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RLIP76 在卵巢黄体中的潜在功能。

A potential function of RLIP76 in the ovarian corpus luteum.

机构信息

College of Animal Life Sciences, Kangwon National University, Chuncheon, 24341, Republic of Korea.

出版信息

J Ovarian Res. 2019 Apr 18;12(1):34. doi: 10.1186/s13048-019-0510-8.

DOI:10.1186/s13048-019-0510-8
PMID:30999946
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6474048/
Abstract

Ral interacting protein of 76 kDa (RLIP76) is multifunctional protein localized and distributed in the plasma membrane, cytosol, and nucleus of the cell. In tumorigenesis, RLIP76 emerges as a common feature for the solid tumor growth. RLIP76 is ubiquitously expressed in various tissues including the ovary. Interestingly, the similar physiological events in obtaining an adequate supply of nutrient by gaining access to the host vascular system are required either for corpus luteum formation or tumor development. In addition, the identical angiogenesis modulators were found in neoplastic and normal ovaries. Our previous study involving RLIP76-/- mice implanted with melanoma or carcinoma cell conclusively demonstrated that RLIP76 is necessary for angiogenesis and neovascularization of primary solid tumors. RLIP76 plays an essential role in tumor angiogenesis through the regulation of pro-angiogenic factors such as vascular endothelial growth factor (VEGF) and hypoxia-inducible factor-1 (HIF-1). In certain previous studies, those pro-angiogenic factors were found significantly to be upregulated during the corpus luteum formation. To that, the following review will discuss the likelihood of RLIP76 role in ovarian corpus luteum.

摘要

RLIP76 是一种多功能蛋白,定位于和分布于细胞膜、细胞质和细胞核。在肿瘤发生过程中,RLIP76 是实体瘤生长的共同特征。RLIP76 在包括卵巢在内的各种组织中广泛表达。有趣的是,黄体形成或肿瘤发展都需要通过进入宿主血管系统来获得足够的营养供应,这是类似的生理事件。此外,在肿瘤性和正常卵巢中都发现了相同的血管生成调节剂。我们之前的研究涉及到植入黑色素瘤或癌细胞的 RLIP76-/- 小鼠,该研究明确表明 RLIP76 对于原发性实体瘤的血管生成和新血管形成是必需的。RLIP76 通过调节血管内皮生长因子 (VEGF) 和缺氧诱导因子-1 (HIF-1) 等促血管生成因子在肿瘤血管生成中发挥重要作用。在某些先前的研究中,发现这些促血管生成因子在黄体形成过程中显著上调。因此,以下综述将讨论 RLIP76 在卵巢黄体中的作用的可能性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4984/6474048/15c44742cbfd/13048_2019_510_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4984/6474048/87e6be1783c9/13048_2019_510_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4984/6474048/b8c9a34e79ad/13048_2019_510_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4984/6474048/15c44742cbfd/13048_2019_510_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4984/6474048/87e6be1783c9/13048_2019_510_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4984/6474048/b8c9a34e79ad/13048_2019_510_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4984/6474048/15c44742cbfd/13048_2019_510_Fig3_HTML.jpg

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Anat Histol Embryol. 2016 Apr;45(2):124-30. doi: 10.1111/ahe.12180. Epub 2015 May 6.
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J Ovarian Res. 2024 Feb 6;17(1):35. doi: 10.1186/s13048-024-01348-w.
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