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Investigation of the Induction of Prostate Cancer Mutagenesis and Development of A Novel Method for Early Detection of Prostate Cancer with Nanoimaging

為了解決Adenoid face的問題，作者Titus Ime Ekanem 這樣論述：

AbstractProstate cancer is a slow growing cancer which affects elderly males worldwide; although 10 percent of the younger population is reported at risk. There have been many hypotheses regarding its origin, but to date no actual cause has been adduced. However, there are many associated risk fact

ors some of which include environmental factors, social and dietary habits. Cooking food at very high temperature generates acrylamide and glycidamide, chemicals previously reported to be mutagenic. Previous studies have reported association of acrylamide with colorectal, brain, lung and ovarian can

cers. It was associated with treatment failures in advanced diseases due to drug resistance. Most conventional chemotherapeutic and hormonal agents have not been able to reduce the high rate of morbidity and mortality associated with the metastatic disease. Since most of these patients have lowered

immunity; recent studies show that stimulation of their immune system could improve their ultimate response to treatment. Although drugs to target the immune checkpoint have been developed for treatment of prostate cancer, there is no appreciable improvement in the overall patient survival, probably

due to poor penetration of the drug to the appropriate sites. Its current detection methods are nonspecific. With a view to developing a novel detection method for its early detection, we have identified androgen receptor as a molecular target as it is overexpressed in about 80 percent of castrate-

resistant prostate cancer. We therefore worked with the aim to synthesize AuNRs@SPIOs-PEG-AR-ab nanoprobes to early detect prostate cancer formation, mutagenesis, and trace the route of metastasis employed by prostate cancer cells in vivo using the nanoprobes. To overcome treatment failures, we have

conjugated CTLA-4-CA21 aptamer to the gold-coated iron oxide nanoprobes which can detect and kill prostate cancer cells even after metastasis has occurred.Method: We synthesized gold-nanorods and iron oxide nanoparticles, functionalized them with organosilanes due to their large surface area to vol

ume ratio, specific optical, electronic, magnetic and chemical properties including high surface energy, conjugated/coupled with the androgen receptor antibody, the CTLA-4-CA21 aptamer and the FITC/CyTE777 dyes. The nanoprobes were characterized, then used to assess cellular uptake efficiency, cytot

oxicity and their ability to detect prostate cancer cells in vitro were assessed using nanoimaging techniques on a more malignant variant of the prostate cancer cell line induced in our laboratory with glycidamide and in nude mice.Results: The nanoprobes have the wavelength maxima at 805 nm, the TEM

images dimensions of gold nanorods and iron oxide nanocrystals were 200 ± 30 nm and 80 nm respectively. Glycidamide-treated cells showed evidence of more nanoprobes uptake, the nanoprobes has low level of toxicity. They have the potential to enter the cancer cells and target androgen receptors in t

he nuclei as shown by the deconvolution/confocal microscopy, near infrared fluorescence imaging and IVIS imaging results. These glycidamide transformed-cells showed reduced doubling time, epithelial mesenchymal transition with invadopodia. They were more proliferative, formed spheroids with invadopo

dia in matrigel invasive assays, and induced changes in androgen receptor, prostate specific antigen, and annexin A2 protein expressions which have been associated with aggressiveness in prostate cancer. The CTLA4-CA21 nanoprobes have the wavelength maxima at 803 nm, the TEM images dimensions which

would enhance movement in the circulation. They show evidence of cell death, and the inhibitory effects on cell proliferation were dose-dependent on LNCaP, DU145, PC3 and BPH cells, with the greatest inhibition at 14.77 picomolar concentration. The near infrared imaging on the live cells showed mar

ked cellular disruptions and apoptotic changes in the cancer cells.Conclusion: With the wavelength maxima of 805 nm and 803 nm for AR nanoprobes and aptamer nanoprobes respectively which are within the “NIR imaging window”, our gold-shell iron oxide-core nanoprobes can penetrate deep tissues and ove

rcome autofluorescence from tissues observed in the visible light region. The aggressiveness such as short doubling time, epithelial mesenchymal transition, formation of invadopodia, and upregulated levels of invasive biomarkers, exhibited by the glycidamide-treated prostate cancer cells compared to

the parental cell lines could be due to the upregulation of androgen receptor promoted by glycidamide. With these great potentials the AuNRs@SPIOs-PEG-AR-ab nanoprobes can be used non-invasively in the early detection of prostate cancer. The inhibitory effects of the aptamer on cell proliferation w

ere dose-dependent at picomolar concentration as well as the marked cellular disruptions and apoptotic changes in the live cancer cells in the near infrared imaging have proved the potency of the modified DNA CTLA-4 aptamer. Therefore they have great potential for use in the treatment of advanced pr

ostate cancers and those associated with drug resistance.Keywords: Glycidamide, prostate cancer cells, mutagenesis, early detection, nanoprobes, nanoimaging .

應用 MicroRNA-124 靶向 LRRC1 以抑制口腔癌

為了解決Adenoid face的問題，作者吳劭皇 這樣論述：

口腔癌為全球最普及的癌症之一，每年被診斷出的口腔癌患者約有35萬人，而死於口腔癌者又有約18萬人。在所有口腔癌的組織型態中，口腔黏膜表皮的鱗狀細胞癌(OSCC)占了95%。在台灣，口腔癌在全國最常見的癌症中，排名於第四名。儘管目前已有多項治療對策，2019年國內口腔癌病例的增加率卻依然居於第五位。因此，了解口腔癌的癌症發展機制是當務之急，藉此找出可靠的口腔癌生物標記、新穎的分子標靶，將有助於提早發現和研發新的治療方式，以進一步提高癌症病患存活率，改善不良的預後。 一般認為，包括OSCC在內的癌變是通過多種遺傳異常(包含突變)的逐步累積而引發的。這些癌變可能透過損壞致癌基因或是抑癌基因(

Tumor suppressor gene, TSG)的功能，而這些致癌基因和抑癌基因在許多癌症的發展中扮演至關重要的角色。而近幾年，發現像是DNA 甲基化或是小型非編碼RNA等的表觀基因機制，在靜默抑癌基因和口腔癌惡性腫瘤的發展中同樣起到重要的作用。 過去這幾年中，MicroRNA在分子生物學中的研究，引發了一場改革性的突破，並發現其在癌變中發揮了關鍵性的作用。MicroRNA 是一種長約19到22個核甘酸組成的微小非蛋白質編碼之內源性單股RNA。其常通過與蛋白質編碼之mRNA上的3’UTR (Untranslated region)或是5’UTR的配對，直接引發mRNA的分解或是間接抑制

轉譯的進行，來調節目標基因的表達。而這類的單股RNA在正常細胞的發展過程中，例如增生、發育、分化、凋亡等，扮演很重要的角色。在近期許多文獻，發現microRNA-124家族(microRNA-124-1、microRNA-124-2、microRNA-124-3)在許多癌症中，扮演抑癌基因的角色。在過去實驗室的研究中，我們在OSCC的病患檢體中，發現microRNA-124-3 (miR-124-3)呈現高度甲基化，進而導致其靜默。而當在OSCC中高度表達miR-124-3時，能夠恢復其抑癌基因的功能。在本研究中，我們想了解更多在口腔癌中microRNA-124(miR-124)作用的分子機制

與功能。 在分析完TargetScan7.1、miRDB、Dianalabs三個資料庫後，我們預測了miR-124在口腔癌中，可能會影響到的數個目標基因。在經過文獻比對後，挑選了LRRC1作為接下來的研究目標。首先我們先透過帶有miR-124的慢病毒載體，感染OSCC cell lines，建立Overexpressing- miR-124 OSCC cell lines。 過去發現在口腔癌中，miR-124高度甲基化，使其無法發揮抑癌功能。本篇研究發現當缺乏miR-124的調控時，會引發下游目標基因LRRC1促進腫瘤細胞的增生。根據qRT-PCR和luciferase assay，發現m

iR-124能夠去直接抑制LRRC1的表達。整合先前的研究，根據檢測miR-124是否處於高度甲基化，能夠更有效對口腔癌發展進行預測。而在口腔癌中，miR-124或許能夠作為一個腫瘤抑制基因。