Regulation by insulin signaling pro

Regulation by insulin signaling prompts the question whetherabnormal RDH expression associates with human disease. Forexample, impaired insulin secretion and insulin resistance duringdiabetes predicts elevated RDH expression and atRA synthesis(71). Conversely, enhancement of insulin signaling through PI3K/Akt from loss of phosphatase and tensin homolog deleted on chromosome10 in cancer implicates decreased RDH (72). ReducedRDH expression would decrease atRA biosynthesis, which could affect tumor differentiation and/or aggressiveness. Various cancersshow alterations in the atRA signaling pathway, such as loss ofatRA receptors (73, 74) and down-regulation of atRA chaperons(75, 76). atRA biosynthesis is impaired in breast cancer cell linesrelative to normal cells (77). Reduced atRA synthesis in the Rbp1-null mouse is consistent with increased mammary tumors, andsuggests consequences of the epigenetic silencing of Rbp1 in 25%of human breast cancers (62). In contrast, overexpression ofRDH10 in HepG2 cells reduces proliferation (70).

結果 (繁體中文) 1:

Regulation by insulin signaling prompts the question whether
abnormal RDH expression associates with human disease. For
example, impaired insulin secretion and insulin resistance during
diabetes predicts elevated RDH expression and atRA synthesis
(71). Conversely, enhancement of insulin signaling through PI3K/
Akt from loss of phosphatase and tensin homolog deleted on chromosome
10 in cancer implicates decreased RDH (72). Reduced
RDH expression would decrease atRA biosynthesis, which could affect tumor differentiation and/or aggressiveness. Various cancers
show alterations in the atRA signaling pathway, such as loss of
atRA receptors (73, 74) and down-regulation of atRA chaperons
（75，76）。全反式維甲酸生物合成在乳腺癌細胞系中受損的
相對於正常細胞（77）。全反式維甲酸降低合成在Rbp1-
無效小鼠是具有增加的乳腺腫瘤一致，並且
表明在25％RBP1的後生沉默的後果
人乳腺癌（62）的。相反，過量表達
在HepG2細胞中降低了RDH10增殖（70）。

結果 (繁體中文) 2:

胰島素信號調節提示問題
異常RDH表達與人類疾病有關。對於
例如，胰島素分泌受損和胰島素抵抗
糖尿病預測RDH表達升高和ATRA合成
（71）. 相反，通過 PI3K 增強胰島素信號/
因失去磷酸酶和在染色體上刪除的張力同源性而消失的Akt
10在癌症暗示減少RDH （72）。減少
RDH表達在RA生物合成時會減少，這可能會影響腫瘤分化和/或攻擊性。各種癌症
顯示 atRA 信令通路的更改，例如
atRA 受體 （73， 74） 和 atRA 伴郎的向下調節
(75, 76).atRA生物合成在乳腺癌細胞系受損
相對於正常細胞 （77）。Rbp1- 中減少RA合成
空小鼠與增加的乳腺腫瘤一致，
建議在25%的Rbp1表觀遺傳沉默的後果
人類乳腺癌（62）。相反，過度表達
HepG2細胞中的RDH10可減少增殖（70）。

結果 (繁體中文) 3:

胰島素訊號調節引發的問題是
RDH表達异常與人類疾病有關。為了
例如，在
糖尿病預測RDH表達和atRA合成的升高
（71）。相反，通過PI3K增强胰島素信號傳導/
從染色體上缺失的磷酸酶和張力素同源物中選取Akt
10例癌症患者RDH降低（72）。减少
RDH的表達會降低atRA的生物合成，從而影響腫瘤的分化和/或侵襲性。各種癌症
顯示atRA訊號通路的改變，如
atRA受體（73，74）與atRA伴子的下調
（75，76）。乳腺癌細胞株atRA生物合成受損
相對於正常細胞（77）。Rbp1中atRA合成的减少-
空鼠與乳腺腫瘤新增一致，並且
提示25%的Rbp1錶觀遺傳沉默的後果
人類乳腺癌（62）。相反，過度表達
HepG2細胞中的RDH10减少增殖（70）。