Hsd17b11, encoding type 11 17β-hydroxysteroid dehydrogenase, catalyzes the conversion of 5α-androstan-3α,17β-diol into androsterone, suggesting its role in androgen metabolism [7]. It is also associated with fatty acid and arachidonic acid absorption and metabolism [2].

In cancer research, its high expression in CRC primary tissues was related to poor prognosis, and it promoted CRC cell proliferation and metastasis through the lnc-HSD17B11-1:1/miR-338-3p/MACC1 axis [1]. In LUAD, low expression of Hsd17b11 was associated with increased recurrence rate [2]. In pancreatic cancer, its differential expression was found, and it was significantly associated with overall survival [5]. In esophageal cancer, FTO promoted lipid droplet formation in cells by enhancing Hsd17b11 expression [6]. Also, Hsd17B11 was identified as a mediator of the selective cytotoxic effects of dehydrofalcarinol in MSL subtype triple-negative breast cancer cells [8]. In addition, phenyl-dialkynylcarbinols can be bio-oxidized by HSD17B11, leading to endoplasmic reticulum stress and apoptosis [3]. Moreover, in hepatocytes, HSD17B11 was found to be an interaction partner contributing to GCKIII-mediated regulation of liver lipid homeostasis [4].

In conclusion, Hsd17b11 is involved in androgen and lipid metabolism. Its dysregulation is associated with various cancers, affecting tumor progression, metastasis, and patient prognosis. Functional studies, especially in the context of cancer, contribute to understanding its role in disease mechanisms, potentially providing new diagnostic and therapeutic targets.