Cancer-Linked Proteins May Reveal Tumors but Help Them Evade Immunity
Researchers at Hiroshima University have discovered that the proteins YAP and TAZ contribute to both tumor visibility and immune evasion in cancer cells. This dual role may explain why certain patients respond better to immune checkpoint inhibitor therapies.
Why it matters
Understanding these protein mechanisms could lead to more effective cancer treatments by helping doctors identify which patients will benefit from specific immunotherapies.
Schematic of YAP/TAZ-mediated immune evasion. YAP/TAZ hyperactivation is associated with genomic instability that may make cancer cells more recognizable to CD8+ T cells, immune cells that can recognize and kill abnormal cells, including cancer cells. At the same time, YAP/TAZ hyperactivation can increase PD-L2, which binds to PD-1 receptors on CD8+ T cells and suppresses their attack. Together, these effects may help explain why certain Hippo pathway alterations were linked to better outcomes following immune checkpoint inhibitor therapy. (Toshinori Ando/Hiroshima University)
The immune system may recognize a cancer cell and still fail to destroy it. Researchers at Hiroshima University (HU) and their international collaborators found that hyperactive YAP and TAZ (YAP/TAZ), two cancer-promoting proteins, were associated with genomic instability that may make cancer cells more recognizable to the immune system, while also increasing PD-L2, which helps the cells suppress T-cell attack.
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