Akt抑制劑MK2206對(duì)舌鱗癌TCA-8113細(xì)胞增殖和凋亡的影響及其作用機(jī)制
發(fā)布時(shí)間:2018-12-07 16:42
【摘要】:目的:探討Akt抑制劑MK2206對(duì)舌鱗狀細(xì)胞癌(舌鱗癌)TCA-8113細(xì)胞增殖和凋亡的影響,并闡明其可能的作用機(jī)制。方法:取處于對(duì)數(shù)生長(zhǎng)期舌鱗癌TCA-8113細(xì)胞株隨機(jī)分為對(duì)照組和1、5、25、125及250nmol·L-1 MK2206實(shí)驗(yàn)組。在不同劑量及時(shí)間處理因素下,采用MTT法檢測(cè)細(xì)胞增殖抑制率,流式細(xì)胞術(shù)(FCM)檢測(cè)細(xì)胞凋亡率,蛋白質(zhì)印跡分析檢測(cè)細(xì)胞中caspase-9、Bad、GSK-3β、p-Akt和T-Akt蛋白表達(dá)水平。結(jié)果:舌鱗癌TCA-8113細(xì)胞在MK2206作用12、24和36h的半數(shù)抑制濃度(IC50)分別為(112.54±1.67)、(79.67±2.01)和(33.33±1.98)nmol·L-1。FCM法檢測(cè),1、5、25、125和250nmol·L-1 MK2206作用舌鱗癌TCA-8113細(xì)胞12h后,細(xì)胞凋亡率分別為(14.2±0.74)%、(19.3±0.45)%、(35.1±0.45)%、(39.6±0.48)%和(52.1±0.19)%,與對(duì)照組比較差異均有統(tǒng)計(jì)學(xué)意義(P0.01)。蛋白質(zhì)印跡分析,隨著MK2206藥物劑量和作用時(shí)間的增加,p-Akt、Bad和GSK-3β蛋白表達(dá)水平下降,與對(duì)照組β-actin比較其條帶的顏色變暗;caspase-9蛋白表達(dá)水平升高,與對(duì)照組β-actin比較其條帶的顏色變深。T-Akt蛋白表達(dá)變化不明顯,與對(duì)照組β-actin比較條帶的顏色無(wú)明顯不同。結(jié)論:Akt抑制劑MK2206可抑制舌鱗癌TCA-8113細(xì)胞增殖并誘導(dǎo)凋亡。
[Abstract]:Aim: to investigate the effects of Akt inhibitor MK2206 on the proliferation and apoptosis of TCA-8113 cells in tongue squamous cell carcinoma (TSCC) and to elucidate its possible mechanism. Methods: TCA-8113 cell lines of tongue squamous cell carcinoma at logarithmic growth stage were randomly divided into three groups: control group and 250nmol L-1 MK2206 group. The inhibition rate of cell proliferation was detected by MTT assay, apoptosis rate was detected by flow cytometry (FCM), and caspase-9,Bad,GSK-3 尾 in cells was detected by Western blot analysis. P-Akt and T-Akt protein expression level. Results: the median inhibitory concentrations (IC50) of TCA-8113 cells in tongue squamous cell carcinoma were (112.54 鹵1.67), (79.67 鹵2.01) and (33.33 鹵1.98) nmol L-1.FCM after MK2206 treatment for 12h and 36h, respectively. The apoptosis rates of TCA-8113 cells treated with 25125 and 250nmol L-1 MK2206 for 12 h were (14.2 鹵0.74)%, (19.3 鹵0.45)%, (35.1 鹵0.45)%, (39.6 鹵0.48)% and (52.1 鹵0.19)%, respectively. Compared with the control group, the difference was statistically significant (P0.01). Western blotting analysis showed that the expression of p-Akttbuad and GSK-3 尾 protein decreased with the increase of MK2206 dosage and action time. Compared with the control group, the band color of p-Aktbud and GSK-3 尾 was darkened. The expression of caspase-9 protein increased, and the color of the band became darker than that of the control group. The expression of T-Akt protein did not change significantly, but the color of the band was not different from that of the control group. Conclusion: Akt inhibitor MK2206 can inhibit the proliferation and induce apoptosis of TCA-8113 cells in tongue squamous cell carcinoma.
【作者單位】: 遼寧醫(yī)學(xué)院附屬第一醫(yī)院口腔科;
【基金】:遼寧省教育廳高等學(xué)?茖W(xué)研究項(xiàng)目資助課題(L2010315)
【分類號(hào)】:R739.86
本文編號(hào):2367479
[Abstract]:Aim: to investigate the effects of Akt inhibitor MK2206 on the proliferation and apoptosis of TCA-8113 cells in tongue squamous cell carcinoma (TSCC) and to elucidate its possible mechanism. Methods: TCA-8113 cell lines of tongue squamous cell carcinoma at logarithmic growth stage were randomly divided into three groups: control group and 250nmol L-1 MK2206 group. The inhibition rate of cell proliferation was detected by MTT assay, apoptosis rate was detected by flow cytometry (FCM), and caspase-9,Bad,GSK-3 尾 in cells was detected by Western blot analysis. P-Akt and T-Akt protein expression level. Results: the median inhibitory concentrations (IC50) of TCA-8113 cells in tongue squamous cell carcinoma were (112.54 鹵1.67), (79.67 鹵2.01) and (33.33 鹵1.98) nmol L-1.FCM after MK2206 treatment for 12h and 36h, respectively. The apoptosis rates of TCA-8113 cells treated with 25125 and 250nmol L-1 MK2206 for 12 h were (14.2 鹵0.74)%, (19.3 鹵0.45)%, (35.1 鹵0.45)%, (39.6 鹵0.48)% and (52.1 鹵0.19)%, respectively. Compared with the control group, the difference was statistically significant (P0.01). Western blotting analysis showed that the expression of p-Akttbuad and GSK-3 尾 protein decreased with the increase of MK2206 dosage and action time. Compared with the control group, the band color of p-Aktbud and GSK-3 尾 was darkened. The expression of caspase-9 protein increased, and the color of the band became darker than that of the control group. The expression of T-Akt protein did not change significantly, but the color of the band was not different from that of the control group. Conclusion: Akt inhibitor MK2206 can inhibit the proliferation and induce apoptosis of TCA-8113 cells in tongue squamous cell carcinoma.
【作者單位】: 遼寧醫(yī)學(xué)院附屬第一醫(yī)院口腔科;
【基金】:遼寧省教育廳高等學(xué)?茖W(xué)研究項(xiàng)目資助課題(L2010315)
【分類號(hào)】:R739.86
【參考文獻(xiàn)】
相關(guān)期刊論文 前1條
1 李勇;林愛(ài)花;;分子靶向治療肺癌的應(yīng)用進(jìn)展[J];中國(guó)實(shí)用醫(yī)藥;2013年02期
【共引文獻(xiàn)】
相關(guān)期刊論文 前1條
1 麥琳;;小分子AKT抑制劑及其在肺癌治療中的研究進(jìn)展[J];中華肺部疾病雜志(電子版);2011年06期
相關(guān)會(huì)議論文 前1條
1 石妍;林鳳;胡瑞謙;;腫瘤分子靶向治療現(xiàn)狀與展望[A];2013年中國(guó)藥學(xué)大會(huì)暨第十三屆中國(guó)藥師周論文集[C];2013年
相關(guān)碩士學(xué)位論文 前2條
1 馬靜;HER2/neu及Akt2蛋白在胃癌中的表達(dá)及意義[D];吉林大學(xué);2011年
2 張麗靜;胃癌組織中AKT-2和PGC的表達(dá)及臨床意義分析[D];鄭州大學(xué);2013年
【二級(jí)參考文獻(xiàn)】
相關(guān)期刊論文 前3條
1 韓寶惠;;肺癌分子靶向治療的現(xiàn)狀與挑戰(zhàn)[J];中華結(jié)核和呼吸雜志;2007年02期
2 蔡莉,隋廣杰;肺癌分子靶向性治療研究的主要成就[J];中華腫瘤雜志;2004年03期
3 張子瑾,程剛;分子靶向藥物治療非小細(xì)胞肺癌的臨床研究進(jìn)展[J];中國(guó)新藥雜志;2005年10期
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