三分文章思路-1
這篇3分文章思路記錄下來，其實(shí)前面沒有展示生信的圖圖唧垦，但是文章introduction部分捅儒，描述了通過TCGA數(shù)據(jù)庫TCGA_CESC_exp_HiSeqV22015-02-24數(shù)據(jù)集，篩選的出的差異基因-KIF18B，應(yīng)該是用了生信方面的分析巧还，后面又用了Human Protein Atlas IHC數(shù)據(jù)庫鞭莽，進(jìn)一步確定了KIF18B在宮頸癌腫瘤組織和正常組織中的表達(dá)量是不一樣的。所以前面生信篩選基因麸祷，后面試驗(yàn)+生信驗(yàn)證澎怒，是這樣的一個(gè)思路吧。
文章是-KIF18B promotes tumor progression through activating the Wnt/β-catenin pathway in cervical cancer
摘要
oncogenes 致癌基因
The Wnt/β-catenin pathway plays key roles in embryogenesis, homeostasis, and stem cell regeneration, and pluripotency. In the canonical pathway, Wnt activation disrupts the destruction complex, allowing β-catenin to accumulate and subsequently translocate to the nucleus,where it interacts with a transcription factor of the TCF/LEF-1 family; the result is increased expression of oncogenes, such as c-Myc and CyclinD1.
Wnt /β-catenin途徑在胚胎發(fā)生阶牍，體內(nèi)穩(wěn)態(tài)喷面，干細(xì)胞再生和多能性中起關(guān)鍵作用。 在經(jīng)典途徑中走孽，Wnt激活破壞了破壞復(fù)合物惧辈，使β-連環(huán)蛋白積累并隨后易位至細(xì)胞核，在其中它與TCF / LEF-1家族的轉(zhuǎn)錄因子相互作用磕瓷； 結(jié)果是增加了癌基因的表達(dá)盒齿，例如c-Myc和CyclinD1。
Regulation of Wnt/β-catenin activity is closely related to the development of various cancers, including lung cancer, breast cancer, liver cancer, colon cancer, and cervical cancer.Thus, targeting Wnt/β-catenin signaling is a promising strategy for treating cancers, with many drugs currently in clinical trials.
Wnt /β-catenin活性的調(diào)節(jié)與多種癌癥的發(fā)生密切相關(guān)困食，包括肺癌边翁，乳腺癌，肝癌硕盹，結(jié)腸癌和宮頸癌符匾。因此，針對Wnt /β-catenin信號傳導(dǎo)是治療癌癥的一種有前途的策略瘩例，目前有許多藥物正在臨床試驗(yàn)中啊胶。
Analysis of The Cancer Genome Atlas (TCGA) database showed that the KIF18B gene is highly expressed in cervical cancer tissue but exhibits low expression in paracancerous tissue. It is also associated positively with a large primary tumor size and an advanced TNM stage. KIF18B is a member of the kinesin family of motor proteins, which is closely related to the pairing and separation of chromosomes in mitosis.
癌癥基因組圖譜（TCGA）數(shù)據(jù)庫的分析表明，KIF18B基因在宮頸癌組織中高表達(dá)垛贤，而在癌旁組織中低表達(dá)创淡。 它也與大的原發(fā)腫瘤大小和晚期TNM分期呈正相關(guān)。 KIF18B是運(yùn)動(dòng)蛋白驅(qū)動(dòng)蛋白家族的成員南吮，其與有絲分裂中染色體的配對和分離密切相關(guān)。
De et al showed that overexpression of KIFC1, KIF1A, KIF5A, and KIFC3 can increase docetaxel chemotherapy resistance in breast cancer cells, and Liao et al21 found that KIF18A is closely related to the overall survival and progression-free survival in hepatic carcinoma patients. Moreover, overexpression of KIF18B indicates a poor prognosis in hepatic carcinoma.
De等顯示KIFC1誊酌，KIF1A部凑，KIF5A和KIFC3的過表達(dá)可以增加乳腺癌細(xì)胞中的多西他賽化療耐藥性，Liao等人21發(fā)現(xiàn)KIF18A與肝癌患者的總體生存和無進(jìn)展生存密切相關(guān)碧浊。 此外涂邀，KIF18B的過度表達(dá)預(yù)示著肝癌的不良預(yù)后。
To predict whether KIF18B is a cancer driver gene with carcinogenic effects, we in a previous study retrieved only literature on the relationship between KIF18B and cancer, which primarily included bioinformatic analyses.22 However, the function of KIF18B in humans has remained unclear. In the present study, we show that KIF18B is a potential oncogene that promotes cervical cancer cell proliferation and migration in vitro and in vivo. Furthermore, our results indicate that the Wnt/β-catenin pathway may contribute to the carcinogenicity of KIF18B overexpression.
為了預(yù)測KIF18B是否是具有致癌作用的癌癥驅(qū)動(dòng)基因箱锐，我們在先前的研究中僅檢索到有關(guān)KIF18B與癌癥之間關(guān)系的文獻(xiàn)比勉，其中主要包括生物信息學(xué)分析。然而，KIF18B在人類中的功能仍不清楚浩聋。 在本研究中观蜗，我們顯示KIF18B是潛在的致癌基因，可在體外和體內(nèi)促進(jìn)宮頸癌細(xì)胞的增殖和遷移衣洁。 此外墓捻，我們的結(jié)果表明Wnt /β-catenin途徑可能與KIF18B過表達(dá)的致癌性有關(guān)。
結(jié)論
1.KIF18B is overexpressed in cervical cancer tumor tissues and correlates with more aggressive clinical characteristics
（1）利用TCGA的數(shù)據(jù)
HeLa and Siha cell這兩種細(xì)胞
siRNA-1, siRNA-2, and siRNA-3三種干擾
通過分析TCGA_CESC_exp_HiSeqV22015-02-24數(shù)據(jù)集坊夫，與正常宮頸組織相比砖第，宮頸癌組織顯示KIF18B的過表達(dá)高3.4倍（P <0.0001），與大的原發(fā)腫瘤大小和晚期FIGO階段密切相關(guān).
（2）利用Human Protein Atlas數(shù)據(jù)庫進(jìn)一步研究KIF18B在正常組織和腫瘤組織中的表達(dá)环凿，原文表述如下
Subsequently, ==Human Protein Atlas IHC== analyses showed that KIF18B was not expressed in normal cervical tissues but was expressed in 11 of 12 (91.7%) cervical cancer tissue samples
(3)自己的數(shù)據(jù)集做驗(yàn)證
KIF18B在30個(gè)腫瘤組織中有26個(gè)高表達(dá)
（4）腫瘤惡性程度代表照片梧兼，免疫組化圖片來自Human Protein Atlas 數(shù)據(jù)庫
（5）KIF18B的表達(dá)量和什么有關(guān)
2.Knockdown of KIF18B inhibits cervical cancer cell proliferation, invasion, and migration in vitro.
（1）KIF18B在3種細(xì)胞中的表達(dá)量
（2）三種干擾RNA的干擾效率
（3）si-KIF18B轉(zhuǎn)染的細(xì)胞現(xiàn)實(shí)較慢的生成速度
（4）si-KIF18B轉(zhuǎn)染的細(xì)胞有較少的菌落
（5）siRNA介導(dǎo)的KIF18B敲低可抑制HeLa和Siha細(xì)胞的遷移
(6）通過流式細(xì)胞術(shù)評估KIF18B對細(xì)胞周期分布和凋亡的影響。
（7）轉(zhuǎn)染si-KIF18B的HeLa細(xì)胞和Siha細(xì)胞在G1期的阻滯性高于轉(zhuǎn)染si-NC的細(xì)胞智听。
（8）對于HeLa和Siha細(xì)胞羽杰，在si-NC和si-KIF18B組之間未觀察到凋亡的顯著差異。
3.Overexpression of KIF18B promotes cervical cancer cell proliferation, invasion, and migration in vitro
（A）傷口愈合試驗(yàn)表明瞭稼，oe-KIF18B C33A細(xì)胞的遷移增加忽洛。
（B）CCK-8分析表明，KIF18B的過度表達(dá)促進(jìn)了C33A細(xì)胞的增殖环肘。
（C）oe-KIF18B轉(zhuǎn)染的C33A細(xì)胞比對照pcDNA3.1轉(zhuǎn)染的細(xì)胞具有更多的集落欲虚。
（D）遷移和侵襲測定表明oe-KIF18B處理損害了C33A細(xì)胞的遷移和侵襲能力。
4.KIF18B plays a carcinogenic role by activating Wnt/β-catenin signaling
（1）與KIF18B共表達(dá)的大多數(shù)基因都發(fā)現(xiàn)了細(xì)胞周期（cell cycle）途徑的富集
（2）考慮到KIF18B敲低會(huì)降低癌細(xì)胞的增殖悔雹，遷移和侵襲并促進(jìn)G1期細(xì)胞周期停滯复哆，我們使用qRT-PCR和Western blot分析方法檢查了KIF18B敲低細(xì)胞中細(xì)胞周期相關(guān)基因的表達(dá)。 與富集分析一致腌零，與si-NC處理相比梯找，si-KIF18B處理可降低CyclinD1的mRNA和蛋白質(zhì)水平，而p21益涧，p27和CyclinE的表達(dá)不受影響锈锤。這個(gè)CyclinD1正好和Wnt /β-catenin以前被證明是相關(guān)的， ==在introduction 做過鋪墊==
（3）評估了與Wnt /β-catenin途徑相關(guān)的蛋白質(zhì)闲询，發(fā)現(xiàn)與si-NC組相比久免，si-KIF18B組的C-myc，β-catenin和GSK3β磷酸化水平降低扭弧，但總 GSK3β水平無明顯差異阎姥。干擾組-C-myc降低，也是 ==在introduction 做過鋪墊==
5.Knockdown of KIF18B suppresses tumor growth in vivo
敲除后對腫瘤的影響
總結(jié)
1.就是我這個(gè)基因的篩選用了TCGA數(shù)據(jù)庫TCGA_CESC_exp_HiSeqV22015-02-24數(shù)據(jù)集鸽捻，篩選的出的差異基因-KIF18B呼巴，應(yīng)該是用了生信方面的分析泽腮，后面又用了Human Protein Atlas IHC數(shù)據(jù)庫，進(jìn)一步確定了KIF18B在宮頸癌腫瘤組織和正常組織中的表達(dá)量是不一樣的衣赶。
2.此外诊赊，作者在introduction對KIF18B家族的其他基因進(jìn)行了描述，英文原文如下：
KIF4 is considered the main tumor trigger, and the absence of this motor protein will lead to aneuploidy in mouse embryonic stem cells or tumor formation in nude mice. A previous study showed that KIF4 is associated with a poor prognosis in breast cancer.Furthermore, Ishikawa et alobserved higher KIF2C mRNA expression in 120 cases of colorectal cancer than in adjacent normal tissues. KIF2C/MCAK is also upregulated in proliferative tumors, suggesting that KIF2C is associated with cell hyperproliferation. Shimo et aldetected 27,648 genes in 81 patients with breast cancer by gene chip analysis and found KIF2C gene expression to be significantly enhanced. Additionally, examination of 10 breast cancer cell lines revealed high KIF2C expression in nine. De et alshowed that overexpression of KIFC1, KIF1A, KIF5A, and KIFC3 can increase docetaxel chemotherapy resistance in breast cancer cells, and Liao et al found that KIF18A is closely related to the overall survival and progression-free survival in hepatic carcinoma patients. Moreover, overexpression of KIF18B indicates a poor prognosis in hepatic carcinoma.
借鑒過來的就是可以如果自己寫作時(shí)屑埋，如果有同一家族的基因豪筝，把其他也寫上。
3.**關(guān)于Human Protein Atlas數(shù)據(jù)庫 **摘能，另一篇思路相近的中文文章-《基于多數(shù)據(jù)庫聯(lián)合挖掘研究PTP4A3的
表達(dá)對肝細(xì)胞癌發(fā)生發(fā)展的影響》也引用了這個(gè)數(shù)據(jù)庫续崖，這篇文章中的方法是：基于Oncomine 及癌癥和腫瘤基因圖譜(the Cancer Genome Atlas，TCGA)數(shù)據(jù)庫聯(lián)合數(shù)據(jù)分析PTP4A3在肝細(xì)胞癌 組織和正常組織中的表達(dá)水平;通過Human Protein Atlas數(shù)據(jù)庫团搞，進(jìn)一步研究PTP4A3在肝細(xì)胞癌和正 常組織中的表達(dá);同時(shí)基于Kaplan-Meier Plotter數(shù)據(jù)庫進(jìn)一步分析PTP4A3表達(dá)水平與肝細(xì)胞癌預(yù)后的 關(guān)系严望。
關(guān)于如何生成==免疫組織化學(xué)圖==方法：生成免疫組織化學(xué)圖 Human Protein Atlas 數(shù)據(jù) 庫(www. proteinatlas.org) 的 免 疫 組 織 化 學(xué) 數(shù) 據(jù) 中，在“Tissue Atlas”和“Pathology Atlas”中輸入 PTP4A3逻恐，分別選擇“l(fā)iver”和“l(fā)iver cancer”像吻，生 成免疫組織化學(xué)圖。
