本文選題：miR-106b + 喉癌��； 參考：《山西醫(yī)科大學(xué)》2013年博士論文

【摘要】：喉癌是頭頸部常見(jiàn)的惡性腫瘤之一,其全世界發(fā)病率呈逐年增長(zhǎng)趨勢(shì)。目前喉癌的治療方法主要是手術(shù)治療,雖然人們一直致力于對(duì)喉癌早診斷、早治療,并在切除癌腫的前提下,盡可能保留或重建喉的功能,但是,患者術(shù)后仍有不同程度發(fā)音障礙和吞咽困難,影響到患者生存質(zhì)量。為了改善療效及提高預(yù)后的生存率,盡管人們不斷探索喉癌發(fā)生、發(fā)展機(jī)制,但喉癌發(fā)生的分子機(jī)制尚不明確。 microRNA(miRNA)是一類存在于生物體內(nèi)非編碼單鏈小分子RNA,長(zhǎng)度約為21-25個(gè)核苷酸,它們通過(guò)堿基互補(bǔ)配對(duì)方式與靶基因mRNA的3’非翻譯區(qū)(3'-untranslated region,3'UTR)完全或不完全結(jié)合,導(dǎo)致靶基因mRNA降解或翻譯抑制,從而調(diào)控靶基因的表達(dá)。目前研究認(rèn)為,miRNA通過(guò)類似癌基因、抑癌基因或其他方式的作用對(duì)細(xì)胞生長(zhǎng)、凋亡和細(xì)胞周期調(diào)控,導(dǎo)致腫瘤發(fā)生發(fā)展。我們前期通過(guò)miRNA芯片技術(shù)篩選到了一系列在喉癌中表達(dá)差異的miRNA,如：miR-106b、miR-151-3p、miR-19b、miR-185、miR-139-5p等。后期我們通過(guò)熒光定量PCR進(jìn)一步研究發(fā)現(xiàn)miR-106b在喉癌中顯著性表達(dá)。因此,本研究以miR-106b為研究對(duì)象,揭示其在喉癌發(fā)生發(fā)展中的作用。 第一部分miR-106b在喉癌組織中的表達(dá)研究 目的 研究miR-106b在喉癌、癌旁組織中表達(dá)水平。 方法 提取14例配對(duì)喉癌手術(shù)新鮮標(biāo)本(喉癌組織和癌旁組織)RNA,用莖環(huán)實(shí)時(shí)熒光定量PCR法檢測(cè)niR-106b在喉癌和癌旁組織中表達(dá)水平。 結(jié)果 喉癌組織中miR-106b表達(dá)水平較癌旁組織顯著增高。 結(jié)論 miR-106b在喉癌組織中高表達(dá),推測(cè)niR-106b可能與喉癌發(fā)生發(fā)展有關(guān)。 第二部分niR-106b對(duì)喉癌細(xì)胞增殖、侵襲和體內(nèi)生長(zhǎng)能力的影響 目的 研究miR-106b對(duì)喉癌細(xì)胞體外增殖、侵襲和體內(nèi)生長(zhǎng)能力的影響。 方法 采用實(shí)時(shí)熒光定量PCR檢測(cè)轉(zhuǎn)染miR-106b ASO后,Hep-2和TU-212喉癌細(xì)胞miR-106b表達(dá)水平,采用體外克隆形成實(shí)驗(yàn)、細(xì)胞侵襲實(shí)驗(yàn)和體內(nèi)生長(zhǎng)實(shí)驗(yàn)觀察miR-106b對(duì)Hep-2和TU-212喉癌細(xì)胞增殖和侵襲能力影響。 結(jié)果 轉(zhuǎn)染了miR-106b ASO的Hep-2和TU-212喉癌細(xì)胞其miR-106b表達(dá)水平降低了約80%,抑制niR-106b表達(dá)可以降低喉癌細(xì)胞體內(nèi)外生長(zhǎng)和體外侵襲能力。 結(jié)論 miR-106b在喉癌細(xì)胞株中高表達(dá),而抑制其表達(dá)可以部分逆轉(zhuǎn)喉癌細(xì)胞體內(nèi)外生長(zhǎng)和體外侵襲能力。 第三部分miR-106b靶向調(diào)控RUNX3的研究 目的 研究miR-106b是否可以直接靶向調(diào)控RUNX3。 方法 生物信息學(xué)方法篩選RUNX3的候選miRNA,熒光素酶報(bào)告基因?qū)嶒?yàn)檢測(cè)候選miRNA對(duì)RUNX3的調(diào)控作用,Western blot檢測(cè)轉(zhuǎn)染了miR-106b模擬劑和抑制劑的喉癌細(xì)胞中RUNX3蛋白表達(dá)變化,采用熒光素酶報(bào)告基因?qū)嶒?yàn)驗(yàn)證miR-106b對(duì)RUNX3直接調(diào)控作用。 結(jié)果 預(yù)測(cè)的RUNX3上游的11個(gè)可能調(diào)控性miRNA,熒光素酶報(bào)告基因?qū)嶒?yàn)顯示共轉(zhuǎn)染miR-130b、miR-106b mimics和RUNX3-3'UTR能夠顯著降低報(bào)告質(zhì)粒熒光素酶的活性,其中miR-130b能夠直接靶定RUNX3在胃癌細(xì)胞中已有報(bào)導(dǎo)。因此,我們進(jìn)一步研究rmiR-106b的作用。轉(zhuǎn)染miR-106b ASO的喉癌細(xì)胞中RUNX3蛋白表達(dá)水平升高2-3倍,轉(zhuǎn)染miR-106b mimics的喉癌細(xì)胞中RUNX3蛋白表達(dá)水平降低約40%～70%。熒光素酶報(bào)告基因?qū)嶒?yàn)顯示niR-106b功能被ASO減弱后,含有野生型RUNX3-3'UTR報(bào)告質(zhì)粒熒光素酶活性顯著增強(qiáng),轉(zhuǎn)染miR-106b mimics后,報(bào)告質(zhì)粒熒光素酶活性顯著降低,而miR-106b mimics和miR-106b ASO對(duì)含有突變型RUNX3-3'UTR的報(bào)告質(zhì)粒的熒光素酶活性則無(wú)顯著影響。 結(jié)論 RUNX3為miR-106b的靶基因。 第四部分喉癌中niR-106b靶向調(diào)控RUNX3作用機(jī)制研究 實(shí)驗(yàn)一喉癌中RUNX3基因啟動(dòng)子甲基化及其蛋白表達(dá)的研究 目的 研究RUNX3基因啟動(dòng)子甲基化狀態(tài)及其蛋白表達(dá)與喉癌發(fā)生發(fā)展的關(guān)系。 方法 采用Western blot檢測(cè)RUNX3在喉癌組織中的表達(dá)水平。用甲基化特異性PCR(MSP)方法檢測(cè)RUNX3基因啟動(dòng)子甲基化發(fā)生狀況。用Western Blot檢測(cè)RUNX3蛋白在RUNX3啟動(dòng)子甲基化喉癌組織、RUNX3啟動(dòng)子非甲基化喉癌組織和正常喉上皮中的表達(dá)情況。免疫組化檢測(cè)正常喉上皮組織、癌旁組織、RUNX3啟動(dòng)子甲基化喉癌組織和RUNX3啟動(dòng)子非甲基化喉癌組織中RUNX3的表達(dá)情況。 結(jié)果 RUNX3啟動(dòng)子甲基化發(fā)生率約為41.67%,無(wú)論RUNX3啟動(dòng)子是否發(fā)生甲基化,RUNX3在喉癌組織中均低表達(dá)。 結(jié)論 除RUNX3基因啟動(dòng)子甲基化在喉癌發(fā)生發(fā)展中起重要作用外,可能還有其它機(jī)制如miR-106b的調(diào)控引起喉癌的發(fā)生發(fā)展。 實(shí)驗(yàn)二研究RUNX3在喉癌細(xì)胞中的作用 目的 過(guò)表達(dá)RUNX3,研究RUNX3在喉癌細(xì)胞中的作用 方法 構(gòu)建過(guò)表達(dá)RUNX3的pCMV6/RUNX3,Western blot檢測(cè)pCMV6/RUNX3質(zhì)粒轉(zhuǎn)染Hep-2和TU-212喉癌細(xì)胞后RUNX3蛋白表達(dá)水平,MTT實(shí)驗(yàn)、克隆形成實(shí)驗(yàn)和Transwell侵襲實(shí)驗(yàn)觀察pCMV6/RUNX3質(zhì)粒轉(zhuǎn)染細(xì)胞后生長(zhǎng)曲線、增殖和侵襲能力變化。 結(jié)果 過(guò)表達(dá)RUNX3后,喉癌細(xì)胞生長(zhǎng)侵襲能力明顯下降。 結(jié)論 上調(diào)RUNX3表達(dá)可以抑制喉癌細(xì)胞的生長(zhǎng)、增殖和侵襲能力。 實(shí)驗(yàn)三miR-106b靶向調(diào)控RUNX3在喉癌細(xì)胞中作用機(jī)制 目的 研究miR-106b通過(guò)靶向調(diào)控RUNX3對(duì)喉癌細(xì)胞功能的影響。 方法 向喉癌細(xì)胞株中同時(shí)轉(zhuǎn)染RUNX3-siRNA和ASO-miR-106b,使得miR-106b和RUNX3的表達(dá)同時(shí)下調(diào),Western Blot檢測(cè)RUNX3表達(dá)水平,實(shí)時(shí)熒光定量PCR法檢測(cè)mR-106b表達(dá)水平,克隆形成實(shí)驗(yàn)和Transwell侵襲實(shí)驗(yàn)檢測(cè)細(xì)胞增殖和侵襲能力變化。 結(jié)果 喉癌細(xì)胞轉(zhuǎn)染ASO-miR-106b+siRNA Control的增殖和侵襲能力顯著低于轉(zhuǎn)染ASO-miR-106b+RUNX3siRNA組,證明RUNX3siRNA能夠部分挽救ASO-miR-106b對(duì)喉癌細(xì)胞的生物學(xué)功能影響。 結(jié)論 miR-106b通過(guò)靶向作用RUNX3參與喉癌的發(fā)生。
[Abstract]:Laryngeal cancer is one of the most common malignant tumors in the head and neck, and its worldwide incidence is increasing year by year. At present, the main treatment method of larynx cancer is surgical treatment. Although people have been working on early diagnosis and treatment of larynx cancer, the function of larynx is retained or reconstructed as much as possible under the premise of cancerous excision, but there are still different degrees after surgery. Dysphonia and dysphagia affect the quality of life of the patient. In order to improve the curative effect and improve the survival rate of the prognosis, although people continue to explore the occurrence and mechanism of larynx, the molecular mechanism of the occurrence of larynx is not clear.
MicroRNA (miRNA) is a class of non coded single strand small molecules, RNA, with 21-25 nucleotides in length. They are completely or incompletely combined with the 3 'non translation region (3'-untranslated region, 3'UTR) of the target gene mRNA by the complementary pairing of bases, causing the target gene mRNA degradation or translation inhibition, thus regulating the target gene table. Da. Current research suggests that miRNA, through the role of oncogenes, tumor suppressor genes, or other ways of regulating cell growth, apoptosis and cell cycle regulation, leads to the development of tumor. We screened a series of miRNA, such as miR-106b, miR-151-3p, miR-19b, miR-185, miR-139-5p, and so on, through miRNA chip technology. In the later period, we found the significant expression of miR-106b in larynx cancer by fluorescence quantitative PCR. Therefore, this study was based on miR-106b and revealed its role in the development of larynx cancer.
Part one expression of miR-106b in laryngeal carcinoma
objective
To study the expression level of miR-106b in laryngeal carcinoma and paracancerous tissues.
Method
RNA was extracted from 14 cases of paired laryngectomy (laryngeal carcinoma tissue and para cancer tissue), and the expression level of niR-106b in laryngeal and paracancerous tissues was detected by real time PCR method.
Result
The expression level of miR-106b in laryngeal carcinoma tissues was significantly higher than that in adjacent tissues.
conclusion
MiR-106b is highly expressed in laryngeal carcinoma. It is speculated that niR-106b may be related to the development of laryngeal carcinoma.
The second part is the effect of niR-106b on the proliferation, invasion and in vivo growth of laryngeal carcinoma cells.
objective
To study the effects of miR-106b on proliferation, invasion and growth of laryngeal carcinoma cells in vitro.
Method
After transfection of miR-106b ASO with real-time fluorescent quantitative PCR, the miR-106b expression level of Hep-2 and TU-212 larynx cancer cells was detected. The effects of miR-106b on the proliferation and invasion ability of Hep-2 and TU-212 larynx cancer cells were observed by in vitro cloning and formation experiments.
Result
The expression level of miR-106b in Hep-2 and TU-212 cells transfected with miR-106b ASO was reduced by about 80%. The inhibition of niR-106b expression could reduce the growth and invasion ability of larynx cells in vitro and in vitro.
conclusion
MiR-106b is highly expressed in laryngeal cancer cell lines, but inhibiting its expression can partially reverse the growth and invasion ability of laryngeal cancer cells in vivo and in vitro.
Study on the third part of miR-106b targeting RUNX3
objective
Whether miR-106b can directly target RUNX3.
Method
The Bioinformatics Method screened the candidate miRNA for RUNX3, and the luciferase reporter gene test detected the role of the candidate miRNA for the regulation of RUNX3. Western blot detected the changes in the expression of RUNX3 protein in the larynx cells transfected with miR-106b analogue and inhibitor, and the luciferase reporter gene was used to verify the direct regulation of miR-106b on RUNX3.
Result
11 possible regulatory miRNA in the upstream of RUNX3 is predicted. The luciferase reporter gene experiment shows that CO transfection of miR-130b, miR-106b mimics and RUNX3-3'UTR can significantly reduce the activity of the reporter plasmid luciferase, and miR-130b can directly target RUNX3 in gastric cancer cells. Therefore, we further study the effect of rmiR-106b. The expression level of RUNX3 protein in the larynx cells transfected with miR-106b ASO increased by 2-3 times. The expression level of RUNX3 protein in the larynx cells transfected with miR-106b mimics decreased by about 40% ~ 70%. luciferase reporter gene experiment showed that the function of niR-106b was weakened by ASO, and the luciferase activity of the wild type RUNX3-3'UTR plasmid was significantly enhanced and the transfection miR-1 was carried out. After 06B mimics, the luciferase activity of the reported plasmid was significantly reduced, while the miR-106b mimics and miR-106b ASO had no significant effect on the luciferase activity of the reported plasmid containing the mutant RUNX3-3'UTR.
conclusion
RUNX3 is the target gene for miR-106b.
The fourth part is the mechanism of niR-106b targeting RUNX3 in laryngeal carcinoma.
Methylation of RUNX3 gene promoter and its protein expression in laryngeal carcinoma
objective
To study the relationship between the methylation status of RUNX3 gene promoter and protein expression and the occurrence and development of laryngeal carcinoma.
Method
The expression level of RUNX3 in the carcinoma of larynx was detected by Western blot. Methylation specific PCR (MSP) method was used to detect the methylation of RUNX3 gene promoter. The expression of RUNX3 protein in RUNX3 promoter methylation laryngeal carcinoma tissue, RUNX3 promoter in non methylated larynx tissues and normal laryngeal epithelium was detected by Western Blot. The expression of RUNX3 in normal laryngeal epithelium, paracancerous tissue, RUNX3 promoter methylation laryngeal carcinoma tissue and RUNX3 promoter non methylation laryngeal carcinoma tissue was detected by histochemical method.
Result
The methylation rate of RUNX3 promoter was about 41.67%. Whether RUNX3 promoter methylation occurred, RUNX3 expression was low in laryngeal carcinoma.
conclusion
Besides the methylation of RUNX3 gene plays an important role in the development of laryngeal carcinoma, there may be other mechanisms, such as the regulation of miR-106b, which may lead to the development of laryngeal carcinoma.
Experiment two to study the role of RUNX3 in laryngeal cancer cells
objective
Overexpression of RUNX3 to study the role of RUNX3 in laryngeal carcinoma cells
Method
The expression of RUNX3 pCMV6/RUNX3 and Western blot were constructed to detect the RUNX3 protein expression level after pCMV6/RUNX3 plasmid transfected to Hep-2 and TU-212 carcinoma cells, MTT experiment, clone formation experiment and Transwell invasion test to observe the growth curve, proliferation and invasiveness of pCMV6/RUNX3 plasmid transfected cells.
Result
After over expression of RUNX3, the growth and invasion ability of laryngeal cancer cells decreased significantly.
conclusion
Up regulation of RUNX3 expression can inhibit the growth, proliferation and invasion of laryngeal cancer cells.
Experiment three the mechanism of miR-106b targeting RUNX3 in laryngeal cancer cells
objective
Objective to study the effect of miR-106b on the function of laryngeal cancer cells by targeting RUNX3.
Method
RUNX3-siRNA and ASO-miR-106b were transfected into the larynx cell line. The expression of miR-106b and RUNX3 was downregulated simultaneously. The expression level of RUNX3 was detected by Western Blot. The level of mR-106b expression was detected by real time fluorescence quantitative PCR method. The colonization and invasion ability of the cells were detected by clone formation experiment and Transwell invasion test.
Result
The proliferation and invasion ability of ASO-miR-106b+siRNA Control transfected by larynx cancer cells were significantly lower than that of transfected ASO-miR-106b+RUNX3siRNA group. It was proved that RUNX3siRNA could partly save the biological function of ASO-miR-106b on larynx cancer cells.
conclusion
MiR-106b participates in laryngeal carcinomas by targeting RUNX3.

【學(xué)位授予單位】：山西醫(yī)科大學(xué)
【學(xué)位級(jí)別】：博士
【學(xué)位授予年份】：2013
【分類號(hào)】：R739.65

【相似文獻(xiàn)】

相關(guān)期刊論文 前10條

1 戴春富，李德堅(jiān)，文三立;喉癌組織中雌激素受體分布的臨床意義[J];臨床耳鼻咽喉科雜志;1995年05期

2 李玉英，孫立群，谷京成;喉癌病人紅細(xì)胞免疫功能初探（摘要）[J];耳鼻咽喉-頭頸外科;1995年03期

3 白素娟;喉癌抑癌基因的研究進(jìn)展[J];國(guó)外醫(yī)學(xué).耳鼻咽喉科學(xué)分冊(cè);1996年05期

4 王銀萍,杜寶東,郭曉峰,鐘李杰;喉癌和癌旁組織P_(53)蛋白的表達(dá)及臨床意義[J];白求恩醫(yī)科大學(xué)學(xué)報(bào);1998年01期

5 劉隆躍,周天明,詹必武;手術(shù)治療喉癌根治性放療后復(fù)發(fā)病人13例報(bào)告[J];臨床耳鼻咽喉科雜志;1998年11期

6 王衛(wèi)華;蘇鴻禧;;人類乳頭狀瘤病毒與喉癌[J];國(guó)際耳鼻咽喉頭頸外科雜志;1991年05期

7 屠規(guī)益;各地腫瘤醫(yī)院喉癌收治情況[J];耳鼻咽喉-頭頸外科;1994年04期

8 ;激光治療喉癌[J];國(guó)外醫(yī)學(xué).耳鼻咽喉科學(xué)分冊(cè);1994年01期

9 程天風(fēng),黃秋生;喉癌切除喉成形術(shù)的護(hù)理體會(huì)[J];江蘇大學(xué)學(xué)報(bào)(醫(yī)學(xué)版);1994年02期

10 周健;手術(shù)治療喉癌88例分析[J];溫州醫(yī)學(xué)院學(xué)報(bào);1995年S1期

相關(guān)會(huì)議論文 前10條

1 李巍;符爽;孫開(kāi)來(lái);富偉能;;SP100基因在喉癌中表達(dá)的研究[A];北方遺傳資源的保護(hù)與利用研討會(huì)論文匯編[C];2010年

2 楊蓓蓓;陳嘉;蔣驊;張守德;凌奕;;靶向表皮生長(zhǎng)因子受體的喉癌基因治療策略研究[A];浙江省醫(yī)學(xué)會(huì)耳鼻咽喉科學(xué)分會(huì)成立60周年慶典暨2011年浙江省醫(yī)學(xué)會(huì)耳鼻咽喉頭頸外科學(xué)學(xué)術(shù)年會(huì)論文匯編[C];2011年

3 符爽;富偉能;;MYCT1-TV在喉癌中的表達(dá)及功能研究[A];中國(guó)的遺傳學(xué)研究——遺傳學(xué)進(jìn)步推動(dòng)中國(guó)西部經(jīng)濟(jì)與社會(huì)發(fā)展——2011年中國(guó)遺傳學(xué)會(huì)大會(huì)論文摘要匯編[C];2011年

4 劉慧光;任偉;;中晚期喉癌病人圍手術(shù)期護(hù)理[A];全國(guó)腫瘤護(hù)理學(xué)術(shù)交流暨專題講座會(huì)議論文匯編[C];2003年

5 王文忠;;白細(xì)胞介素-18在人喉鱗狀細(xì)胞癌中的表達(dá)[A];安徽省第五屆“興皖之光”青年學(xué)術(shù)年會(huì)論文集（醫(yī)科卷）[C];2005年

6 孫紹華;馬會(huì)平;劉劍利;李福才;;靶向干擾Hep-2細(xì)胞P/N1的研究[A];中國(guó)的遺傳學(xué)研究——遺傳學(xué)進(jìn)步推動(dòng)中國(guó)西部經(jīng)濟(jì)與社會(huì)發(fā)展——2011年中國(guó)遺傳學(xué)會(huì)大會(huì)論文摘要匯編[C];2011年

7 孫麗麗;鄭穎;高虹;;低劑量輻射對(duì)人喉癌細(xì)胞Hep—2生長(zhǎng)的影響[A];吉林省醫(yī)學(xué)會(huì)第九次耳鼻咽喉—頭頸外科學(xué)術(shù)會(huì)議論文匯編[C];2011年

8 張劍;;甲苯胺藍(lán)染色對(duì)喉癌切緣作用的評(píng)估[A];西部大開(kāi)發(fā) 科教先行與可持續(xù)發(fā)展——中國(guó)科協(xié)2000年學(xué)術(shù)年會(huì)文集[C];2000年

9 劉吉祥;;早期喉癌的CO_2激光微創(chuàng)手術(shù)治療[A];第四屆全國(guó)中西醫(yī)結(jié)合耳鼻咽喉科學(xué)術(shù)會(huì)論文匯編[C];2003年

10 陳鳴;楊蓓蓓;;IL-17對(duì)喉癌的血管形成和轉(zhuǎn)移作用的研究[A];浙江省醫(yī)學(xué)會(huì)耳鼻咽喉科學(xué)分會(huì)成立60周年慶典暨2011年浙江省醫(yī)學(xué)會(huì)耳鼻咽喉頭頸外科學(xué)學(xué)術(shù)年會(huì)論文匯編[C];2011年

相關(guān)重要報(bào)紙文章 前10條

1 楊陽(yáng);喉癌與HP兩者存在聯(lián)系[N];醫(yī)藥經(jīng)濟(jì)報(bào);2001年

2 秦皇島市腫瘤醫(yī)院放療科主任 趙成會(huì);警惕喉癌的早期信號(hào)[N];河北科技報(bào);2009年

3 劉江峰 趙成會(huì);十個(gè)喉癌九個(gè)是煙民[N];衛(wèi)生與生活報(bào);2009年

4 吳正虎;切除喉癌還能說(shuō)話嗎？[N];浙江日?qǐng)?bào);2001年

5 黃志純　程守勤 （黃志純 南京中大醫(yī)院耳鼻咽喉科主任）;聲音嘶啞當(dāng)心喉癌[N];健康報(bào);2008年

6 陳默;中山“協(xié)和”“喉癌全切術(shù)”喜獲成功[N];中山日?qǐng)?bào);2008年

7 宋雯;舌、唇、喉癌的早期有什么信號(hào)[N];衛(wèi)生與生活報(bào);2003年

8 復(fù)旦大學(xué)附屬腫瘤醫(yī)院放療科 胡超蘇;早期喉癌不用切喉[N];健康時(shí)報(bào);2009年

9 雄縣醫(yī)院耳鼻喉科 劉江峰;喉癌和肺心病 都是吸煙惹的禍[N];河北科技報(bào);2009年

10 謝環(huán)馳;中國(guó)喉癌研究取得新突破[N];保健時(shí)報(bào);2003年

相關(guān)博士學(xué)位論文 前10條

1 許瑩;miR-106b在喉癌中對(duì)RUNX3表達(dá)的調(diào)控及其機(jī)制研究[D];山西醫(yī)科大學(xué);2013年

2 劉杰;細(xì)胞生長(zhǎng)調(diào)節(jié)基因遺傳變異與喉癌風(fēng)險(xiǎn)及預(yù)后[D];中國(guó)協(xié)和醫(yī)科大學(xué);2010年

3 崔朝陽(yáng);喉癌及復(fù)發(fā)癌微衛(wèi)星雜合性丟失的研究[D];山東大學(xué);2011年

4 汪超;正常人喉的三維重建及喉癌生長(zhǎng)浸潤(rùn)特征的研究[D];山西醫(yī)科大學(xué);2010年

5 尹萬(wàn)忠;喉癌多藥耐藥相關(guān)基因的篩查及中藥逆轉(zhuǎn)機(jī)制的研究[D];吉林大學(xué);2010年

6 劉巖;喉癌側(cè)群細(xì)胞生物學(xué)特性的研究[D];吉林大學(xué);2011年

7 李巍;喉癌中SP100表達(dá)及生物學(xué)功能研究[D];中國(guó)醫(yī)科大學(xué);2010年

8 馮彥;喉癌外科療效的系統(tǒng)評(píng)價(jià)及TopoⅡ-α表達(dá)與喉癌臨床特征的相關(guān)研究[D];山西醫(yī)科大學(xué);2011年

9 陳偉;端粒酶抑制后存活喉癌細(xì)胞端粒機(jī)制和關(guān)鍵蛋白的研究[D];武漢大學(xué);2010年

10 張勇;羅格列酮和曲格列酮對(duì)人喉癌Hep-2細(xì)胞影響的實(shí)驗(yàn)研究[D];鄭州大學(xué);2010年

相關(guān)碩士學(xué)位論文 前10條

1 江黎珠;FoxM1在喉癌中的表達(dá)及其在姜黃素抑制喉癌細(xì)胞株Hep-2增殖、侵襲、轉(zhuǎn)移中的作用[D];重慶醫(yī)科大學(xué);2011年

2 溫曉霞;喉癌大體分型的病理特點(diǎn)與臨床意義[D];中國(guó)醫(yī)科大學(xué);2004年

3 周q，

本文編號(hào)：1786099