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AKR7A3 通过调节 PHGDH 抑制的自噬来调节胰腺导管腺癌的转移。

AKR7A3 modulates the metastasis of pancreatic ductal adenocarcinoma through regulating PHGDH-suppressed autophagy.

机构信息

Department of Oncology Tangdu Hospital, Air Force Medical University, Xi'an, 710038, Shanxi, China.

出版信息

Cancer Sci. 2023 Aug;114(8):3101-3113. doi: 10.1111/cas.15798. Epub 2023 May 29.

DOI:10.1111/cas.15798
PMID:36951402
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10394148/
Abstract

AKR7A3 is a member of the aldo-keto reductase (AKR) protein family, whose primary purpose is to reduce aldehydes and ketones to generate primary and secondary alcohols. It has been reported that AKR7A3 is downregulated in pancreatic cancer (PC). However, the mechanism underlying the effects of AKR7A3 in PC remains largely unclarified. Here, we explored the biological function, molecular mechanism and clinical relevance of AKR7A3 in pancreatic ductal adenocarcinoma (PDAC). AKR7A3 expression was downregulated in PDAC compared with adjacent normal tissues, and the lower AKR7A3 expression was related to poor prognosis. In addition, our results demonstrated that AKR7A3 could be a potential diagnostic marker for PDAC, especially in the early stages. Knockdown of AKR7A3 promoted PDAC progression and chemoresistance, while inhibiting autophagy flux. Mechanistically, AKR7A3 affected the metastasis, autophagy, and chemoresistance of PDAC by regulating PHGDH. Overall, the present study suggests that AKR7A3 inhibits PDAC progression by regulating PHGDH-induced autophagy. In addition, AKR7A3 inhibits chemoresistance via regulating PHGDH and may serve as a new therapeutic target for PDAC.

摘要

AKR7A3 是醛酮还原酶 (AKR) 蛋白家族的成员，其主要作用是将醛和酮还原为生成一级和二级醇。有报道称 AKR7A3 在胰腺癌 (PC) 中下调。然而，AKR7A3 在 PC 中的作用机制在很大程度上仍不清楚。在这里，我们探讨了 AKR7A3 在胰腺导管腺癌 (PDAC) 中的生物学功能、分子机制和临床相关性。与相邻正常组织相比，AKR7A3 在 PDAC 中的表达下调，较低的 AKR7A3 表达与预后不良相关。此外，我们的结果表明 AKR7A3 可能是 PDAC 的潜在诊断标志物，尤其是在早期阶段。AKR7A3 的敲低促进了 PDAC 的进展和化疗耐药性，同时抑制了自噬流。在机制上，AKR7A3 通过调节 PHGDH 影响 PDAC 的转移、自噬和化疗耐药性。总的来说，本研究表明 AKR7A3 通过调节 PHGDH 诱导的自噬抑制 PDAC 的进展。此外，AKR7A3 通过调节 PHGDH 抑制化疗耐药性，可能成为 PDAC 的新治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8c4/10394148/ce5456b98f2b/CAS-114-3101-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8c4/10394148/bc7d7dd452ce/CAS-114-3101-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8c4/10394148/bc7d7dd452ce/CAS-114-3101-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8c4/10394148/c4f598bc7b86/CAS-114-3101-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8c4/10394148/01af317b4116/CAS-114-3101-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8c4/10394148/991e2dcca4ec/CAS-114-3101-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8c4/10394148/df8c6b4adfac/CAS-114-3101-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8c4/10394148/396642c6c429/CAS-114-3101-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8c4/10394148/ce5456b98f2b/CAS-114-3101-g002.jpg

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