Roles of PLODs in Collagen Synthesis and Cancer Progression.

Roles of PLODs in Collagen Synthesis and Cancer Progression.
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DOI:
10.3389/fcell.2018.00066
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发表时间:
2018
影响因子:
5.5
通讯作者:
Xu R
Xu R
中科院分区:
生物学2区
文献类型:
--
作者:
Qi Y;Xu R

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胶原蛋白是细胞外基质的主要成分。胶原交联和沉积依赖于赖氨酰羟基化,该羟基化由原胶原-赖氨酸,2-酮戊二酸5-双加氧酶(PLOD)催化。赖氨酰羟基化和胶原交联异常导致许多胶原相关疾病的进展,如纤维化和癌症。鉴定了三种赖氨酰羟化酶(LH1、LH2和LH3),其由PLOD 1、PLOD 2和PLOD 3基因编码。PLODs的表达受多种细胞因子、转录因子和microRNA的调控。PLODs的失调促进癌症的进展和转移,表明靶向PLODs是癌症治疗的潜在策略。本文就PLODs在正常组织发育和疾病进展,特别是肿瘤中的作用和调控的研究进展作一综述。
Collagen is the major component of extracellular matrix. Collagen cross-link and deposition depend on lysyl hydroxylation, which is catalyzed by procollagen-lysine, 2-oxoglutarate 5-dioxygenase (PLOD). Aberrant lysyl hydroxylation and collagen cross-link contributes to the progression of many collagen-related diseases, such as fibrosis and cancer. Three lysyl hydroxylases (LH1, LH2, and LH3) are identified, encoded by PLOD1, PLOD2, and PLOD3 genes. Expression of PLODs is regulated by multiple cytokines, transcription factors and microRNAs. Dysregulation of PLODs promotes cancer progression and metastasis, suggesting that targeting PLODs is potential strategy for cancer treatment. Here, we summarize the recent progress in the investigation of function and regulation of PLODs in normal tissue development and disease progression, especially in cancer.
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