本文選題：腎透明細胞癌 + miR-182�。� 參考：《鄭州大學(xué)》2016年博士論文

【摘要】：背景腎細胞癌(renal cell carcinoma,RCC)也稱為腎腺癌或腎癌,是來源于腎實質(zhì)小管上皮細胞的惡性腫瘤。據(jù)流行病學(xué)統(tǒng)計,腎細胞癌在所有類型的泌尿系統(tǒng)惡性腫瘤中排名第二位。最近幾年來的研究表明,腎細胞癌的發(fā)病率較過去明顯增高。流行病學(xué)研究表明,腎細胞癌約占成年人每年新發(fā)惡性腫瘤的3%,且其發(fā)病率在過去的二十年中呈不斷上升趨勢。腎透明細胞癌(clear cell renal cell carcinoma,CCRCC)為腎細胞癌中最為多見的病理類型,其發(fā)病率約占所有類型腎癌發(fā)病率的80~85%�，F(xiàn)階段臨床上對腎癌的治療仍是以根治性腎切除為主,對于沒有累及腎周筋膜的腫瘤來說,采取手術(shù)切除的方法療效最好,但對于腎癌晚期以及腎癌術(shù)后發(fā)生復(fù)發(fā)和轉(zhuǎn)移的患者依然缺乏行之有效的治療方法。盡管目前分子靶向治療藥物已經(jīng)應(yīng)用于臨床上腎癌的治療當中,且患者的預(yù)后亦有了較大改善,但腎癌患者的總體治療效果依然不佳。過去的研究表明,機體內(nèi)多種因素促進了腎透明細胞癌的發(fā)生以及惡性化進程,因此開展基礎(chǔ)實驗進行深入研究,探討腎細胞癌的發(fā)病原因以及癌細胞內(nèi)信號轉(zhuǎn)導(dǎo)通路的改變以及癌基因/抑癌基因的變化情況,對于尋找出更具有針對性的關(guān)鍵靶點以及更加有效的臨床治療藥物具有重要意義。mi R-182為一種mi RNA。目前已有研究證實,mi R-182在多種實體惡性腫瘤中的表達量發(fā)生異常增高或降低,從而提示其對腫瘤的發(fā)生和發(fā)展具有促癌或者抑癌基因的作用,但其在腎透明細胞癌中的表達情況以及作用機制仍尚未探明。胰島素樣生長因子(insulin-like growth factors,IGFS)是生長因子的重要成員之一,其在人類機體骨骼以及肌肉的生長和分化過程中發(fā)揮著十分重要的作用,而IGFS的大部分生物學(xué)活性均由IGF-1R介導(dǎo)產(chǎn)生。IGF-1R廣泛表達于生物機體各種類型的細胞中,其信號轉(zhuǎn)導(dǎo)途徑與惡性腫瘤的發(fā)生和發(fā)展之間存在密切聯(lián)系。IGF-1R經(jīng)由多種信號轉(zhuǎn)導(dǎo)通路介導(dǎo)了腫瘤細胞的惡性化增殖、侵襲以及轉(zhuǎn)移過程,同時還介導(dǎo)了腫瘤血管的生成以及腫瘤細胞抗凋亡等作用。除此之外,IGF-1R對透明細胞癌的發(fā)生和發(fā)展亦具有重要影響。目的本研究通過熒光定量PCR檢測mi R-182在腎透明細胞癌患者腫瘤組織中的表達,并探討其與患者的重要臨床病理參數(shù)的相關(guān)性,同時分析mi R-182的表達對腎透明細胞癌細胞增殖、侵襲及轉(zhuǎn)移過程的影響,探究mi R-182信號活化或抑制對于腎透明細胞癌細胞中IGF-1R表達的調(diào)控作用,研究其對腎透明細胞癌細胞侵襲和轉(zhuǎn)移的影響,旨在了解腎透明細胞癌的發(fā)生和發(fā)展機制,同時為腎透明細胞癌的臨床診斷以及靶向治療提供可靠依據(jù)。方法(1)采集2010年4月~2015年8月期間就診于鄭州大學(xué)第一附屬醫(yī)院泌尿外科行根治性腎切除手術(shù)57例腎透明細胞癌患者。其中男性患者為38例,女性患者為19例,年齡范圍在50~79歲之間。腎透明細胞癌組織學(xué)分級根據(jù)Fuhrman分級系統(tǒng)進行劃分:I級為15例,II期為26例,III~IV級16例。臨床分期按照Robson法進行劃分:I期22例、II期16例,III~IV期19例。按照是否發(fā)生轉(zhuǎn)移進行劃分:發(fā)生轉(zhuǎn)移者為19例,無轉(zhuǎn)移者為38例。此外選取10例于本院進行健康體檢的志愿者外周血作為健康對照組。采用熒光實時定量PCR檢測mi R-182在腎透明細胞癌組織及其相應(yīng)癌旁正常組織、患者血漿及健康志愿者血漿中的表達,分析mi R-182與腎透明細胞癌患者臨床病理參數(shù)的相關(guān)性。(2)設(shè)計并合成mi R-182 mimic、mi R-182 inhibitor和mi R-control,隨后將三者分別轉(zhuǎn)染人腎透明細胞癌Caki-1細胞,以此構(gòu)建mi R-182過表達或抑制表達的Caki-1細胞系,并通過熒光實時定量PCR法檢測轉(zhuǎn)染后上述三組細胞中mi R-182的表達用以驗證。隨后采用MTT法檢測轉(zhuǎn)染后上述三組細胞的增殖活性;克隆形成實驗檢測生長情況;Transwell侵襲小室法檢測細胞的遷移和侵襲能力。(3)運用生物信息學(xué)軟件篩選mi R-182的靶基因。采用熒光定量PCR和western blot對分別檢測轉(zhuǎn)染mi R-182 control、mi R-182 mimic以及mi R-182 inhibitor的人透明細胞癌Caki-1細胞中IGF-1R m RNA和蛋白的表達情況。采用IGF-1R 3’UTR定點突變的方法構(gòu)建含有熒光素酶報告基因的IGF-1R 3’UTR Mut(突變型)質(zhì)粒載體,同時構(gòu)建IGF-1R 3’UTR WT(野生型)質(zhì)粒載體,將兩者分別與mi R-182 mimic共轉(zhuǎn)染Caki-1細胞。采用熒光素酶報告系統(tǒng)進行檢測上述細胞中熒光素酶的表達量。使用si-IGF1R構(gòu)建IGF-1R表達抑制的Caki-1細胞系,并用熒光定量PCR和western blot法分別檢測細胞中IGF-1Rm RNA和蛋白的表達。將人透明細胞癌Caki-1細胞分為3組,采用Transwell小室法分別檢測Control組、mi R-182 inhibitor組以及si-IGF1R+mi R-182 inhibitor組細胞的侵襲以及遷移能力。結(jié)果(1)熒光定量PCR檢測結(jié)果表明,腎透明細胞癌組織中mi R-182的表達量明顯低于其在癌旁相應(yīng)正常組織中的表達(P0.05);mi R-182在腎透明細胞癌患者血漿中的表達明顯低于健康志愿者(P0.05)。mi R-182與腎透明細胞癌患者臨床病理參數(shù)分析結(jié)果表明,mi R-182的表達與腎透明細胞癌患者的組織學(xué)分級、臨床分期以及轉(zhuǎn)移有關(guān),而與患者的性別和年齡因素?zé)o關(guān)。(2)熒光定量PCR檢測結(jié)果表明,與control組相比,mi R-182 mimic組細胞中mi R-182的表達水平明顯增高(P0.05),mi R-182 inhibitor組細胞中mi R-182的表達量明顯降低(P0.05),表明mi R-182過表達/抑制表達Caki-1細胞系構(gòu)建成功。MTT法檢測結(jié)果表明,轉(zhuǎn)染mi R-182 mimic的Caki-1細胞在48 h、72 h、96 h時的增殖率明顯低于對照組(P0.05);轉(zhuǎn)染mi R-182 inhibitor的Caki-1細胞在48 h、72 h、96 h時的增殖率明顯高于對照組(P0.05)�？寺⌒纬蓪嶒灲Y(jié)果表明,mi R-182 mimic組Caki-1細胞的克隆形成數(shù)明顯低于對照組(P0.05);mi R-182 inhibitor組Caki-1細胞的克隆形成數(shù)明顯高于對照組(P0.05)。Transwell小室法檢測結(jié)果表明,mi R-182 mimic組Caki-1細胞的遷移和侵襲細胞數(shù)均明顯低于對照組(P0.05);而mi R-182 inhibitor組Caki-1細胞的遷移和侵襲細胞數(shù)均明顯高于對照組(P0.05)。(3)生物信息學(xué)軟件預(yù)測結(jié)果表明,IGF-1R為mi R-182的靶基因。轉(zhuǎn)染mi R-182 mimic后,Caki-1細胞中IGF-1R m RNA和蛋白的表達量明顯降低(P0.05);轉(zhuǎn)染mi R-182 inhibitor后,Caki-1細胞中IGF-1R m RNA和蛋白的表達量明顯增高(P0.05)。熒光素酶檢測結(jié)果表明,與對照組相比,mi R-182 mimic與IGF1R 3’UTR WT共轉(zhuǎn)染組的熒光素酶表達量明顯降低(P0.05);而mi R-182 mimic和IGF1R 3’UTR Mut共轉(zhuǎn)染組細胞中的熒光素酶表達量則與對照組相比無顯著差異(P0.05)。si-IGF1R干擾表達后Caki-1細胞IGF-1R m RNA和蛋白的表達量明顯降低。Transwell小室法檢測結(jié)果表明,與對照組相比,mi R-182 inhibitor組細胞的遷移和侵襲細胞數(shù)明顯增高(P0.05),而si-IGF1R+mi R-182 inhibitor組細胞的遷移和侵襲細胞數(shù)則明顯降低(P0.05)。結(jié)論mi R-182在腎透明細胞癌組織以及患者外周血中呈低表達,且其表達量與腎透明細胞癌患者的組織學(xué)分級、臨床分期以及有無轉(zhuǎn)移密切相關(guān)。mi R-182能夠通過直接抑制IGF-1R的表達來實現(xiàn)對腎透明細胞癌細胞增殖、侵襲以及轉(zhuǎn)移的調(diào)控,從而抑制腎透明細胞癌的發(fā)生和發(fā)展。
[Abstract]:Renal cell carcinoma (RCC), also known as renal adenocarcinoma or renal carcinoma, is a malignant tumor derived from renal tubular epithelial cells. According to epidemiological statistics, renal cell carcinoma is ranked second in all types of urological malignancies. Recent studies have shown that the incidence of renal cell carcinoma is significantly higher than that in the past. Epidemiological studies have shown that renal cell carcinoma accounts for about 3% of new malignant tumors in adults, and its incidence is increasing in the past twenty years. Clear cell renal cell carcinoma (CCRCC) is the most common pathological type of renal cell carcinoma, and its incidence is about 80~85 in the incidence of all types of renal cancer. At this stage, the treatment of renal carcinoma is still mainly radical nephrectomy. For the tumor without involvement of the perirenal fascia, surgical resection is the best treatment. However, there is still a lack of effective treatment for patients with late renal cancer and recurrence and metastasis of renal carcinoma. Drugs have been used in the treatment of clinical renal cancer, and the prognosis of the patients has been improved greatly, but the overall treatment effect of renal cancer patients is still poor. Past studies have shown that many factors in the body promote the occurrence and malignant process of renal clear cell carcinoma. The cause of cell carcinoma and the change of signal transduction pathway in cancer cells and the change of oncogene / tumor suppressor gene are of great significance for finding more targeted key targets and more effective clinical drugs.Mi R-182 for a kind of MI RNA., MI R-182 is in a variety of malignant swelling. The expression of insulin-like growth factors (IGFS) is an important member of the growth factor. First, it plays a very important role in the growth and differentiation of human skeleton and muscle, and most of the biological activity of IGFS is mediated by IGF-1R to produce.IGF-1R widely expressed in various types of cells. The signal transduction pathway is closely related to the occurrence and development of malignant swollen tumor,.IGF-1 R mediated the malignant proliferation, invasion and metastasis of tumor cells via a variety of signal transduction pathways, and also mediates the formation of tumor vessels and the anti apoptosis effect of tumor cells. In addition, IGF-1R also plays an important role in the development and development of clear cell carcinoma. Objective this study was to detect mi R-182 by fluorescence quantitative PCR The expression in the tumor tissue of patients with renal clear cell carcinoma and its correlation with the important clinicopathological parameters of the patients, and the effect of the expression of MI R-182 on the proliferation, invasion and metastasis of renal clear cell carcinoma cells, and to explore the regulation of the activation or inhibition of the MI R-182 signal to the expression of IGF-1R in the renal clear cell carcinoma cells. The purpose of this study is to investigate the invasion and metastasis of renal clear cell carcinoma cells, to understand the mechanism of the occurrence and development of renal clear cell carcinoma, and to provide a reliable basis for the clinical diagnosis and target treatment of renal clear cell carcinoma. Method (1) collected in the Department of Urology, the First Affiliated Hospital of Zhengzhou University, April 2010, during the period of August ~2015. 57 cases of renal clear cell carcinoma were treated with radical nephrectomy, of which 38 cases were male and 19 female patients, age range was between 50~79 years. The histological grading of renal clear cell carcinoma was divided according to Fuhrman classification system: 15 cases of I grade, 26 cases of II stage, 16 cases of III~IV grade. The clinical stages were divided according to Robson method: 22 cases in I phase, II 16 cases and 19 cases of III~IV phase were divided into 19 cases and 38 cases without metastasis. In addition, the peripheral blood of 10 cases of healthy volunteers in our hospital was selected as the healthy control group. The fluorescence real-time quantitative PCR was used to detect mi R-182 in the tissues of renal hyaline cell carcinoma and the corresponding normal tissue adjacent to the cancer. Plasma and healthy volunteers were expressed in plasma, and the correlation between MI R-182 and the clinicopathological parameters of patients with renal clear cell carcinoma was analyzed. (2) mi R-182 mimic, MI R-182 inhibitor and MI R-control were designed and synthesized. Then the three persons were transfected into the Caki-1 cell of human renal clear cell carcinoma. Cell lines were detected by fluorescence real-time quantitative PCR method to detect the expression of MI R-182 in these three groups of cells after transfection. Then MTT method was used to detect the proliferation activity of the three groups of the above transfected cells; the clone formation test was used to detect the growth of the cells; Transwell invaded the cell to detect the cell migration and invasion ability. (3) use bioinformatics soft. The target gene of MI R-182 was screened by using the fluorescent quantitative PCR and Western blot to detect the expression of MI R-182 control, MI R-182 mimic and the human transparent cell carcinoma cell carcinoma cells. 1R 3 'UTR Mut (mutant) plasmid vector, simultaneously constructed IGF-1R 3' UTR WT (wild type) plasmid vector, and co transfected Caki-1 cells with MI R-182 mimic respectively. The luciferase expression was detected by the luciferase reporter system. The expression of IGF-1Rm RNA and protein in the cells was detected by PCR and Western blot. The Caki-1 cells of human transparent cell carcinoma were divided into 3 groups. The invasion and migration ability of Control group, MI R-182 inhibitor group and si-IGF1R+mi MI group were detected by Transwell chamber method. Results (1) the results of quantitative fluorescence detection showed that The expression of MI R-182 in the tissues of renal clear cell carcinoma was significantly lower than that in the normal tissues near the carcinoma (P0.05). The expression of MI R-182 in the plasma of patients with renal clear cell carcinoma was significantly lower than that of healthy volunteers (P0.05).Mi R-182 and renal clear cell carcinoma. The expression of MI R-182 and the transparency of renal transparency were revealed. The histological grade, clinical staging and metastasis of the patients were not related to the sex and age factors of the patients. (2) the results of fluorescence quantitative PCR showed that the expression level of MI R-182 in the MI R-182 mimic group was significantly higher than that in the control group (P0.05), and the expression of MI in MI R-182 inhibitor group was significantly reduced. .05) showed that MI R-182 overexpressed / suppressed expression of Caki-1 cell lines was successfully constructed by.MTT assay. The proliferation rate of Caki-1 cells transfected with MI R-182 mimic in 48 h, 72 h and 96 h was significantly lower than that of the control group, and the proliferation rate of the cells transfected in 48, 72, and 96 was significantly higher than that of the control group. The experimental results showed that the number of clone formation of Caki-1 cells in MI R-182 mimic group was significantly lower than that of the control group (P0.05), and the number of Caki-1 cells in the MI R-182 inhibitor group was significantly higher than that of the control group (P0.05).Transwell chamber method. 05), and the number of migration and invasion of Caki-1 cells in MI R-182 inhibitor group was significantly higher than that of the control group (P0.05). (3) the prediction results of bioinformatics software showed that IGF-1R was the target gene of MI R-182. The expression of IGF-1R m RNA and protein in the cells increased significantly (P0.05). The luciferase expression of MI R-182 mimic and IGF1R 3 'UTR WT co transfection group was significantly lower than that of the control group (P0.05), while the luciferase expression in the cells of the MI R-182 and the co transfected group was compared with the control group. The expression of IGF-1R m RNA and protein in Caki-1 cells decreased significantly after the expression of.Si-IGF1R interference without significant difference (P0.05), and the results of.Transwell compartment assay showed that the number of cell migration and invasion cells in MI R-182 inhibitor group increased significantly (P0.05) compared with the control group. The number of cells decreased significantly (P0.05). Conclusion the expression of MI R-182 in the tissues of renal clear cell carcinoma and the peripheral blood of the patients was low, and the expression of R-182 was closely related to the histological grade of the patients with clear cell carcinoma of the kidney, the clinical stages and the close correlation between the metastasis and the metastasis of the renal clear cell carcinoma cells by directly inhibiting the expression of IGF-1R. Regulation of proliferation, invasion and metastasis can inhibit the occurrence and development of renal clear cell carcinoma.

【學(xué)位授予單位】：鄭州大學(xué)
【學(xué)位級別】：博士
【學(xué)位授予年份】：2016
【分類號】：R737.11

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