KDM1B antibodies are monoclonal or polyclonal reagents that bind specifically to the KDM1B protein. They are validated for use in techniques such as Western blot (WB), flow cytometry (FC), and enzyme-linked immunosorbent assay (ELISA). Key properties include:
Oncogenic Role: KDM1B is overexpressed in breast, colorectal, and lung cancers, where it promotes tumor growth and chemoresistance by demethylating H3K4me1/me2 . Antibodies enable detection of KDM1B in cancer cell lines and patient tissues.
Stemness Regulation: In breast cancer, KDM1B overexpression enriches cancer stem cell (CSC) populations (e.g., CD44+/EpCAM-, ALDHhigh) and upregulates pluripotency markers (NANOG, SOX2) . Neutralizing KDM1B with inhibitors like tranylcypromine reduces CSC expansion .
Chromatin Remodeling: KDM1B antibodies facilitate ChIP-seq analyses to map KDM1B’s interaction with genes involved in stemness, DNA repair, and immune evasion .
Enzyme Activity: Studies show KDM1B demethylates H3K4 but not H3K9 or H3K27, distinguishing it from LSD1/KDM1A .
IFN-I → KDM1B Axis: Type I interferons (IFN-I) upregulate KDM1B during chemotherapy, driving CSC plasticity and immune escape. KDM1B inhibition blocks this process, improving tumor control in murine models .
Morphological Changes: Overexpression of KDM1B in MDA-MB-231 breast cancer cells induces cobblestone-like morphology and alters epigenetic modifiers (e.g., LSD1, HDAC1/2) .
Prognostic Marker: High KDM1B expression correlates with poor survival in basal-like breast cancer and HER2-negative tumors .
Therapeutic Target: Preclinical data support combining KDM1B inhibitors (e.g., tranylcypromine) with immunogenic therapies to prevent CSC-driven relapse .