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转化酶 2 alpha 同源物是缺氧诱导因子 1 亚单位 alpha 的下游基因，参与胰腺癌的进展。

Transformer 2 alpha homolog is a downstream gene of hypoxia-inducible factor 1 subunit alpha and is involved in the progression of pancreatic cancer.

机构信息

Department of Anatomy, School of Basic Medicine, Guizhou Medical University, Guiyang, Guizhou, China.

Department of Physiology, School of Basic Medicine, Guizhou Medical University, Guiyang, Guizhou, China.

出版信息

Bioengineered. 2022 May;13(5):13238-13251. doi: 10.1080/21655979.2022.2079243.

DOI:10.1080/21655979.2022.2079243
PMID:35635094
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9275993/
Abstract

Intratumoral hypoxia is a common feature of pancreatic cancer (PC) and also plays a role in its progression. However, hypoxia-regulated signatures in PC are still not completely understood. This study aimed to identify core hypoxia-associated genes and determine their underlying molecular mechanisms in PC cells. Transformer 2 alpha homolog (TRA2A) was found to be an important hypoxia-associated gene, which was upregulated in PC tissues and in PC cells cultured under hypoxia. High TRA2A expression was associated with advanced stage, poor differentiation, and lymph node metastasis. Under normoxic and hypoxic conditions, knockdown of TRA2A both markedly suppressed PC cell proliferation and motility and , as well as activation of the AKT pathway. Hypoxia-inducible factor 1 subunit alpha (HIF1α) upregulated the transcription of TRA2A by directly binding to its promoter. TRA2A showed a co-expression relationship with HIF1α in PC tissues. Overexpression of TRA2A alleviated the pro-inhibitive functions of HIF1α-inhibition on PC cell proliferation and motility under hypoxia. In conclusion, TRA2A is a crucial downstream gene of HIF1α that accelerates the proliferation and motility of PC cells. TRA2A may be a novel and practical molecular target for investigating the hypoxic response of PC cells.: TRA2A, transformer 2A protein; PC, pancreatic cancer; HIF1α, hypoxia-inducible factor 1-alpha; GEO, Gene Expression Omnibus; IHC, immunohistochemical staining.

摘要

肿瘤内缺氧是胰腺癌（PC）的一个常见特征，也在其进展中起作用。然而，PC 中缺氧调节的特征仍然不完全清楚。本研究旨在鉴定核心缺氧相关基因，并确定其在 PC 细胞中的潜在分子机制。Transformer 2 alpha 同源物（TRA2A）被发现是一个重要的缺氧相关基因，在 PC 组织和在缺氧条件下培养的 PC 细胞中上调。高 TRA2A 表达与晚期、低分化和淋巴结转移有关。在常氧和缺氧条件下，下调 TRA2A 均明显抑制 PC 细胞增殖和运动，以及 AKT 通路的激活。缺氧诱导因子 1 亚基 alpha（HIF1α）通过直接结合其启动子上调 TRA2A 的转录。TRA2A 在 PC 组织中与 HIF1α 呈共表达关系。TRA2A 的过表达减轻了 HIF1α 抑制在缺氧下对 PC 细胞增殖和运动的抑制作用。总之，TRA2A 是 HIF1α 的关键下游基因，可加速 PC 细胞的增殖和运动。TRA2A 可能是研究 PC 细胞缺氧反应的一个新的、实用的分子靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4bb/9275993/d12eae48bbe2/KBIE_A_2079243_F0008_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4bb/9275993/664e41e3bb15/KBIE_A_2079243_UF0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4bb/9275993/64b815483b14/KBIE_A_2079243_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4bb/9275993/bed3ea6b3f64/KBIE_A_2079243_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4bb/9275993/8a46cfc30ad0/KBIE_A_2079243_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4bb/9275993/b8ad610d42a4/KBIE_A_2079243_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4bb/9275993/4c00bebea686/KBIE_A_2079243_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4bb/9275993/d0c6744ac717/KBIE_A_2079243_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4bb/9275993/3045756a8925/KBIE_A_2079243_F0007_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4bb/9275993/d12eae48bbe2/KBIE_A_2079243_F0008_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4bb/9275993/664e41e3bb15/KBIE_A_2079243_UF0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4bb/9275993/64b815483b14/KBIE_A_2079243_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4bb/9275993/bed3ea6b3f64/KBIE_A_2079243_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4bb/9275993/8a46cfc30ad0/KBIE_A_2079243_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4bb/9275993/b8ad610d42a4/KBIE_A_2079243_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4bb/9275993/4c00bebea686/KBIE_A_2079243_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4bb/9275993/d0c6744ac717/KBIE_A_2079243_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4bb/9275993/3045756a8925/KBIE_A_2079243_F0007_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4bb/9275993/d12eae48bbe2/KBIE_A_2079243_F0008_OC.jpg

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