Kdm1b, also known as lysine-specific demethylase 2 (LSD2), is an epigenetic modifier with demethylase activity against H3K4 and H3K9 histones. It plays crucial roles in regulating gene transcription, participating in various biological processes such as tumor progression, tumor stem cell enrichment, and somatic cell reprogramming. It is also involved in pathways related to cancer cell stemness, drug resistance in cancers, and spermatogenesis [1-7].

In cancer research, inhibition of Kdm1b prevents the appearance of type I interferon-induced cancer stem cells in vitro and in vivo, indicating its role in promoting cancer cell stemness and immune escape [1]. In enzalutamide-resistant prostate cancer, down-regulation of Kdm1b can improve treatment response by suppressing AGR2 transcription [2]. In pancreatic cancer, knockdown of Kdm1b inhibits cell proliferation and induces apoptosis [3]. In cisplatin-resistant ovarian cancer cells, down-regulation of Kdm1b promotes cell death [5]. In prenatal dexamethasone-exposed rats, changes in Kdm1b expression affect sperm quality and blood-testis barrier function [4].

In conclusion, Kdm1b is a significant epigenetic regulator involved in multiple biological processes. Studies on Kdm1b, especially through loss-of-function experiments in various models, have revealed its importance in cancer development, drug resistance, and male reproductive health. These findings provide potential therapeutic targets for treating related diseases.