小瞼裂綜合征相關(guān)基因Foxl2對(duì)Hela和Siha的生物學(xué)作用
發(fā)布時(shí)間：2018-07-25 08:45
【摘要】：小瞼裂綜合癥(blephar-ophimosis-ptosis-epicanthus inversus syndrome,BPES)是常染色體顯性遺傳疾病,臨床科室均有發(fā)現(xiàn)。其相關(guān)基因-Foxl2是一個(gè)單一的外顯子編碼的叉頭轉(zhuǎn)錄因子,基因突變可導(dǎo)致小瞼裂綜合征的發(fā)生。在女性患者之中,BPES被分為兩種類型:Ⅰ型伴有卵巢早衰,而II型卵巢功能及生育力正常[1,2]。Foxl2的轉(zhuǎn)錄m RNA先前主要被發(fā)現(xiàn)在小鼠胚胎的眼瞼、胚胎及性成熟小鼠的卵巢中[1,3]。Foxl2一直表達(dá)在卵巢的顆粒細(xì)胞上[4]。在青少年群體,卵巢顆粒細(xì)胞腫瘤(OGCTs)中,其表達(dá)下降[5]。另外,Shah等在2009年發(fā)現(xiàn)體細(xì)胞Foxl2的突變即402C突變?yōu)镚[5]。這個(gè)突變出現(xiàn)在97%的成人卵巢顆粒細(xì)胞腫瘤(OGCTs)中,且對(duì)這個(gè)腫瘤類型是特異的[6-10]。另發(fā)現(xiàn)在結(jié)直腸癌中存在Foxl2位點(diǎn)失活,是體細(xì)胞超甲基化導(dǎo)致的[11]。更有趣的是,Foxl2的這個(gè)突變?cè)谌魏我环N性-索基質(zhì)細(xì)胞腫瘤及不相關(guān)的卵巢癌或乳腺癌中未發(fā)現(xiàn)[12,13]。另外,Wegman P等[14]在乳腺癌中發(fā)現(xiàn)Foxl2基因的表達(dá),并且這可能與芳香化酶的表達(dá)及其臨床預(yù)后相關(guān)。BPES相關(guān)基因Foxl2的功能越來越多的被發(fā)現(xiàn)。小瞼裂綜合征的相關(guān)基因Foxl2被相繼被研究,如在眼瞼、遺傳學(xué)、婦產(chǎn)科卵巢功能及少量腫瘤等方面。腫瘤相關(guān)的研究僅僅局限于直結(jié)腸癌、其他性索間質(zhì)細(xì)胞腫瘤、乳腺癌及卵巢癌之中。據(jù)我們所知,Foxl2尚未在宮頸癌中研究過,因此我們分析并探討了Foxl2在宮頸癌中的表達(dá)及對(duì)Foxl2對(duì)宮頸癌細(xì)胞的生物學(xué)作用。第一部分小瞼裂綜合征相關(guān)基因Foxl2在宮頸癌中的表達(dá)目的檢測(cè)小瞼裂綜合征相關(guān)基因Foxl2在宮頸癌組織中的表達(dá),并檢測(cè)Foxl2在宮頸腺癌及鱗癌這兩種細(xì)胞系中的轉(zhuǎn)錄RNA的水平。方法收集的宮頸癌37例患者的癌變組織,分為兩組:一組為腺癌,一組為鱗狀細(xì)胞癌;取宮頸上皮內(nèi)瘤變(CIN)的8例患者的病變組織,其中包括了低度鱗狀內(nèi)上皮瘤變(LSIL)患者5例,高度鱗狀上皮內(nèi)瘤變(HSIL)患者10例;取宮頸炎的10例患者的病變組織作為對(duì)照組。采用免疫組織化學(xué)染色技術(shù),分別檢測(cè)Foxl2在宮頸癌組織組、宮頸上皮內(nèi)瘤變組和對(duì)照組中的表達(dá);然后,培養(yǎng)人類宮頸癌的腺癌細(xì)胞系(Hela細(xì)胞)及鱗癌細(xì)胞系(Siha細(xì)胞),提取RNA,利用逆轉(zhuǎn)錄聚合酶鏈?zhǔn)椒磻?yīng)(Reverse transcription polymerase chain reaction,RT-PCR)技術(shù)分別檢測(cè)Foxl2基因在這這種癌癥的兩種細(xì)胞系中的表達(dá)水平。結(jié)果免疫組織化學(xué)染色結(jié)果顯示,Foxl2在宮頸鱗癌組織的切片中表達(dá)的陽性率顯著高于CIN組和對(duì)照組,Foxl2在宮頸鱗癌的組織中蛋白的表達(dá)水平相比宮頸腺癌及其他組,呈現(xiàn)為高表達(dá)狀態(tài)。在宮頸腺癌組、CIN組及宮頸炎組中并不表達(dá)Foxl2蛋白,也不存在顯著差異。RT-PCR結(jié)果顯示Hela細(xì)胞和Siha細(xì)胞可轉(zhuǎn)錄Foxl2的m RNA。結(jié)論在宮頸鱗癌中Foxl2的表達(dá)量顯著高于相對(duì)于宮頸腺癌、宮頸CIN組織及宮頸炎組織;Hela細(xì)胞及Siha細(xì)胞能轉(zhuǎn)錄Foxl2的m RNA。根據(jù)Foxl2在宮頸腺癌和鱗狀細(xì)胞癌,這兩種組織中的表達(dá)水平的不同,我們將進(jìn)一步研究Foxl2基因在宮頸癌細(xì)胞中的生物學(xué)作用。第二部分小瞼裂綜合征相關(guān)基因Foxl2對(duì)宮頸癌細(xì)胞系的生物學(xué)作用目的構(gòu)建兩種細(xì)胞系的模型,過表達(dá)Foxl2的Hela細(xì)胞和沉默F(xiàn)oxl2的Siha細(xì)胞模型,研究Foxl2對(duì)這兩種細(xì)胞的增殖、凋亡、粘附及侵襲能力的影響,從而分析Foxl2對(duì)宮頸癌的生物學(xué)作用。方法利用攜帶Foxl2的質(zhì)粒轉(zhuǎn)染Hela細(xì)胞,使其過表達(dá)Foxl2,同時(shí)沉默F(xiàn)oxl2基因在Siha細(xì)胞中的表達(dá),利用蛋白免疫印跡法(Western Blotting)驗(yàn)證轉(zhuǎn)染的效率,鑒定過表達(dá)及沉默模型;Foxl2過表達(dá)或者沉默后,Brdu法檢測(cè)Hela和Siha的增殖能力;Annexin V/PI法檢測(cè)Hela和Siha細(xì)胞的凋亡率;采用粘附試劑盒檢測(cè)Hela和Siha細(xì)胞的粘附能力;采用侵襲實(shí)驗(yàn)分別檢測(cè)過表達(dá)和沉默F(xiàn)oxl2的宮頸癌的兩種細(xì)胞系的侵襲力;采用流式細(xì)胞術(shù)(FCM)檢測(cè)過表達(dá)Foxl2的Hela細(xì)胞及沉默F(xiàn)oxl2的Siha細(xì)胞中Ki67、細(xì)胞增殖核抗原(proliferating cell nuclear antigen,PCNA)和Fas L的表達(dá)量,進(jìn)一步檢測(cè)和分析調(diào)節(jié)增殖和凋亡的相關(guān)因子的表達(dá)。結(jié)果Western Blotting結(jié)果,與對(duì)照組相比,過表達(dá)Hela細(xì)胞中Foxl2的表達(dá)量明顯增加;沉默Siha細(xì)胞中Foxl2的表達(dá)量顯著減少(P0.01),可見轉(zhuǎn)染模型構(gòu)建成功。Brdu及Annexin V/PI結(jié)果表明,與對(duì)照組相比,過表達(dá)Foxl2后,Hela的增殖能力明顯被抑制(P0.01);沉默組的增殖能力增加,同時(shí)其凋亡顯著降低(P0.001)。過表達(dá)Hela細(xì)胞的粘附無明顯改變,但是沉默F(xiàn)oxl2可促進(jìn)Siha的粘附。侵襲實(shí)驗(yàn)提示,過表達(dá)組細(xì)胞侵襲能力明顯減低(P0.05);沉默組細(xì)胞侵襲能力提高(P0.05)。PCM結(jié)果顯示,過表達(dá)的Hela中Ki67的表達(dá)水平明顯降低(P0.001),Fas L的表達(dá)增加(P0.01)。沉默的Siha中Ki67的表達(dá)量顯著增加(P0.001),并且Fas L的表達(dá)水平降低(P0.01)。但是,無論過表達(dá)還是沉默細(xì)胞組中PCNA的表達(dá)無明顯變化。結(jié)論結(jié)果表明,小瞼裂相關(guān)基因Foxl2抑制宮頸癌細(xì)胞Hela和Siha的增殖并促進(jìn)凋亡;抑制Hela和Siha的侵襲能力;與此同時(shí),促進(jìn)Siha的粘附,但Foxl2對(duì)Hela細(xì)胞的粘附能力無顯著作用。另外,Foxl2下調(diào)Ki67在Hela和Siha細(xì)胞的表達(dá)水平,其同時(shí)上調(diào)Fas L在Hela和Siha的表達(dá)。綜上所述,我們的實(shí)驗(yàn)研究結(jié)果表明,Foxl2在宮頸鱗癌中高表達(dá)。一方面,Foxl2抑制宮頸癌細(xì)胞的增殖,并抑制其凋亡,這個(gè)生物學(xué)作用主要是Foxl2通過下調(diào)Ki67的表達(dá)和上調(diào)Fas L的表達(dá)水平發(fā)揮作用的;另一方面,Foxl2可能是一個(gè)新的腫瘤抑制因子,至少在宮頸癌里面。這可能對(duì)于評(píng)價(jià)宮頸癌的轉(zhuǎn)移和復(fù)發(fā)是有價(jià)值的,但是仍需要進(jìn)一步的研究。
[Abstract]:Blephar-ophimosis-ptosis-epicanthus inversus syndrome (BPES) is an autosomal dominant hereditary disease, which is found in the clinical department. Its related gene -Foxl2 is a single exon encoded fork head transcription factor, and gene mutation can lead to the occurrence of small eyelid cleft syndrome. In female patients, BPES is divided into Two types: type I with premature ovarian failure, and II type ovarian function and normal [1,2].Foxl2 transcript of normal fertility, m RNA was previously found in the eyelids of mouse embryos, and in embryos and sexually mature mice, [1,3].Foxl2 has been expressed on the ovarian granulosa cells, [4]. in the adolescent population, ovarian granulosa cell tumor (OGCTs), and in the ovarian granulosa cells (OGCTs). To decrease [5]., Shah and so on in 2009 found that the mutation of the somatic cell Foxl2, that is, the mutation of 402C to G[5]., appears in 97% of the adult ovarian granulosa cell tumor (OGCTs), and that the tumor type is a specific [6-10]. and there is a Foxl2 site inactivation in the present colorectal cancer, which is more interesting in the hypermethylation of somatic cells. Yes, this mutation of Foxl2 has not been found in any of the sexual cord stromal cell tumors and unrelated ovarian and breast cancers, and the expression of the Foxl2 gene is found in Wegman P, such as Wegman P, and this may be associated with the increasing function of the.BPES related gene Foxl2 related to the expression of aromatase and its clinical prognosis. Now. Foxl2 related genes of the cleft palpebral syndrome have been studied, such as eyelids, genetics, ovarian function and a small number of tumors. Tumor related studies are limited to colorectal, other sexual stromal tumors, breast and ovarian cancers. As we know, Foxl2 has not been studied in cervical cancer. We analyzed and discussed the expression of Foxl2 in cervical cancer and the biological effect of Foxl2 on cervical cancer cells. Part 1 the expression of Foxl2 in cervical cancer was detected in cervical cancer, and the expression of Foxl2 in cervix cancer tissues was detected, and the two types of Foxl2 were detected in cervical adenocarcinoma and squamous cell carcinoma. The level of transcriptional RNA in the cell lines. Methods the cancerous tissues of 37 patients with cervical cancer were divided into two groups: a group of adenocarcinoma, a group of squamous cell carcinoma, and 8 cases of cervical intraepithelial neoplasia (CIN), including 5 cases of low degree squamous intraepithelial neoplasia (LSIL), and 10 cases of high squamous intraepithelial neoplasia (HSIL). The pathological tissue of 10 patients with cervicitis was used as the control group. Immunohistochemical staining was used to detect the expression of Foxl2 in cervical cancer tissue, cervical intraepithelial neoplasia and control group. Then, the adenocarcinoma cell lines (Hela cells) and squamous cell carcinoma cell lines (Siha cells) were cultured for human cervical cancer, and RNA was extracted, and reverse transcriptase was used. The expression of the Foxl2 gene in the two cell lines of this cancer was detected by the Reverse transcription polymerase chain reaction (RT-PCR) technique. The results of immunohistochemical staining showed that the positive rate of Foxl2 in the slices of cervical squamous cell carcinoma was significantly higher than that of the CIN group and the control group, and Foxl2 was in the uterus. The expression level of protein in the tissues of cervical squamous cell carcinoma was higher than that of cervical adenocarcinoma and other groups. In the cervical adenocarcinoma group, the Foxl2 protein was not expressed in the CIN group and the cervicitis group, and there was no significant difference between the.RT-PCR results and the m RNA. conclusion that Hela cells and Siha cells could transcribe Foxl2 in the squamous cell carcinoma of the cervix. Compared with cervical adenocarcinoma, cervical CIN tissue and cervicitis, Hela and Siha cells can transcribe Foxl2 m RNA. based on Foxl2 in cervical adenocarcinoma and squamous cell carcinoma, and the expression level of these two tissues is different. We will further study the biological role of Foxl2 gene in cervical cancer cells. Second part of the small lid cleft synthesis. The biological effect of the associated gene Foxl2 on cervical cancer cell lines, aim to construct a model of two cell lines, overexpress the Hela cells of Foxl2 and the Siha cell model of the silent Foxl2, and study the effects of Foxl2 on the proliferation, apoptosis, adhesion and invasion of these two cells, so as to analyze the biological effects of Foxl2 on cervical cancer. Hela cells were transfected with Foxl2 plasmid to express Foxl2, and the expression of Foxl2 gene in Siha cells was silenced. The transfection efficiency was verified by protein immunoblotting (Western Blotting), and the expression and silence model was identified. The proliferation ability of Hela and Siha was detected by Brdu method after the Foxl2 was overexpressed or silenced. The apoptosis rate of a and Siha cells, the adhesion ability of Hela and Siha cells was detected by the adhesive kit, and the invasiveness of two kinds of cell lines expressing and silent Foxl2 were detected by invasive assay, and FCM was used to detect Hela cells expressing Foxl2 and Ki67 in Siha cells with silent Foxl2, and cell proliferating nuclear antigen ( The expression of proliferating cell nuclear antigen, PCNA) and Fas L was used to further detect and analyze the expression of the related factors regulating proliferation and apoptosis. Results Western Blotting results, compared with the control group, the Foxl2 expression in the overexpressed Hela cells was significantly increased; the expression of the silent Siha cells decreased significantly, and the transfection was visible. The results of the successful model construction of.Brdu and Annexin V/PI showed that compared with the control group, the proliferation ability of Hela was obviously inhibited after overexpression of Foxl2 (P0.01), the proliferation ability of the silent group increased and its apoptosis decreased significantly (P0.001). The adhesion of over expressed Hela cells was not significantly altered, but the silence of Foxl2 could promote the adhesion of Siha. The invasion ability of the cells in the overexpressed group decreased significantly (P0.05), and the cell invasiveness in the silent group increased (P0.05).PCM results showed that the expression level of Ki67 in the overexpressed Hela was significantly decreased (P0.001), the expression of Fas L increased (P0.01). The expression of Ki67 in the silent Siha increased significantly (P0.001), and the expression level of Fas L decreased. There was no obvious change in the expression of PCNA in the over expression or silent cell group. Conclusion the results showed that the small lid fissure related gene Foxl2 inhibited the proliferation of Hela and Siha in cervical cancer cells and promoted apoptosis, and inhibited the invasion ability of Hela and Siha; at the same time, it promoted the adhesion of Siha, but Foxl2 had no significant effect on the adhesion ability of Hela cells. In addition, Foxl2 (Foxl2) had no significant effect on the adhesion of Hela cells. Down regulation of the expression level of Ki67 in Hela and Siha cells, and up regulation of the expression of Fas L in Hela and Siha. To sum up, our experimental results show that Foxl2 is highly expressed in cervical squamous cell carcinoma. On the one hand, Foxl2 inhibits the proliferation of cervical cancer cells and inhibits its apoptosis. This biological effect is mainly Foxl2 by down Ki67 expression and in the expression of Foxl2. Up - regulation the expression level of Fas L; on the other hand, Foxl2 may be a new tumor suppressor, at least in cervical cancer. This may be of value in the evaluation of metastasis and recurrence of cervical cancer, but further research is still needed.
【學(xué)位授予單位】：濰坊醫(yī)學(xué)院
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2014
【分類號(hào)】：R737.33
本文編號(hào)：2143272
[Abstract]:Blephar-ophimosis-ptosis-epicanthus inversus syndrome (BPES) is an autosomal dominant hereditary disease, which is found in the clinical department. Its related gene -Foxl2 is a single exon encoded fork head transcription factor, and gene mutation can lead to the occurrence of small eyelid cleft syndrome. In female patients, BPES is divided into Two types: type I with premature ovarian failure, and II type ovarian function and normal [1,2].Foxl2 transcript of normal fertility, m RNA was previously found in the eyelids of mouse embryos, and in embryos and sexually mature mice, [1,3].Foxl2 has been expressed on the ovarian granulosa cells, [4]. in the adolescent population, ovarian granulosa cell tumor (OGCTs), and in the ovarian granulosa cells (OGCTs). To decrease [5]., Shah and so on in 2009 found that the mutation of the somatic cell Foxl2, that is, the mutation of 402C to G[5]., appears in 97% of the adult ovarian granulosa cell tumor (OGCTs), and that the tumor type is a specific [6-10]. and there is a Foxl2 site inactivation in the present colorectal cancer, which is more interesting in the hypermethylation of somatic cells. Yes, this mutation of Foxl2 has not been found in any of the sexual cord stromal cell tumors and unrelated ovarian and breast cancers, and the expression of the Foxl2 gene is found in Wegman P, such as Wegman P, and this may be associated with the increasing function of the.BPES related gene Foxl2 related to the expression of aromatase and its clinical prognosis. Now. Foxl2 related genes of the cleft palpebral syndrome have been studied, such as eyelids, genetics, ovarian function and a small number of tumors. Tumor related studies are limited to colorectal, other sexual stromal tumors, breast and ovarian cancers. As we know, Foxl2 has not been studied in cervical cancer. We analyzed and discussed the expression of Foxl2 in cervical cancer and the biological effect of Foxl2 on cervical cancer cells. Part 1 the expression of Foxl2 in cervical cancer was detected in cervical cancer, and the expression of Foxl2 in cervix cancer tissues was detected, and the two types of Foxl2 were detected in cervical adenocarcinoma and squamous cell carcinoma. The level of transcriptional RNA in the cell lines. Methods the cancerous tissues of 37 patients with cervical cancer were divided into two groups: a group of adenocarcinoma, a group of squamous cell carcinoma, and 8 cases of cervical intraepithelial neoplasia (CIN), including 5 cases of low degree squamous intraepithelial neoplasia (LSIL), and 10 cases of high squamous intraepithelial neoplasia (HSIL). The pathological tissue of 10 patients with cervicitis was used as the control group. Immunohistochemical staining was used to detect the expression of Foxl2 in cervical cancer tissue, cervical intraepithelial neoplasia and control group. Then, the adenocarcinoma cell lines (Hela cells) and squamous cell carcinoma cell lines (Siha cells) were cultured for human cervical cancer, and RNA was extracted, and reverse transcriptase was used. The expression of the Foxl2 gene in the two cell lines of this cancer was detected by the Reverse transcription polymerase chain reaction (RT-PCR) technique. The results of immunohistochemical staining showed that the positive rate of Foxl2 in the slices of cervical squamous cell carcinoma was significantly higher than that of the CIN group and the control group, and Foxl2 was in the uterus. The expression level of protein in the tissues of cervical squamous cell carcinoma was higher than that of cervical adenocarcinoma and other groups. In the cervical adenocarcinoma group, the Foxl2 protein was not expressed in the CIN group and the cervicitis group, and there was no significant difference between the.RT-PCR results and the m RNA. conclusion that Hela cells and Siha cells could transcribe Foxl2 in the squamous cell carcinoma of the cervix. Compared with cervical adenocarcinoma, cervical CIN tissue and cervicitis, Hela and Siha cells can transcribe Foxl2 m RNA. based on Foxl2 in cervical adenocarcinoma and squamous cell carcinoma, and the expression level of these two tissues is different. We will further study the biological role of Foxl2 gene in cervical cancer cells. Second part of the small lid cleft synthesis. The biological effect of the associated gene Foxl2 on cervical cancer cell lines, aim to construct a model of two cell lines, overexpress the Hela cells of Foxl2 and the Siha cell model of the silent Foxl2, and study the effects of Foxl2 on the proliferation, apoptosis, adhesion and invasion of these two cells, so as to analyze the biological effects of Foxl2 on cervical cancer. Hela cells were transfected with Foxl2 plasmid to express Foxl2, and the expression of Foxl2 gene in Siha cells was silenced. The transfection efficiency was verified by protein immunoblotting (Western Blotting), and the expression and silence model was identified. The proliferation ability of Hela and Siha was detected by Brdu method after the Foxl2 was overexpressed or silenced. The apoptosis rate of a and Siha cells, the adhesion ability of Hela and Siha cells was detected by the adhesive kit, and the invasiveness of two kinds of cell lines expressing and silent Foxl2 were detected by invasive assay, and FCM was used to detect Hela cells expressing Foxl2 and Ki67 in Siha cells with silent Foxl2, and cell proliferating nuclear antigen ( The expression of proliferating cell nuclear antigen, PCNA) and Fas L was used to further detect and analyze the expression of the related factors regulating proliferation and apoptosis. Results Western Blotting results, compared with the control group, the Foxl2 expression in the overexpressed Hela cells was significantly increased; the expression of the silent Siha cells decreased significantly, and the transfection was visible. The results of the successful model construction of.Brdu and Annexin V/PI showed that compared with the control group, the proliferation ability of Hela was obviously inhibited after overexpression of Foxl2 (P0.01), the proliferation ability of the silent group increased and its apoptosis decreased significantly (P0.001). The adhesion of over expressed Hela cells was not significantly altered, but the silence of Foxl2 could promote the adhesion of Siha. The invasion ability of the cells in the overexpressed group decreased significantly (P0.05), and the cell invasiveness in the silent group increased (P0.05).PCM results showed that the expression level of Ki67 in the overexpressed Hela was significantly decreased (P0.001), the expression of Fas L increased (P0.01). The expression of Ki67 in the silent Siha increased significantly (P0.001), and the expression level of Fas L decreased. There was no obvious change in the expression of PCNA in the over expression or silent cell group. Conclusion the results showed that the small lid fissure related gene Foxl2 inhibited the proliferation of Hela and Siha in cervical cancer cells and promoted apoptosis, and inhibited the invasion ability of Hela and Siha; at the same time, it promoted the adhesion of Siha, but Foxl2 had no significant effect on the adhesion ability of Hela cells. In addition, Foxl2 (Foxl2) had no significant effect on the adhesion of Hela cells. Down regulation of the expression level of Ki67 in Hela and Siha cells, and up regulation of the expression of Fas L in Hela and Siha. To sum up, our experimental results show that Foxl2 is highly expressed in cervical squamous cell carcinoma. On the one hand, Foxl2 inhibits the proliferation of cervical cancer cells and inhibits its apoptosis. This biological effect is mainly Foxl2 by down Ki67 expression and in the expression of Foxl2. Up - regulation the expression level of Fas L; on the other hand, Foxl2 may be a new tumor suppressor, at least in cervical cancer. This may be of value in the evaluation of metastasis and recurrence of cervical cancer, but further research is still needed.
【學(xué)位授予單位】：濰坊醫(yī)學(xué)院
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2014
【分類號(hào)】：R737.33
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