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探討 ADAM9 下游調控 UBN2 及 AKR1C3 在前列腺癌症惡化過程中的生物機轉

為了解決cf. abbreviation的問題，作者LE THI HUYNH TRANG 這樣論述：

A progressively diagnosed resistance mechanism to androgen deprivation in prostate cancer (PCa) is still lacking in understanding. Many genes involved in the androgen and androgen receptor (AR) pathway contribute to this aggressive subset. The essential role of the disintegrin and metalloproteinase

domain-containing protein 9 (ADAM9) in driving the solid tumor aggressiveness and metastasis has been well-defined. In PCa, ADAM9 is promoted the metastasis state through an activation by androgen. A secreted isoform of ADAM9 (sADAM9) is released by stromal cells and upregulated the cancer cell inv

asion. In our study, by stimulating PCa cells with sADAM9, we noticed an increased ubinuclein 2 (UBN2) expression and a positive association between ADAM9 with UBN2 expression was also observed in the PCa cell lines and clinical tissues. Latterly, by analysis of the genetic modification approach we

revealed UBN2 as a downstream target gene of ADAM9 in androgen-dependent PCa cell lines. Here, we showed that UBN2 expression was up-regulated in PCa with those normal samples by Oncomine database and immunohistochemistry. Moreover, PCa tissues and clinical relevance confirmed the certainly correlat

ion between AR with ADAM9 and UBN2 expression for which ADAM9 and UBN2 expression were induced in PCa cells by AR genetic modification or treatment with synthetic androgen (R1881). Remarkably, this study provides a novel mechanism of progression in PCa by which the regulatory role of UBN2 and its up

stream ADAM9 on the aldo-keto reductase family 1 member C3 (AKR1C3) expression regulated PCa cell growth against androgen-targeted therapy . We also supported the causal relationship of ADAM9-UBN2-AKR1C3 in promoting the progression to castration-resistant PCa (CRPC) of androgen-dependent PCa. Coll

ectively, our finding of the ADAM9/UBN2/AKR1C3 axis might be considered as a new driver in resistance to androgen-deprivation therapy of PCa progression .

淋病雙球菌假設性蛋白質之免疫特性分析

為了解決cf. abbreviation的問題，作者曾怡嘉 這樣論述：

淋病 (gonorrhea) 是由淋病雙球菌 (Neisseria gonorrhoeae, Ng) 感染所導致之疾病，主要藉由性行為途徑感染，感染後多數患者無明顯癥兆並且可能經由垂直傳染給下一代。除此之外，康復患者體內不具有免疫記憶性，早期只要使用抗生素治療就能達到有效療效，但 Ng 菌多重抗藥性的問題逐漸增加，使得治療變得棘手，開發有效疫苗是目前最佳解決方式。本研究以反向疫苗學 (Reverse vaccinology) 方法作為基礎，從全序列定序完成的參考菌株 FA 1090 的假設性蛋白質 (hypothetical protein) 中挑選標的，首先藉由電腦軟體 SignalP-5

.0 Server 預測蛋白質是否為分泌性蛋白質，再以 Gneg-mPLoc 預測蛋白質在菌體位置並以 Blast 比對，選擇高保守性的目標製備重組蛋白質以進行免疫原性 (immunogenicity) 分析。本研究以台灣分離的臨床菌株為模板共分析14個基因，其中有8個基因透過 PCR 成功被增幅出，分別為 NGO1889、NGO1484、NGO0783、NGO2002、NGO2133、NGO0782、NGO0666和NGO2054 。將上述8個基因分別構築至表現載體，送入 E. coli 表現並純化重組蛋白質，純化後的蛋白質進行小鼠免疫試驗，以獲得之抗血清進行西方墨點分析各蛋白質在 Ng 菌

的表現情形，證實有5個蛋白質之抗血清具有認回原菌能力且在不同的臨床菌株都有表現。Whole- cell ELISA與免疫螢光染色法分析結果顯示只有 NGO1889、NGO1484、NGO0783和NGO2002 暴露於菌體表面，繼而分析 這些抗血清的殺菌力，結果只有 NGO0783 抗血清對不同臨床菌株具有殺菌活性。進一步進行in vivo 小鼠保護力分析，證實事先接種NGO0783 可增加小鼠對 Ng 菌感染的抵抗力，因此 NGO0783 具有成為開發Ng疫苗之潛力抗原。