HIF-1alpha inhibitor at translation level (HITT)

HIF-1alpha inhibitor at translation level (HITT, also known as LINC00637 and PPP1R13B divergent transcript) is a long non-coding RNA (lncRNA) that does not encode a protein but plays a regulatory role in cellular stress responses. HITT inhibits translation of HIF-1alpha, a protein involved in hypoxic response, and also suppresses ATM activity linked to DNA damage. In cancer, HITT is downregulated in advanced stages of several types (colon, bladder, breast, liver), where its decreased expression is associated with tumor progression. Mechanistically, HITT inhibits translation of PD-L1, a key immune checkpoint molecule, by forming a complex with the translational regulator protein RGS2, and possibly helps modulate immune evasion by tumor cells. HITT expression is induced by the cytokine IFN-γ and may act as a responsive regulator in inflammatory microenvironments. Overall, HITT is recognized as a functionally relevant lncRNA in tumor suppression and immune modulation, but it is not a canonical therapeutic target such as a receptor or enzyme[1][3].

Other names

LINC00637PPP1R13B divergent transcriptPPP1R13B-DTlong intergenic non-protein coding RNA 637HIF-1alpha inhibitor at translation levelHITT

Not applicable (no drugs known to specifically target this lncRNA)