本文選題：結(jié)直腸癌 + NIBP�。� 參考：《廣西醫(yī)科大學(xué)》2015年博士論文

【摘要】：背景和目的結(jié)直腸癌是臨床最常見的惡性腫瘤之一,在全世界范圍內(nèi),結(jié)直腸癌的發(fā)病率和死亡率均處于惡性腫瘤的第3位。在我國(guó),隨著生活水平的不斷提高,發(fā)病率呈上升態(tài)勢(shì)。結(jié)直腸癌的發(fā)生發(fā)展是遺傳和環(huán)境等多種因素作用導(dǎo)致多基因改變及其相互作用的結(jié)果,其中涉及到多個(gè)信號(hào)轉(zhuǎn)導(dǎo)通路,比NF-κB信號(hào)通路。它們通過(guò)NF-kB轉(zhuǎn)錄因子,調(diào)節(jié)炎癥和腫瘤相關(guān)的至關(guān)重要的幾個(gè)途徑,影響腫瘤細(xì)胞的生存、血管生成、腫瘤細(xì)胞的運(yùn)動(dòng)性和侵襲力,從而促進(jìn)腫瘤細(xì)胞的增殖,抑制細(xì)胞凋亡,并引起腫瘤的侵襲和轉(zhuǎn)移。NIBP是一種支架蛋白,它將NF-κB經(jīng)典途徑中的關(guān)鍵激活子-IKKβ和非經(jīng)典途徑中的關(guān)鍵酶-NIK連接成為三聚體。研究發(fā)現(xiàn),NIBP的表達(dá)升高可以促進(jìn)IKKβ及其下游p65的磷酸化,由此推測(cè),NIBP在NF-κB經(jīng)典途徑中發(fā)揮激活劑的作用。另一方面,抑制NIBP的表達(dá)則能減少由NIK和IKKβ分別介導(dǎo)的INF-κB信號(hào)通路的活化。此外,NIBP可能提高由TNF-a刺激引起NF-κB信號(hào)通路的活化從而促進(jìn)腫瘤細(xì)胞的侵襲能力。最近研究還發(fā)現(xiàn),NIBP在人結(jié)腸癌組織中的表達(dá)明顯升高,推測(cè)這種升高可能與NF-κB信號(hào)通路的活化有關(guān),NIBP可能參與腺瘤向腺癌的演變過(guò)程。因此,本研究以NIBP為研究對(duì)象,檢測(cè)結(jié)直腸癌組織中NIBP、NF-κB活性因子p-p65和c-myc、cyclinD1的表達(dá),了解其表達(dá)與結(jié)直腸癌的臨床分期及臨床病理關(guān)系。利用基因工程構(gòu)建NIBP基因沉默載體,在體外試驗(yàn)中驗(yàn)證NIBP基因表達(dá)水平變化對(duì)結(jié)腸癌細(xì)胞增殖的影響,探討其在結(jié)直腸癌的發(fā)生、發(fā)展及侵襲轉(zhuǎn)移中的作用和意義。方法1.采用免疫組化SP法分別檢測(cè)16例正常結(jié)腸粘膜、21例結(jié)直腸腺瘤以及114例結(jié)直腸癌患者結(jié)直腸組織中NIBP、NF-κB活性因子p-p65、c-myc和cyclinD1的表達(dá),分析NIBP等在結(jié)直腸癌臨床分期和臨床病理的關(guān)系,推測(cè)其在結(jié)直腸癌的發(fā)生發(fā)展和侵襲轉(zhuǎn)移中的作用。2.利用基因工程,以人結(jié)腸癌細(xì)胞HCT116株為研究對(duì)象,設(shè)計(jì)并構(gòu)建人NIBP基因的慢病毒表達(dá)載體pLenti6.3-EGFP-NIBP-miR-1/2/3;另外,同時(shí)還設(shè)計(jì)無(wú)關(guān)的序列作為陰性對(duì)照(negative control, NC);人結(jié)腸癌細(xì)胞HCT1 16作為空白對(duì)照。用NIBP基因干擾的慢病毒及慢病毒陰性對(duì)照病毒液Lenti-EGFP感染靶細(xì)胞、空白細(xì)胞作對(duì)照,抽提細(xì)胞的蛋白,WB檢測(cè)目的蛋白的表達(dá),篩選出最佳干擾靶點(diǎn)。目的基因干擾靶點(diǎn)慢病毒Lenti-EGFP-NIBP-miR感染HCT 116細(xì)胞后加入BSD(Blasticidin, BSD)進(jìn)行篩選,獲得穩(wěn)定轉(zhuǎn)染NIBP低表達(dá)的單克隆HCT116細(xì)胞。應(yīng)用QRT-PCR檢測(cè)轉(zhuǎn)染效率,選擇NIBP干擾效率高的穩(wěn)轉(zhuǎn)株細(xì)胞株用于后續(xù)的細(xì)胞功能試驗(yàn)。3.以空白對(duì)照組(blank control,簡(jiǎn)稱CON組,即未轉(zhuǎn)染的HCT116細(xì)胞株)、陰性對(duì)照組(NC組,Lenti-EGFP-miR轉(zhuǎn)染HCT116細(xì)胞株)、NIBP低表達(dá)組(NIBP組,Lenti-EGFP-NIBP-miR轉(zhuǎn)染HCT 116細(xì)胞株)和NIBP低表達(dá)組細(xì)胞加NF-κB經(jīng)典途徑激活劑TNF-a組(NIBPT組)作為研究對(duì)象,采用CCK-8檢測(cè)試驗(yàn)盒檢測(cè)各組細(xì)胞的增殖能力；流式細(xì)胞儀檢測(cè)各組細(xì)胞的凋亡和細(xì)胞周期分布情況；透射電子顯微鏡觀察細(xì)胞凋亡情況；QRT-PCR和Western Blot檢測(cè)細(xì)胞相關(guān)周期蛋白c-myc和cyclinD1的表達(dá)情況。結(jié)果1.免疫組化顯示結(jié)直腸癌組織中NIBP、NF-κB活性因子p-p65、c-myc和cyclinD1的陽(yáng)性表達(dá)率均高于結(jié)直腸腺瘤和正常結(jié)腸粘膜組織,P0.05；而且NIBP、NF-κB活性因子p-p65、c-myc和cyclinDl在結(jié)腸癌組織中的表達(dá)與腫瘤的分化程度、組織類型、浸潤(rùn)深度、TNM和Duke's分期、淋巴結(jié)轉(zhuǎn)移及遠(yuǎn)處轉(zhuǎn)移相關(guān),P0.05。同時(shí),NIBP、c-myc和cyclinD1與NF-κB活化因子p-p65呈正相關(guān)關(guān)系。2.建立NIBP沉默載體和穩(wěn)定轉(zhuǎn)染HCT116細(xì)胞株。我們利用質(zhì)粒載體pLenti6.3-MCS/V5 DEST系列慢病毒表達(dá)載體成功構(gòu)建人NIBP基因的慢病毒表達(dá)載體Lenti-EGFP-NIBP-miR(NIBP)和Lenti-EGFP-miR(NC);經(jīng)酶切、重組克隆及鑒定等,證實(shí)載體構(gòu)建成功。設(shè)計(jì)的NIBP基因1#,2#,3#干擾靶點(diǎn)進(jìn)行慢病毒包裝并感染HCT116細(xì)胞后3個(gè)靶點(diǎn)的敲減效率均非常明顯,NIBP蛋白均沒有出現(xiàn)明顯的條帶。我們選擇了其中的第3#靶點(diǎn)進(jìn)行后續(xù)穩(wěn)轉(zhuǎn)株篩選。將這些載體轉(zhuǎn)染HCT116細(xì)胞株,放在熒光顯微鏡下觀察,看到綠色熒光；可以篩選出穩(wěn)定轉(zhuǎn)染的單克隆細(xì)胞株；通過(guò)QRT-PCR和Western Blot試驗(yàn)證實(shí)NIBP干擾效果滿意,HCT116細(xì)胞NIBP干擾穩(wěn)轉(zhuǎn)株與陰性對(duì)照穩(wěn)轉(zhuǎn)株相比,NIBP干擾效率高。3. NIBP對(duì)結(jié)腸癌細(xì)胞生長(zhǎng)的影響到試驗(yàn)研究：CCK-8試驗(yàn)顯示,NIBP轉(zhuǎn)染細(xì)胞組和NIBPT組的細(xì)胞生長(zhǎng)較空白組和陰性對(duì)照組減慢,P0.05；細(xì)胞凋亡檢測(cè)四組細(xì)胞的凋亡率差異無(wú)統(tǒng)計(jì)學(xué)意義,P0.05；細(xì)胞周期檢測(cè)結(jié)果顯示NIBP和NIBPT組的細(xì)胞多處于Go/G1期(分別為73.500%±3.061%和70.133%±5.181%),明顯高于HCT116細(xì)胞組和NC細(xì)胞組(55.933%±3.963%和52.000%±2.193%),P0.05；NIBP和NIBPT組細(xì)胞的S期分別為6.700%±1.249%和9.467%±4.858%,低于HCT116細(xì)胞組和NC細(xì)胞組(11.300%±3.751%和13.567%±1.563%),差異有統(tǒng)計(jì)學(xué)意義,P0.05;NIBP和NIBPT組的細(xì)胞處于G2/M期分別為14.967%±1.041%和16.067%±1.380%,明顯低于HCT116細(xì)胞組和NC細(xì)胞組(29.933%±2.309%和31.200%±2.007%),P0.05；說(shuō)明NIBP轉(zhuǎn)染后結(jié)腸癌細(xì)胞的凋亡無(wú)明顯增加,但其增殖能力下降,而且即使使用NF-κB信號(hào)通路經(jīng)典途徑激活劑TNF-a也不能使其增殖能力恢復(fù)。透射電鏡觀察發(fā)現(xiàn)NIBP轉(zhuǎn)染細(xì)胞的凋亡亦無(wú)明顯增加。而QRT-PCR和WB的檢測(cè)結(jié)果顯示四組細(xì)胞中c-myc和cyclinD1的表達(dá)無(wú)顯著差異。結(jié)論1、NIBP、p-p65、c-myc和cyclinD1在結(jié)直腸癌組織中高表達(dá)。2. NIBP、p-p65、c-myc和cyclinD1的表達(dá)與腫瘤的分化程度、浸潤(rùn)深度、TNM和Duke's分期及有無(wú)淋巴結(jié)轉(zhuǎn)移或/和遠(yuǎn)處轉(zhuǎn)移有關(guān)。3、NIBP基因促進(jìn)結(jié)腸癌HCT116細(xì)胞的增殖能力,可能是通過(guò)激活NF-κB經(jīng)典途徑來(lái)實(shí)現(xiàn)的。4、NIBP對(duì)結(jié)腸癌HCT116細(xì)胞株的凋亡無(wú)明顯影響。5、NIBP對(duì)結(jié)腸癌HCT116細(xì)胞株的c-myc和cyclinD1的表達(dá)也無(wú)明顯影響。
[Abstract]:Background and objective colorectal cancer is one of the most common malignant tumors in clinical. In the world, the incidence and mortality of colorectal cancer are third in the malignant tumor. In China, with the continuous improvement of the living standard, the incidence of colorectal cancer is on the rise. The development of colorectal cancer is caused by many factors such as heredity and environment. The results of multiple gene changes and their interactions involving multiple signal transduction pathways, which are more important than the NF- kappa B signaling pathway. They regulate several important pathways associated with inflammation and cancer through NF-kB transcription factors, affecting the survival of tumor cells, angiogenesis, motility and invasiveness of tumor cells, thus promoting tumor cells. Proliferation, inhibition of apoptosis, and the invasion and metastasis of tumors,.NIBP is a scaffold protein, which connects the key activator -IKK beta in the classical pathway of NF- kappa B and the key enzyme in the non classical pathway, -NIK, to be a trimer. The study shows that the increase of NIBP expression can promote the phosphorylation of IKK beta and its downstream p65, thus speculating that NIBP is in NF- kappa B. On the other hand, inhibition of the expression of NIBP can reduce the activation of the INF- kappa B signaling pathway mediated by NIK and IKK beta, respectively. In addition, NIBP may improve the activation of the NF- kappa B signaling pathway by TNF-a stimulation to promote the invasion of tumor cells. The recent study also found that NIBP is in human colon cancer tissue. The expression in the NF- kappa B signaling pathway may be related to the activation of the signal pathway. NIBP may be involved in the evolution of adenoma to adenocarcinoma. Therefore, this study uses NIBP as a study object to detect the expression of NIBP, NF- kappa B active factor p-p65, c-myc, cyclinD1, and to understand the expression of the colorectal cancer and the clinical stages of colorectal cancer. The effect and significance of the changes of NIBP gene expression level on the proliferation of colon cancer cells and the role and significance of NIBP gene expression level on the occurrence, development and invasion and metastasis of colorectal cancer were examined in vitro by using gene engineering to construct a NIBP gene silencing carrier. Methods 16 cases of normal colon mucosa were detected by the immunization of SP. 21 cases of colorectal adenoma and 114 cases of colorectal cancer, NIBP, NF- kappa B active factor p-p65, c-myc and cyclinD1 expression, analysis of the relationship between NIBP and the clinical staging and clinicopathological features of colorectal cancer, and speculate that its role in the development of colorectal cancer and invasion and metastasis of.2. using genetic engineering, with human colon cancer cell HC The T116 strain was used to design and construct the Lentivirus Expression Vector pLenti6.3-EGFP-NIBP-miR-1/2/3 of human NIBP gene. In addition, unrelated sequences were designed as negative control (negative control, NC); human colon cancer cell HCT1 16 was used as a blank control. Lentivirus and lentivirus negative control virus liquid Lenti-EG with NIBP gene interference were used as control. FP infected target cells, blank cells as control, extract cell protein, WB to detect the expression of target protein, screening out the best interference target. Target gene interfered with lentivirus Lenti-EGFP-NIBP-miR infection HCT 116 cells after BSD (Blasticidin, BSD) screening, obtained stable transfection of low expression of NIBP of the monoclonal HCT116 cells. QRT application of QRT. The transfection efficiency was detected by -PCR, and the stable cell line with high NIBP interference efficiency was selected for subsequent cell function test,.3. was used as a blank control group (blank control, CON group, or untransfected HCT116 cell line), negative control group (NC group, Lenti-EGFP-miR transfected HCT116 cell line), NIBP low expression group (NIBP group, transfected 116) Cell lines and NIBP low expression group cells plus NF- kappa B classical pathway activator TNF-a group (NIBPT group) were used as the research object. CCK-8 test box was used to detect the proliferation ability of each cell. Flow cytometry was used to detect the cell apoptosis and cell cycle distribution; transmission electron microscopy was used to observe the cell apoptosis; QRT-PCR and Weste. RN Blot was used to detect the expression of cell related cyclin c-myc and cyclinD1. Results 1. immunohistochemical staining showed that NIBP, NF- kappa B active factor p-p65, c-myc and cyclinD1 positive rates were higher than those of colorectal adenoma and normal colon mucosa, P0.05. The expression in cancer tissue is related to the degree of differentiation, type of tissue, depth of invasion, TNM and Duke's staging, lymph node metastasis and distant metastasis, P0.05., NIBP, c-myc and cyclinD1 are positively related to NF- kappa B activator p-p65.2.,.2. to establish NIBP silencing carrier and stable transfection HCT116 cell strain. /V5 DEST series lentivirus vector successfully constructed the Lentivirus Expression Vector Lenti-EGFP-NIBP-miR (NIBP) and Lenti-EGFP-miR (NC) of human NIBP gene. Through enzyme digestion, recombinant cloning and identification, it confirmed the success of the vector construction. The designed NIBP gene 1#, 2#, 3# interfered the target of the lentivirus packaging and infected the HCT116 cells after the knockout effect of 3 targets. The NIBP protein had no obvious bands. We selected the 3# target for subsequent stable strain screening. These vectors were transfected into HCT116 cell lines and observed under the fluorescence microscope to see the green fluorescence; the stable transfected monkon cell lines could be screened; the QRT-PCR and Western Blot tests were used. The effect of NIBP interference was satisfactory. Compared with the negative control stable strain of HCT116 cell NIBP interference, the effect of NIBP interference efficiency.3. NIBP on the growth of colon cancer cells was studied. The CCK-8 test showed that the cell growth of NIBP transfected cell group and NIBPT group was slower than that of the blank group and the negative control group, P0.05; the apoptosis detection was four. There was no significant difference in the apoptosis rate of the group cells, P0.05. The cell cycle detection showed that the cells in the NIBP and NIBPT groups were mostly in the Go/G1 phase (73.500% + 3.061% and 70.133% + 5.181% respectively), obviously higher than the HCT116 cell group and the NC cell group (55.933% + 3.963% and 52% + 2.193%), and the S period of the P0.05; NIBP and NIBPT groups was 6.700%, respectively. 1.249% and 9.467% + 4.858%, lower than the HCT116 cell group and the NC cell group (11.300% + 3.751% and 13.567% + 1.563%), the difference was statistically significant. The cells in the group NIBP and NIBPT were 14.967% + 1.041% and 16.067% +, respectively, lower than the HCT116 cell group and NC cell group (29.933% + 2.309% and 31.200% + 3.751%), P0.05. The apoptosis of colon cancer cells was not significantly increased after NIBP transfection, but its proliferation ability decreased, and the proliferation ability could not be restored even with the use of NF- kappa B signaling pathway activator TNF-a. The transmission electron microscopy showed that the apoptosis of NIBP transfected cells was not significantly increased. The results of QRT-PCR and WB detection showed that c-myc in four groups of cells. Conclusion 1, 1, NIBP, p-p65, c-myc and cyclinD1 express the expression of.2. NIBP, p-p65, c-myc and cyclinD1 in colorectal cancer tissues, which are related to the degree of differentiation, depth of invasion, TNM and Duke's stages, and whether there is lymph node metastasis or / and distant transfer. The ability, possibly through the activation of the classical pathway of NF- kappa B, is.4. NIBP has no significant effect on the apoptosis of HCT116 cell line of colon cancer, and NIBP has no significant effect on the expression of c-myc and cyclinD1 in colon cancer HCT116 cell lines.
【學(xué)位授予單位】：廣西醫(yī)科大學(xué)
【學(xué)位級(jí)別】：博士
【學(xué)位授予年份】：2015
【分類號(hào)】：R735.34

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