Menin regulates YBX1 nuclear translocation to drive HKDC1 transcription and restrain glycolysis in pancreatic ductal adenocarcinoma

Menin suppresses glycolysis in PDAC by binding YBX1, promoting its nuclear import, and up-regulating HKDC1 transcription. RNA-seq on PL45 cells over-expressing Menin versus vector control identified 413 DEGs; key metabolic genes GLUT1 and LDHA were down-regulated, while HKDC1 was up-regulated. Findings highlight a Menin-YBX1-HKDC1 axis as a potential therapeutic target. Homo sapiens PL45 PDAC cells (triplicate). Group A: pcDNA3.1-Menin over-expression (Menin-OE). Group B: empty-vector control (Vector). Total RNA isolated 48 h post-transfection, rRNA depleted, stranded paired-end (2 × 150 bp) libraries prepared with NEBNext Ultra, sequenced on Illumina NovaSeq 6000.