In this paper, a cross-institutional team led by the Harvey N. Cushing Neuro-oncology Laboratories (HCNL) at Harvard, explains how checkpoint inhibitors, such as programmed cell death 1 ligand 1 (PD-L1), have introduced a whole new approach to fighting cancer.
The team recently discovered that a poorly characterized long noncoding RNA (lncRNA) — known as Interferon-stimulated Non-Coding RNA1 (INCR1) — regulates IFNɣ signaling of PD-L1.
Specifically, silencing of INCR1 leads to the repression of interferon-stimulated genes (ISG), including PD-L1 which has an inhibitory effect on the cancer-fighting abilities of cytotoxic T cells. When PD-L1 is suppressed, it leaves tumor cells more susceptible to cytotoxic T cells and thus becomes a great target for immunotherapy.
The first step in discovery efforts into regulator effects of INCR1 included whole-transcriptome sequencing (RNAseq) of known cancer cell lines with and without IFNɣ stimulation. Comparison of upregulated lncRNA in the IFNɣ stimulated cells led to all subsequent findings.
All RNAseq work was completed at Psomagen Inc. in Rockville, MD USA. Psomagen is a CLIA-certified, CAP-accredited next-generation sequencing services company whose laboratory operations are located within the United States.
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