Polyclonal LSD1 (IN), (Lysine-specific histone demethylase)
- Known as:
- Polyclonal LSD1 (IN), (Lysine-specific histone demethylase)
- Catalog number:
- pc-543
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Kamiya biomedical company
- Gene target:
- Polyclonal LSD1 () (Lysine-specific histone demethylase)
Related genes to: Polyclonal LSD1 (IN), (Lysine-specific histone demethylase)
- Gene:
- KDM1A NIH gene
- Name:
- lysine demethylase 1A
- Previous symbol:
- AOF2, KDM1
- Synonyms:
- KIAA0601, BHC110, LSD1
- Chromosome:
- 1p36.12
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-26
- Date modifiied:
- 2018-03-06
Related products to: Polyclonal LSD1 (IN), (Lysine-specific histone demethylase)
Related articles to: Polyclonal LSD1 (IN), (Lysine-specific histone demethylase)
- Colorectal cancer (CRC) remains poorly responsive to immune checkpoint blockade in a substantial proportion of patients, highlighting the need to identify druggable mechanisms that regulate tumor immune evasion. CD155, a ligand of the inhibitory receptor TIGIT, is highly expressed in CRC and contributes to impaired natural killer (NK) cell-mediated antitumor immunity. Lysine-specific demethylase 1 (LSD1/KDM1A) is a pharmacologically targetable epigenetic enzyme with emerging roles in tumor immunogenicity, but whether LSD1 inhibition modulates the CD155/TIGIT immune checkpoint axis in CRC remains unclear. In this study, we found that LSD1 and CD155 were highly expressed in CRC tissues and showed a significant positive correlation. Genetic depletion of LSD1 reduced CD155 expression at both the mRNA and protein levels in CRC cells. Importantly, pharmacological inhibition of LSD1 with two small-molecule inhibitors, CC-90011 and ORY-1001, markedly decreased CD155 expression and membrane abundance in multiple CRC cell lines. Mechanistically, LSD1 depletion or inhibition increased H3K4me2 enrichment at the CD155 promoter, suggesting that LSD1 activity is required for maintaining CD155 transcription in CRC cells. Functionally, LSD1 inhibition decreased CD155 expression and cell-surface abundance, resulting in reduced CD155/TIGIT interaction and enhanced NK cell-mediated cytotoxicity, accompanied by increased secretion of IFN-γ and TNF-α. In a CT26 syngeneic tumor model, LSD1 knockdown suppressed tumor growth and decreased CD155 expression in vivo. Collectively, these findings reveal that pharmacological inhibition of LSD1 attenuates CRC immune escape, at least in part, by epigenetically suppressing the CD155/TIGIT axis. This study provides a rationale for exploiting LSD1 inhibitors as immunomodulatory agents to enhance antitumor immunity in CRC. - Source: PubMed
Publication date: 2026/08/11
Dai Xing-JieWu Jiang-WanZhu Jin-ManHu Jing-YingLiu Hong-MinLiu Hui-MinZheng Yi-Chao - Selective lysine-specific demethylase 1 (LSD1) inhibition has emerged as a robust strategy for small cell lung cancer (SCLC) eradication. Herein, we describe the structural design, synthesis, and biological evaluation of novel reversible LSD1 inhibitors containing a carboxamido pyrazole core with a pyrrolidine-substituted phenyl ring. Notably, compound 10q demonstrated potent LSD1 inhibition with an IC50 value of 7.2 nM and effective H1417 cell growth inhibition with a GI50 value of 20.0 nM. Moreover, it showed notable selectivity against homologous proteins and demethylases. The oral administration of compound 10q demonstrated encouraging pharmacokinetic profiles and remarkable antitumor efficacy in the NCI-H1417 SCLC xenograft model using NOD/Shi-scid/IL-2Rγnull mice without notable toxicity. Furthermore, the potential of compound 10q is proposed by combinatorial therapy with chemotherapeutic agents for treating SCLC. Therefore, compound 10q can be considered a promising candidate as a selective and orally bioavailable LSD1 inhibitor. - Source: PubMed
Choi JaeyulKim JihunLee SeungyeonKim JisookKim Wong JungKang Seok JongJung Seung HyunAhn YounggilSingh PargatKim In Su - Pancreatic ductal adenocarcinoma (PDAC) remains a highly lethal malignancy due to its aggressive biology and therapeutic resistance. Lysine-specific demethylase 1 (LSD1), an epigenetic regulator, is overexpressed in PDAC and linked to poor prognosis, yet its context-dependent roles in metabolic subtypes and chemoresistance remain undefined. Here, we show that LSD1 knockdown has opposing, subtype-specific effects on chemotherapeutic responses: it sensitized RSK-subtype cells (L3.6pl, PANC-1) to chemotherapy but induced resistance in KRAS-subtype cells (BxPC-3, TBO368). Integrated analyses revealed mitochondrial dysfunction and defective mitophagy as hallmarks distinguishing KRAS- from RSK-subtype PDAC. Critically, mitochondrial targeting through respiratory modulation or mitophagy manipulation overrides LSD1-mediated subtype-specific chemoresistance, establishing mitochondrial fitness as the mechanistic determinant. Mechanistically, LSD1 transcriptionally regulates GLS2 to drive glutamine metabolic reprogramming, promoting reductive carboxylation in KRAS-subtype cells and oxidative metabolism in RSK-subtype cells. Our work establishes the LSD1-GLS2 axis as a metabolic switch controlling PDAC chemosensitivity and provides a framework for subtype-specific therapeutic strategies. - Source: PubMed
Publication date: 2026/07/20
Wang ZhefangHuang QiuZhao JiangangLyu ZichengJu FengYou BoWang JieDong QiongzhuOdenthal MargareteQuaas AlexanderDiakopoulos Kalliope NAlgül HanaReichert MaximilianBruns Christiane JZhao Yue - Ureteral scar formation is a fibrotic process linked with collagen synthesis. Although autophagy prevents collagen synthesis, its role in ureteral scarring remains unclear. Therefore, this study investigated the modulation of SESN2-mediated autophagy by verapamil during ureteral scar formation. - Source: PubMed
Publication date: 2026/07/17
He JunhuanLi JunWu XuechengZhu ZhiweiChen JunjieLu QiangTang ZhengyanLi YuanweiZeng Mingqiang - Sickle cell disease and cancer represent fundamentally distinct classes of human disease-one is driven by a defined mutation in β-globin, whereas the other arises through complex genetic and epigenetic alterations that reshape cellular identity and behavior. Despite these differences, both contexts illustrate how transcription factors, chromatin regulators, and cis-regulatory elements can impose disease-relevant gene expression states. In β-hemoglobinopathies, therapeutic reactivation of fetal hemoglobin through modulation of γ-globin (HBG1/2) regulatory pathways, most notably disruption of the erythroid-specific BCL11A enhancer, has emerged as a clinically validated strategy. These advances have been facilitated in part by the HUDEP-2 erythroid progenitor cell line, which provides a tractable adult erythroid model for identifying fetal hemoglobin regulators, validating their function, and evaluating relevant gene editing and gene-regulatory therapies. Many of the regulators implicated in γ-globin silencing, including BCL11A, ZBTB7A, NuRD-associated proteins, DNMT1, KDM1A/LSD1, MYB, and ATF4, also function in cancer-associated transcriptional or epigenetic networks. In cancer, these factors can support oncogenic transcription, tumor suppressor repression, impaired differentiation, stress adaptation, invasion, or therapy resistance. This review summarizes discoveries enabled by HUDEP-2 cells in fetal hemoglobin regulation and hemoglobinopathy therapeutic development, then discusses how these mechanisms provide conceptual parallels for understanding and targeting regulatory dependencies in cancer. - Source: PubMed
Publication date: 2026/07/16
Yu MeigenDas PuspaZhang XingCheng Xiaodong