28P Hijacking CCAT1/miR-17-5p axis alleviates immune checkpoint blockers resistance in PDL1+ TNBC patients

The hot tumor nature of triple-negative breast cancer (TNBC) tumors serves as a key player in the prognosis such patients. Giving strong rational to support immune-based therapeutic approaches for this hard-to-treat group Immune checkpoint blockades (ICBs) have been extensively studied especially PDL1/PD1 blockers. Yet, number resistant cases started escalate. Therefore, it became crucial probe molecular engines regulating PDL1 expression. Currently, unveiling novel networks between non-coding RNAs (ncRNAs) and their roles TNBC has become research hotspot. Our recently reported that miR-17-5p represses immune suppressive IL-10 production. However, its role is still unprobed TNBC. CCAT1 an oncogenic long ncRNA. acts sponge several suppressor miRNAs affecting downstream targets. aim study investigate part interactive ncRNA network BC patients (n=35) were recruited. Bioinformatics analysis was executed. cell lines cultured transfected with different oligonucleotides using HiPerFect Transfection Reagent. Total RNA extracted, reverse transcribed quantified qRT-PCR. Cellular viability, colony forming ability migration measured MTT, scratch assays, respectively. In-silico revealed potential target CCAT1. found be under-expressed PDL1+/CCAT+ tissues compared normal counterparts. Ectopic expression and/or knocking down resulted prominent reduction PDL1. On other hand, mutual loop observed cells; mimics repressed levels while siRNAs induction levels. Functionally, markedly halted hallmarks. This highlights circuit Thus, targeting CCAT1/miR-17-5p axis might provide solution overcoming ICBs resistance arises some