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. 2021 Jan 28;134(9):1052-1054.
doi: 10.1097/CM9.0000000000001379.

Roles of AKR1C3 in malignancy

Xin-Zhu Xiao  1 , Li-Ying Lin, Ming-Kai Zhuang, Can-Mei Zhong, Feng-Lin Chen
Affiliations

Roles of AKR1C3 in malignancy

Xin-Zhu Xiao et al. Chin Med J (Engl). .
No abstract available

PubMed Disclaimer

Conflict of interest statement

None.

Figures

Figure 1
Figure 1
Overview of the major pathways for AKR1C3's action on tumor cells. AKR1C3 promotes the proliferation, survival, radio-resistance, EMT, metastasis, invasion, and angiogenesis and inhibits the apoptosis, differentiation of tumor cells through the above signal pathway. 5d-PGJ2: 15-d prostaglandin J2; AKR1C3: C3 subtype of aldosterone reductase family 1; AKT: Protein kinase B; AR: Androgen receptor; CREB: cAMP-response element-binding protein; EMT: Epithelial-to-mesenchymal transition; ER: Estrogen receptor; FR: Prostaglandin receptor; IGF-1: Insulin-like growth factor-1; NF-κB: Nuclear factor kappa-B; p-AKT: Phosphorylated protein kinase B; PCD2: Prostaglandin D2; p-ERK1/2: Phosphorylated extracellular-regulated protein kinases 1/2; PGF2α: Prostaglandin F2α; PI3K: Phosphatidylinositol 3 kinase; p-MEK: Phosphorylated mitogen-activated protein kinase kinase; PPARγ: Peroxisome proliferator-activated receptor γ; PR: Progesterone receptor; PTEN: Phosphatase and tensin homolog deleted on chromosome ten; Twist1: Twist family BHLHT transcription factor 1; VEGF: Vascular endothelial growth factor; ZEB1: Zinc finger box-binding homeobox 1.
See this image and copyright information in PMC

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