HIP2在放射线处理后喉癌Hep-2细胞中的增殖、凋亡及细胞周期中作用

Abstract
Figure/Table
References (21)
Related Citation (10)

Download: PDF (935 KB) HTML (1 KB)
Export: BibTeX | EndNote (RIS)

Abstract Objective To explore the relation between the expression of SHIP2 and proliferation, apoptosis and cell cycle in Hep-2 cells after radiotherapy. Methods Lupine carcinoma Hep-2 cells were divided into the experiment group (treated with 2, 4, 8 Gy X- ray) and the control group (treated with 0 Gy). CCK-8 was repeatedly used to detect the proliferation of the cells 12, 24, 36 h and 48 h after the treatment. The most appropriate and exact time to detect cells in the subsequent experiment was set up following the result of proliferation. Then apoptosis was evaluated by AnnexinV- FITC/PI double staining flow cytometry and cell cycle was evaluated by PI single staining flow cytometry. RT-qPCR and Western-blot were used to detect the expression of SHIP2 mRNA and its protein. Results Compared with the control group, Hep-2 cells' proliferation in the experiment group was inhibited (all P ＜ 0.05) . As the dose of ray increased, the viability descended, and the most remarkable result arose 48 h after the treatment. There was a remarkable increase in apoptosis of the experiment group (all P ＜ 0.01). After treated with 4 Gy and 8 Gy X-ray G2/M phase arrest was remarkable too (all P ＜ 0.01). The expression of SHIP2 mRNA and SHIP2 protein in the experiment group was lower than those of the control group (all P ＜ 0.01). Conclusion In Hep-2 cells, low expression of SHIP2 after the treatment with X-ray, may be one important pathway of X-ray inhibiting cell proliferation and increasing cell apoptosis and G2/M phase arrest.

Key words： X-ray SHIP2 Proliferation Apoptosis Cell cycle

	Service

	E-mail this article
	Add to my bookshelf
	Add to citation manager
	E-mail Alert
	RSS
	Articles by authors
	LIANG Huiling HE Xiaoqin GAN Yuanyuan ZHOU Yujie XIONG Lin TANG Tian XU Ximing

Cite this article:

LIANG Huiling HE Xiaoqin GAN Yuanyuan ZHOU Yujie XIONG Lin TANG Tian XU Ximing. Study on the relation of SHIP2 with proliferation, apoptosis and cell cycle in Hep-2 cells after radiation[J]. 中国医药导报, 2017, 14(36): 4-8,20.

URL:

http://www.yiyaodaobao.com.cn/EN/ OR http://www.yiyaodaobao.com.cn/EN/Y2017/V14/I36/4

[1] Siegel RL，Miller KD，Jemal A. Cancer Statistics，2016 [J]. CA Cancer J Clin，2016，66（1）：7-30.
[2] 汤钊猷.现代肿瘤学[M].第3版.上海：复旦大学出版社，2014.
[3] Jines TM，De M，Foran B，et al. Laryngeal caner：United Kingdom National Multidisciplinary guidelines [J]. Laryngeal Otol，2016，130（S2）：S75-S82.
[4] Aypar U，Morgan WF，Baulch JE. Radiation- induced genomic instability：are epigenetic mechanisms the missing link? [J] Int J Radiat Biol，2011，87（2）：179-191.
[5] Kim JS，Kim SY，Lee M，et al. Radioresistance in a human laryngeal squamous cell carcinoma cell line is associated with DNA methylation changes and topoisomeraseⅡα [J]. Cancer Biol Ther，2015，16（4）：558-566.
[6] Ye Y，Qian XY，Xiao MM，et al. Decreased Sp1 Expression Mediates Downregulation of SHIP2 in Gastric Cancer Cell [J]. Int J Mol Sci，2017，18（1）.pii：E220.
[7] Ye Y，Ge YM，Xiao MM，et al. Suppression of SHIP2 contributes to tumorigenesis and proliferation of gastric cancer cells via activation of Akt [J]. J Gastroenterol，2016， 51（3）：230-240.
[8] Bao YY，Zhou SH，Lu ZJ，et al. Inhibiting GLUT-1 expression and PI3K/Akt signaling using apigenin improves the radiosensitivity of laryngeal carcinoma in vivo [J]. Oncol Rep，2015，34（4）：1805-1814.
[9] 陈犹白，柴密，乌兰哈斯，等.放射性损伤：类型、症状和机制[J].中华损伤与修复杂志，2017，12（3）：203-206.
[10] 周妮娜，张利英，刘永琦，等.不同X线剂量照射对骨髓间充质干细胞的增殖及DNA损伤的影响[J].医学研究生报，2016，29（9）：923-927.
[11] Pan Y，Zhang Q，Atsaves V，et al. Suppression of Jab1/CSN5 induces radio- and chemo-sensitivity in nasopharyngeal carcinoma through changes to the DNA damage and repair pathways [J]. Onco gene，2013，32（22）：2756-2766.
[12] Antwih DA，Gabbara KM，Lancaster WD，et al. Radiation-induced epigenetic DNA methylation modification of radiation-response pathways [J]. Epigenetics，2013，8（8）：839-848.
[13] Bae JH，Kim JG，Heo K. Identification of radiation-induced aberrant hypomethylation in colon cancer [J]. BMC Genomics，2015，16（1）：1-12.
[14] Erneux C，Edimo WE，Deneubourg L，et al. SHIP2 multiple functions：a balance between a negative control of PtdIns（3，4，5）P 3 level，a positive control of PtdIns（3，4）P 2 production，and intrinsic docking properties [J]. J Cell Biochem，2011，112（9）：2203-2209.
[15] Le CJ，Heredia GL，Lietha D. Expression，Purification，Crystallisation and X-ray Crystallographic Analysis of a Truncated Form of Human Src Homology 2 Containing Inositol 5-Phosphatase 2 [J]. Protein J，2016，35（3）：225-230.
[16] Thomas MP，Erneux C，Potter BV. SHIP2：Structure，Function and Inhibition [J]. Chembiochem，2017，18（3）：233-247.
[17] 邹力，李法琦.SHIP2通过抑制PI3K/Akt信号通路降低胰岛素敏感性[J].生理科学进展，2010，41（1）：62- 64.
[18] Elong EW，Ghosh S，Derua R，et al. SHIP2 controls plasma membrane PI（4，5）P2 Thereby participating in the control of cell migration in 1321 N1 glioblastoma cells [J]. J Cell Sci，2016，129（6）：1101-1114.
[19] Fu M，Gu X，Ni H，et al. High expression of inositol polyphosphate phosphatase-like 1 associates with unfavorable survival in hepatocellular carcinoma [J]. Int J Clin Exp Pathol，2013，6（11）：2515- 2522.
[20] Yang J， Fu M， Ding Y， et al. High SHIP2 Expression Indicates Poor Survival in Colorectal Cancer [J]. Dis Markers，2014，（3）：218 968.
[21] Zhou X，Liu Y，Tan G. Prognostic Value of Elevated SHIP2 Expression in Laryngeal Squamous Cell Carcinoma [J]. Arch Med Res，2011，42（7）：589- 595.