目的 研究多柔比星对非霍奇金淋巴瘤细胞株Raji体外增殖、迁移侵袭的作用及PTEN(gene of phosphate and tension homology deleted on chromsome ten)的影响。方法 四甲基偶氮唑蓝(MTT)法测定不同浓度多柔比星对Raji细胞生长活力的影响;Transwell法检测多柔比星和PTEN对Raji细胞迁移侵袭的影响;RT-qPCR检测多柔比星对Raji细胞中PTENM表达的影响。结果 多柔比星具有显著抑制Raji细胞增殖的作用,且呈浓度依赖效应(r=-0.925, P<0.001);多柔比星能够抑制Raji细胞的侵袭和迁移;多柔比星能够促进PTEN在Raji细胞中的表达,过表达PTEN能显著抑制Raji细胞的侵袭和迁移;多柔比星和PTEN联合使用能够显著降低Raji细胞活力、抑制Raji细胞侵袭和迁移能力。结论 多柔比星和PTEN均能够抑制Raji细胞增殖、侵袭和迁移,PTEN可显著增强多柔比星对Raji细胞增殖、迁移侵袭的抑制作用。
Abstract
OBJECTIVE To investigate the inhibitiom effect of PTEN(gene of phosphate and tension homology deleted on chromsome ten) combined with adriamycin on proliferation, migration and invasion of non-Hodgkin lymphoma cell line Raji in vitro. METHODS Cell proliferation was determined by MTT in Raji cells response to adriamycin with different concentrations. Transwell assay was performed to evaluate the effects of adriamycin and PTEN on migration and invasion of Raji cells. RT-qPCR was conducted to measure the expression of PTEN in Raji cells after adriamycin treatment. RESULTS Adriamycin significantly inhibited the proliferation of Raji cells in a concentration dependent manner (r=-0.925, P<0.001). Adriamycin inhibited invasion and migration in Raji cells. Moreover, adriamycin promoted the expression of PTEN. Overexpression of PTEN markedly suppressed invasion and migration in Raji cells. The combination of adriamycin and PTEN strikingly decreased the proliferation, invasion and migration of Raji cells. CONCLUSION Adriamycin and PTEN would inhibite the proliferation, invasion and migration of Raji cells. PTEN drastically enhances the inhibition of adriamycin on the proliferation, migration and invasion of Raji cells.
关键词
PTEN /
多柔比星 /
非霍奇金淋巴瘤细胞 /
生长抑制
{{custom_keyword}} /
Key words
PTEN /
adriamycin /
Raji cells /
growth inhibition
{{custom_keyword}} /
中图分类号:
R965
{{custom_clc.code}}
({{custom_clc.text}})
{{custom_sec.title}}
{{custom_sec.title}}
{{custom_sec.content}}
参考文献
[1] LL Y B, LIU Y X, LU Y Q. Non-Hodgkin′s lymphoma research:a review of the literature[J]. Mod Oncol(现代肿瘤医学), 2010, 18(3):620-624.
[2] KUPPERS R. The biology of Hodgkin′s lymphoma[J]. Nat Rev Cancer, 2009, 9(1):15-27.
[3] SKARIN A T, ROSENTHAL D L, MOLONEY W C, et al. Combination chemotherapy of advanced non-Hodgkin lymphoma with bleomycin, adriamycin, cyclophosphamide, vincristine, and prednisone (BACOP)[J]. Blood, 1977, 49(5):759-770.
[4] DABICH L, ENSMINGER W D, ZUCKERMAN K S, et al. High-dose adriamycin combination chemotherapy for intermediate and high-grade non-Hodgkin′s lymphomas[J]. Semin Oncol, 1985, 12(3):212-217.
[5] XU X Y, ZHOU J P, LI L, et al. Preparation and research on the anti-tumor activity of doxorubicin loaded high polymer micelles[J]. Chin Pharm J (中国药学杂志), 2008, 43(7):514-518.
[6] GAO J, ZHU X Y, SHI Q F, et al. Mechanism and inhibition of thalidomide combined with epirubicine on the growth of transplanted H22 hepatocellular carcinoma in mice[J]. Chin J Clin Pharmacol (中国临床药理学杂志), 2016,32(2):170-173.
[7] SUN F J, ZHANG Y D, ZHANG M X, et al. Roles of β-AR/PKA/CaMK Ⅱ signaling pathway in cardiomyocyte apoptosis induced by adriamycin in rats[J]. Chin Pharmacol Bull (中国药理学通报), 2017, 33(3):360-365.
[8] ZHANG D, WU W, NA D, et al. Mxd1 mediates hypoxia-induced cisplatin resistance in osteosarcoma cells by repression of the PTEN tumor suppressor gene[J]. Mol Carcinog, 2017, 56(10):2234-2244.
[9] ZHAO H X. Research progress in PTEN and tumor development[J]. Med J Wuhan Univ (武汉大学学报:医学版), 2014, 35(1):155-159.
[10] LIU D, XU J H, JIAO Z L, et al. Advances in research on PTEN gene function and its regulation[J]. Med Pharm J Chin PLA (解放军医药杂志), 2014, 26(4):111-116.
[11] XIAO M, ZUO L. Clinical observation of gemcitabine combined with cisplatin and dexamethasone in the treatment of relapsed or refractory non-Hodgkin′s lymphoma[J]. Chin J Clin (Elect Ed) (中华临床医师杂志电子版), 2013,7(3):205-206.
[12] CHEN C, ZHANG Y H, WANG M H, et al. Effect of the long non-coding RNA CAF on doxorubicin-induced cardiotoxicity and its possible mechanisms[J]. Translat Med J (转化医学杂志), 2018, 7(2):68-73.
[13] LI J, YEN C, LIAW D, et al. PTEN a putative tyrosine phosphatase gene mutated in human brain, breast, and prostate cancer[J]. Science, 1997, 275(5308):1943-1947.
[14] SUZUKI A, JI D L P, STAMBOLIC V, et al. High cancer susceptibility and embryonic lethality associated with mutation of the PTEN tumor suppressor gene in mice[J]. Curr Biol, 1998, 8(21):1169-1178.
[15] LIAO Y, SHEN L, ZHAO H, et al. LncRNA CASC2 interacts with miR-181a to modulate glioma growth and resistance to TMZ through PTEN pathway[J]. J Cell Biochem, 2017, 118(7):1889-1899.
[16] LI B, LU Y, WANG H, et al. miR-221/222 enhance the tumorigenicity of human breast cancer stem cells via modulation of PTEN/Akt pathway[J]. Biomed Pharmacother, 2016, 79:93-101.
[17] WEI Z, CUI L, MEI Z, et al. miR-181a mediates metabolic shift in colon cancer cells via the PTEN/AKT pathway[J]. Febs Letter, 2016, 588(9):1773-1779.
[18] YANG Y, GUO J X, SHAO Z Q. miR-21 targets and inhibits tumor suppressor gene PTEN to promote prostate cancer cell proliferation and invasion: an experimental study [J]. Asian Pac J Trop Med, 2017, 10(1):87-91.
{{custom_fnGroup.title_cn}}
脚注
{{custom_fn.content}}