A primary cilium is a single tail-like structure that protrudes out of most cells in our body.2 It functions as a signaling hub that receives and transmits a variety of signals inside and outside the cell. Most notably, it plays a key role in cellular growth and development though the hedgehog pathway3, and the dysfunction in this pathway is implicated in many diseases including cancer.4,5,6
Three key proteins are involved in the hedgehog pathway: smoothened (SMO), patched (PTCH), and hedgehog (HH).3 In normal conditions, PTCH reside on the surface of the cell near the primary cilium, while SMO reside within the cell.7 Through mechanisms that are not fully understood, PTCH prevents SMO from translocating to the primary cilium.
However, when HH binds to PTCH, PTCH is inactivated and is transported within the cell. This allows SMO to translocate to the primary cilium, where it is able to transmit signal for the cell to grow.7 Since this process is dependent on the presence of HH, it is a controllable one - when cellular growth is no longer needed, the production of HH simply ceases.
However, SMO or PTCH are mutated in certain types of cancer that allows SMO to bypass PTCH or for PTCH to be unable to block SMO.4,8 This allows SMO-mediated growth signal to be transmitted uncontrollably even without hedgehog. These cancer cells rely on growth signal from the constitutively active hedgehog pathway to proliferate.6
Vismodegib is a drug that binds to SMO and inactivates it.9 This turns off the growth signal transmitted by SMO, and as a result, cancer growth is halted.10,11