癌細胞的生長速度遠大於正常細胞，當癌細胞生長到相當體積時，腫瘤組織內處於嚴重高度缺氧、酸性環境且充滿大量活性氧物質(ROS)等逆境壓力。在這些逆境下，癌細胞啟動一連串改變腫瘤微環境內外部的反應措施，維持一定含量的ROS，增加癌細胞的活性與增加其相關發炎因子的利用，並促進癌細胞的增殖。因此其中一種抗癌方法便是去除ROS，而過去的研究指出許多維生素(Vitamin)被認為具有抗發炎作用並消除ROS的功能，也表明維生素可能對癌症治療是很重要，因此在本篇研究中我們想針對與維生素相關的基因去進行癌症治療的研究。
在本篇研究中我們所找尋到的一個標靶目標為核黃素轉運蛋白:GPR172A。它是一個結合G 蛋白質之穿膜蛋白，其主要功能在負責將核黃素從細胞外傳送的細胞內作用。過去的研究中提到GPR172A 與癌症似乎有些許關聯性,其被發現在胃癌及卵巢癌病人檢體中表現量有比較高的情況,被認為可能可作為癌症標記。但GPR172A 與乳癌的關係性過去並未有太多的研究,所以我們在本篇研究想要了解他們之間的關聯。
我們使用生物資訊分析在三種不同的乳癌數據庫中搜索過量表達基因。為了分析GPR172A表達與乳癌患者存活的關聯，構建了Kaplan-Meier存活曲線。我們發現在存活率的分析中, GPR172A 高表現量的情況伴隨著一個比較不好的預後,這裡可能暗示著他在乳癌中可能扮演的一個oncogenic 的角色。為了研究GPR172A在乳癌中的影響,我們利用shRNA的技術去抑制其在細胞中的表現量並進行細胞功能性分析。實驗結果中發現抑制GPR172A的表現量會使得乳癌細胞的增殖和遷移能力下降,而且調節細胞週期相關蛋白的表現量也同時有被抑制的情況發生。結果顯示GPR172A可能在細胞增殖，遷移和細胞週期進程中發揮重要作用。為了鑑定共表達基因，我們使用用於癌症基因體學數據庫的cBioPortal。共表達數據顯示了與細胞週期進展的關聯並提供了對潛在機制的理解。我們推測GPR172A在乳癌治療中可能是潛在的標靶基因。

Cancer cells grow much faster than normal cells, when cancers cells grow to a considerable volume, the tumors are highly hypoxic, acidic and filled with a large amount of reactive oxygen species (ROS). Under such circumstances, cancer cells initiate a series of reaction measures, maintain a certain amount of reactive oxygen species, cause the increase activity of cancer cells and the utilization of related inflammatory factors, and promote the proliferation of cancer cells. One of the anti-cancer methods is to remove ROS. In the previous studies, many vitamins were thought to have anti-inflammatory effects and can eliminate ROS. It also suggests that vitamins may be important for cancer treatment, so in this study we want to conduct cancer treatment research on vitamin-related genes.
We proposed target therapy for the treatment of breast cancer. GPR172A is a G protein-coupled receptor (GPCR) and a transmembrane protein that mediates cellular uptake of riboflavin (vitamin B2). In previous study, GPR172A has been a potential biomarker in ovarian and gastric cancer. Furthermore, the up-regulated of GPR172A in human malignancies. However, the effect of GPR172A in breast cancer is not clear. Therefore, the aim of this study is to identify the function of GPR172A in breast cancer.
To find out the role of GPR172A in breast cancer, we used bioinformatics analysis searching the overexpression gene in three different databases of breast carcinoma. To analyze the association of GPR172A expression with breast cancer patient survival, Kaplan-Meier survival curves were constructed. A significant association was identified between GPR172A mRNA and survival. GPR172A predicts a poor survival in breast carcinoma. We examined the effects of GPR172A on breast cancer and using vector-mediated short hairpin RNA (shRNA) to suppress GPR172A expression. GPR172A shRNA suppressed the cell proliferation and migration of breast cancer cells in vitro. The cell cycle-related protein expression was also altered by GPR172A shRNA. In order to identify the coexpression genes, we used the cBioPortal for Cancer Genomics database. The co-expression data revealed the association with cell cycle progression and provided insight into the potential underlying mechanism. The results suggested that GPR172A may play an important role in cell proliferation, migration and cell cycle progression. GPR172A is a potential target gene for breast cancer treatment.

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