40880-018-0335-7 [5] Ghanavat M,Shahrouzian M,Deris Zayeri Z,et al. Digging deeper through glucose metabolism and its regulators in cancer and metastasis[J]. Life Sci,2021,264:118603. doi: 10.1016/j.lfs.2020.118603 [6] Somashekar B S,Kamarajan P,Danciu T,et al. Magic angle spinning NMR-based metabolic profiling of head and neck squamous cell carcinoma tissues[J]. Journal of Proteome Research,2011,10(11):5232-5241. doi: 10.1021/pr200800w [7] Boffetta P,Hashibe M. Alcohol and cancer[J]. The Lancet Oncology,2006,7(2):149-156. doi: 10.1016/S1470-2045(06)70577-0 [8] Nguyen A, Kim A H, Kang M K, et al. Chronic alcohol exposure promotes cancer stemness and glycolysis in oral/oropharyngeal squamous cell carcinoma cell lines by activating NFAT signaling [J]. International Journal of Molecular Sciences, 2022, 23(17): 9779. [9] Zhou X,Xue D,Qiu J. Identification of biomarkers related to glycolysis with weighted gene co-expression network analysis in oral squamous cell carcinoma[J]. Head and Neck-Journal for the Sciences and Specialties of the Head and Neck,2022,44(1):89-103. [10] Robey R B,Hay N. Is AKT the “Warburg kinase”?-AKT-energy metabolism interactions and oncogenesis[J]. Seminars in cancer biology,2009,19(1):25-31. doi: 10.1016/j.semcancer.2008.11.010 [11] Marquard F, Jücker M J B P. PI3K/AKT/mTOR signaling as a molecular target in head and neck cancer [J]. 2020, 172: 113729. [12] Raggi C,Taddei M L,Rae C,et al. Metabolic reprogramming in cholangiocarcinoma[J]. J Hepatol,2022,77(3):849-864. doi: 10.1016/j.jhep.2022.04.038 [13] Tang Y C,Hsiao J R,Jiang S S,et al. c-MYC-directed NRF2 drives malignant progression of head and neck cancer via glucose-6-phosphate dehydrogenase and transketolase activation[J]. Theranostics,2021,11(11):5232-5247. doi: 10.7150/thno.53417 [14] Wang L W,Yu Y,Chen J,et al. Protein kinase D1 regulates the growth and metabolism of oral squamous carcinoma cells in tumor microenvironment[J]. West China Journal of Stomatology,2019,37(6):577-582. [15] Chen J,Cui B,Fan Y,et al. Protein kinase D1 regulates hypoxic metabolism through HIF-1 and glycolytic enzymes incancer cells[J]. Oncology Reports,2018,40(2):1073-1082. [16] Fu L,Pelicano H,Liu J,et al. The circadian gene Period2 plays an important role in tumor suppression and DNA damage response in vivo[J]. Cell,2002,111(1):41-50. doi: 10.1016/S0092-8674(02)00961-3 [17] Zheng B,Larkin D W,Albrecht U,et al. The mPer2 gene encodes a functional component of the mammalian circadian clock[J]. Nature,1999,400(6740):169-173. doi: 10.1038/22118 [18] Long W, Gong X, Yang Y, et al. Downregulation of PER2 promotes tumor progression by enhancing glycolysis via the phosphatidylinositol 3-kinase/Protein kinase B pathway in oral squamous cell carcinoma [J]. Journal of Oral and Maxillofacial Surgery, 2020, 78(10): 10. [19] Zheng M,Cao M X,Yu X H,et al. STAT3 promotes invasion and aerobic glycolysis of human oral squamous cell carcinoma via inhibiting foxO1[J]. Front Oncol,2019,9:1175. doi: 10.3389/fonc.2019.01175 [20] Grimm M, Cetindis M, Lehmann M, et al. Association of cancer metabolism-related proteins with oral carcinogenesis - indications for chemoprevention and metabolic sensitizing of oral squamous cell carcinoma? [J]. Journal of Translational Medicine, 2014, 12: 208. [21] Brizel D M,Schroeder T,Scher R L,et al. Elevated tumor lactate concentrations predict for an increased risk of metastases in head-and-neck cancer[J]. International Journal of Radiation Oncology Biology Physics,2001,51(2):349-353. doi: 10.1016/S0360-3016(01)01630-3 [22] Wang Y,Zhang X,Zhang Y,et al. Overexpression of pyruvate kinase M2 associates with aggressive clinicopathological features and unfavorable prognosis in oral squamous cell carcinoma[J]. Cancer Biology & Therapy,2015,16(6):839-845. [23] Yang W,Xia Y,Hawke D,et al. PKM2 Phosphorylates Histone H3 and Promotes Gene Transcription and Tumorigenesis[J]. Cell,2014,158(5):1210. [24] Kurihara-shimomura M, Sasahira T, Nakashima C, et al. The multifarious functions of pyruvate kinase M2 in oral cancer cells [J]. International Journal of Molecular Sciences, 2018, 19(10): 2907. [25] Cai H, Li J, Zhang Y, et al. LDHA promotes oral squamous cell carcinoma progression through facilitating glycolysis and epithelial-mesenchymal transition[J]. Frontiers in Oncology, 2019, 9: 1446. [26] Yuan C,Li Z,Wang Y,et al. Overexpression of metabolic markers PKM2 and LDH5 correlates with aggressive clinicopathological features and adverse patient prognosis in tongue cancer[J]. Histopathology,2014,65(5):595-605. doi: 10.1111/his.12441 [27] Wigfield S M,Winter S C,Giatromanolaki A,et al. PDK-1 regulates lactate production in hypoxia and is associated with poor prognosis in head and neck squamous cancer[J]. British Journal of Cancer,2008,98(12):1975-1984. doi: 10.1038/sj.bjc.6604356 [28] Pai S, Yadav V K, Kuo K T, et al. PDK1 inhibitor BX795 improves cisplatin and radio-efficacy in oral squamous cell carcinoma by downregulating the PDK1/CD47/Akt-mediated glycolysis signaling pathway[J]. International Journal of Molecular Sciences, 2021, 22(21): 11492. [29] Guo D,Tong Y,Jiang X,et al. Aerobic glycolysis promotes tumor immune evasion by hexokinase2-mediated phosphorylation of IκBα[J]. Cell Metabolism,2022,34(9):1312-24.e6. doi: 10.1016/j.cmet.2022.08.002 [30] Patra K C,Wang Q,Bhaskar P T,et al. Hexokinase 2 is required for tumor initiation and maintenance and its systemic deletion is therapeutic in mouse models of cancer[J]. Cancer Cell,2013,24(2):213-228. doi: 10.1016/j.ccr.2013.06.014 [31] Christison T, Wang J, Huang Y, et al. Profiling anionic polar metabolites in oral cancer using capillary ion chromatography and high resolution accurate mass spectrometry [J]. Abstracts of Papers of the American Chemical Society, 2015, 249: 49. [32] Wang L, Wang J, Shen Y, et al. Fructose-1, 6-bisphosphatase 2 inhibits oral squamous cell carcinoma tumorigenesis and glucose metabolism via downregulation of c-myc[J]. Oxidative Medicine and Cellular Longevity, 2022, 2022. [33] Simoes-sousa S,Granja S,Pinheiro C,et al. Prognostic significance of monocarboxylate transporter expression in oral cavity tumors[J]. Cell Cycle,2016,15(14):1865-1873. doi: 10.1080/15384101.2016.1188239 [34] Nakazato K,Mogushi K,Kayamori K,et al. Glucose metabolism changes during the development and progression of oral tongue squamous cell carcinomas[J]. Oncology Letters,2019,18(2):1372-1380. [35] Gholami S,Chamorro-petronacci C,Pérez-sayáns M,et al. Immunoexpression profile of hypoxia-inducible factor (HIF) targets in potentially malignant and malignant oral lesions: a pilot study[J]. Journal of Applied Oral Science:Revista FOB,2023,31:e20220461. doi: 10.1590/1678-7757-2022-0461 [36] Chang Y C, Chi L H, Chang W M, et al. Glucose transporter 4 promotes head and neck squamous cell carcinoma metastasis through the TRIM24-DDX58 axis [J]. Journal of Hematology & Oncology, 2017, 10(1): 11. [37] Zhang Y,Cai H,Liao Y,et al. Activation of PGK1 under hypoxic conditions promotes glycolysis and increases stem cell-like properties and the epithelial-mesenchymal transition in oral squamous cell carcinoma cells via the AKT signalling pathway[J]. International Journal of Oncology,2020,57(3):743-755. doi: 10.3892/ijo.2020.5083 [38] Nakashima C,Yamamoto K,Fujiwara-tani R,et al. Expression of cytosolic malic enzyme (ME1) is associated with disease progression in human oral squamous cell carcinoma[J]. Cancer Science,2018,109(6):2036-2045. doi: 10.1111/cas.13594 [39] Li Y J,Huang T H,Hsiao M,et al. Suppression of fructose-bisphosphate aldolase C expression as a predictor of advanced oral squamous cell carcinoma[J]. Head and Neck-Journal for the Sciences and Specialties of the Head and Neck,2016,38:E1075-E85. [40] Wilde L,Roche M,Domingo-vidal M,et al. Metabolic coupling and the Reverse Warburg Effect in cancer: Implications for novel biomarker and anticancer agent development[J]. Seminars in Oncology,2017,44(3):198-203. doi: 10.1053/j.seminoncol.2017.10.004 [41] Muhammad S N H, Safuwan N A M, Yaacob N S, et al. Regulatory mechanism on anti-Glycolytic and anti-metastatic activities induced by strobilanthes crispus in breast cancer, in vitro [J]. Pharmaceuticals (Basel, Switzerland), 2023, 16(2): 153. [42] Bai R, Meng Y, Cui J. Therapeutic strategies targeting metabolic characteristics of cancer cells [J]. Critical Reviews in Oncology/Hematology, 2023, 104037. [43] Samuel S M,Varghese E,Satheesh N J,et al. Metabolic heterogeneity in TNBCs: A potential determinant of therapeutic efficacy of 2-deoxyglucose and metformin combinatory therapy[J]. Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie,2023,164:114911. [44] Huang G, Chen S, Washio J, et al. Glycolysis-related gene analyses indicate that DEPDC1 promotes the malignant progression of oral squamous cell carcinoma via the WNT/β-catenin signaling pathway[J]. International Journal of Molecular Sciences, 2023, 24(3): 1992. [45] Liu X, Zhao T, Yuan Z, et Al. MIR600HG sponges miR-125a-5p to regulate glycometabolism and cisplatin resistance of oral squamous cell carcinoma cells via mediating RNF44 [J]. Cell Death Discovery, 2022, 8(1): 216. [46] Li M, Gao F, Zhao Q, et al. Tanshinone IIA inhibits oral squamous cell carcinoma via reducing AKT-c-MYC signaling-mediated aerobic glycolysis [J]. Cell Death & Disease, 2020, 11(5): 381. [47] Wei J, Wu J, Xu W, et al. Salvanic acid B inhibits glycolysis in oral squamous cell carcinoma via targeting PI3K/AKT/HIF-1 alpha signaling pathway [J]. Cell Death & Disease, 2018, 9: 599. [48] Wei J,Xie G,Ge S,et al. Metabolic transformation of DMBA-induced carcinogenesis and inhibitory effect of salvianolic acid B and breviscapine treatment[J]. Journal of Proteome Research,2012,11(2):1302-1316. doi: 10.1021/pr2009725 [49] Lee N, Jang W J, Seo J H, et al. 2-Deoxy-d-Glucose-Induced Metabolic Alteration in Human Oral Squamous SCC15 Cells: Involvement of N-Glycosylation of Axl and Met [J]. Metabolites, 2019, 9(9): 3515-3524. [50] Lin C X,Tu C W,Ma Y K,et al. Nobiletin inhibits cell growth through restraining aerobic glycolysis via PKA-CREB pathway in oral squamous cell carcinoma[J]. Food Science & Nutrition,2020,8(7):3515-3524. [51] Zhang G,Fu J,Su Y,et al. Opposite effects of garcinol on tumor energy metabolism in oral squamous cell carcinoma cells[J]. Nutrition and Cancer-an International Journal,2019,71(8):1403-1411. doi: 10.1080/01635581.2019.1607409 [52] Sur S, Nakanishi H, Flaveny C, et al. Inhibition of the key metabolic pathways, glycolysis and lipogenesis, of oral cancer by bitter melon extract [J]. Cell Communication and Signaling, 2019, 17(1): 131. [53] Kawata M,Ogi K,Nishiyama K,et al. Additive effect of radiosensitization by 2-deoxy-D-glucose delays DNA repair kinetics and suppresses cell proliferation in oral squamous cell carcinoma[J]. Journal of Oral Pathology & Medicine,2017,46(10):979-985.
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