[an error occurred while processing this directive] | [an error occurred while processing this directive]
Effect of compound UC2288 on radiosensitivity of CNE-2R cell line and nude mouse transplanted tumor
Liang Renba1, Zhu Xiaodong1,2
1Department of Oncology, Wuming Hospital of Guangxi Medical University, Nanning 530021, China; 2Key Laboratory of Early Prevention and Treatment for Regional High-Incidence-Tumor, Guangxi MedicalUniversity, Ministry of Education, Nanning 530021, China
AbstractObjective To evaluate the effect of compound UC2288 on the radiosensitivity of CNE-2R cell line and nude mouse transplanted tumor. Methods The UC2288 concentration was referenced to previous experimental results (IC50=12.20μmol/L). The effect of UC2288 combined with 2,4,6,8Gy X-ray irradiation on the radiosensitivity of CNE-2R cell line was detected by clone formation experiment. The effect of UC2288 combined with 2,4,6,8Gy X-ray irradiation on the proliferation of CNE-2R cell line was determined by CCK8 assay. The nude mouse model of transplanted tumor was constructed with CNE-2R cell line. The radiosensitivity of transplanted tumor of UC2288 combined with 2Gy/fraction X-ray irradiation for three consecutive days was evaluated. Results The experimental concentration of UC2288 was 8μmol/L. The clonality of CNE-2R cell line was reduced under UC2288 combined with X-ray 2,4,6, and 8Gy irradiation, andthe radiosensitizationratio was 1.60. The proliferation of CNE-2R cell line was significantly decreased under UC2288 combined with X-ray 2,4,6, and 8Gy irradiation. UC2288 inhibited the growth of transplanted tumor in nude mice, and the inhibitory effect was strengthened with the extension of observation time, and the most obvious effect was observed at 16d.(P<0.01). Theradiosensitizationratio was 4.33. The proliferation of CNE-2R cell line was decreased under UC2288 combined with X-ray irradiation. Conclusion UC2288 can increase the radiosensitivity of nasopharyngeal carcinoma radioresistant cell line CNE-2R.
Liang Renba,Zhu Xiaodong. Effect of compound UC2288 on radiosensitivity of CNE-2R cell line and nude mouse transplanted tumor[J]. Chinese Journal of Radiation Oncology, 2022, 31(2): 196-200.
Liang Renba,Zhu Xiaodong. Effect of compound UC2288 on radiosensitivity of CNE-2R cell line and nude mouse transplanted tumor[J]. Chinese Journal of Radiation Oncology, 2022, 31(2): 196-200.
[1] Chen YP, Chan A, Le QT, et al. Nasopharyngeal carcinoma[J]. Lancet, 2019, 394(10192):64-80. DOI:10.1016/S0140-6736(19)30956-0. [2] Mao YP, Tang LL, Chen L, et al. Prognostic factors and failure patterns in non-metastatic nasopharyngeal carcinoma after intensity-modulated radiotherapy[J]. Chin J Cancer, 2016, 35(1):103-112. DOI:10.1186/s40880-016-0167-2. [3] Xiao BD, Zhao YJ, Jia XY, et al. Multifaceted p21 in carcinogenesis, stemness of tumor and tumor therapy[J]. World J Stem Cells, 2020, 12(6):481-487. DOI:10.4252/wjsc.v12.i6.481. [4] Zhang Q, Yang X, Luo L, et al. Targeted p21 activation by a new double stranded RNA suppresses human prostate cancer cells growth and metastasis[J]. Am J Transl Res, 2020, 12(8):4175-4188. [5] Wettersten HI, Hee HwangS, Li C, et al. A novel p21 attenuator which is structurally related to sorafenib[J]. Cancer Biol Ther, 2013, 14(3):278-285. DOI:10.4161/cbt.23374. [6] Gupta R, Dong Y, Solomon PD, et al. Synergistic tumor suppression by combined inhibition of telomerase and CDKN1A[J]. Proc Natl Acad Sci USA, 2014, 111(30):E3062-E3071. DOI:10.1073/pnas.1411370111. [7] 梁仁拔,李欣晓,朱小东. P21抑制剂UC2288诱导鼻咽癌放射抗拒细胞CNE-2R凋亡的研究[J]. 中国比较医学杂志,2020, 30(8):16-22. DOI:10. 3969/j.issn.1671-7856. Liang RB, Li XX, Zhu XD. Study on UC2288-induced radiation resistance to CNE-2R apoptosis by P21 Inhibitor P21[J]. Chin J Comparat Med, 2020, 30(8):16-22. DOI:10.3969/j.issn.1671-7856. [8] Liang R, Zhu X. UC2288 induces cell apoptosis of nasopharyngeal carcinoma cells via inhibiting EGFR/ERK pathway[J]. J Cancer, 2021, 12(4):988-995. DOI:10.7150/jca.48282. [9] 苏芳,朱小东,曲颂,等. 人鼻咽癌放射抗拒细胞株建立及其细胞周期的观察[J]. 中华肿瘤防治杂志,2009, 16(16):1221-1224. DOI:10.16073/j.cnki.cjcpt. Su F, Zhu XD, Qu S, et al. The observation of its cell cycle[J]. Chin J Cancer Prevent Treat, 2009, 16(16):1221-1224. DOI:10.16073/j.cnki.cjcpt. [10] Chen KH, Guo Y, Li L, et al. Cancer stem cell-like characteristics and telomerase activity of the nasopharyngeal carcinoma radioresistant cell line CNE-2R[J]. Cancer Med, 2018, 7(9):4755-4764. DOI:10.1002/cam4.1729. [11] Sung H, Ferlay J, Siegel RL, et al. Global cancer statistics 2020:GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries[J]. CA Cancer J Clin, 2021, 71(3):209-249. In press. DOI:10.3322/caac.21660. [12] Wang HY, Chang YL, To KF, et al. A new prognostic histopathologic classification of nasopharyngeal carcinoma[J]. Chin J Cancer, 2016, 35(1):41-56. DOI:10.1186/s40880-016-0103-5. [13] Pathmanathan R, Prasad U, Chandrika G, et al. Undifferentiated, nonkeratinizing, and squamous cell carcinoma of the nasopharynx. Variants of Epstein-Barr virus-infected neoplasia[J]. Am J Pathol, 1995, 146(6):1355-1367. [14] Young LS, Dawson CW. Epstein-Barr virus and nasopharyngeal carcinoma[J]. Chin J Cancer, 2014, 33(12):581-590. DOI:10.5732/cjc.014.10197. [15] Peng G, Wang T, Yang KY, et al. A prospective, randomized study comparing outcomes and toxicities of intensity-modulated radiotherapy vs. conventional two-dimensional radiotherapy for the treatment of nasopharyngeal carcinoma[J]. Radiother Oncol, 2012, 104(3):286-293. DOI:10.1016/j.radonc.2012.08.013. [16] Zhang MX, Li J, Shen GP, et al. Intensity-modulated radiotherapy prolongs the survival of patients with nasopharyngeal carcinoma compared with conventional two-dimensional radiotherapy:a 10-year experience with a large cohort and long follow-up[J]. Eur J Cancer, 2015, 51(17):2587-2595. DOI:10.1016/j.ejca.2015.08.006. [17] Xiao WW, Huang SM, Han F, et al. Local control, survival, and late toxicities of locally advanced nasopharyngeal carcinoma treated by simultaneous modulated accelerated radiotherapy combined with cisplatin concurrent chemotherapy:long-term results of a phase 2 study[J]. Cancer, 2011, 117(9):1874-1883. DOI:10.1002/cncr.25754. [18] Bruix J, Raoul JL, Sherman M, et al. Efficacy and safety of sorafenib in patients with advanced hepatocellular carcinoma:subanalyses of a phase Ⅲ trial[J]. J Hepatol, 2012, 57(4):821-829. DOI:10.1016/j.jhep.2012.06.014. [19] Pressiani T, Boni C, Rimassa L, et al. Sorafenib in patients with Child-Pugh class A and B advanced hepatocellular carcinoma:a prospective feasibility analysis[J]. Ann Oncol, 2013, 24(2):406-411. DOI:10.1093/annonc/mds343. [20] Niu L, Liu L, Yang S, et al. New insights into sorafenib resistance in hepatocellular carcinoma:Responsible mechanisms and promising strategies[J]. Biochim Biophys Acta Rev Cancer, 2017, 1868(2):564-570. DOI:10.1016/j.bbcan.2017.10.002. [21] Tang W, Chen Z, Zhang W, et al. The mechanisms of sorafenib resistance in hepatocellular carcinoma:theoretical basis and therapeutic aspects[J]. Signal Transduct Target Ther, 2020, 5(1):87-101. DOI:10.1038/s41392-020-0187-x. [22] Elser C, Siu LL, Winquist E, et al. Phase Ⅱ trial of sorafenib in patients with recurrent or metastatic squamous cell carcinoma of the head and neck or nasopharyngeal carcinoma[J]. J Clin Oncol, 2007, 25(24):3766-3773. DOI:10.1200/JCO.2006.10.2871.