It has been discovered by an international research team that the IFT20 protein helps some cancer cells to invade by facilitating the transportation of membranes and proteins within parts of the cell. Most human cells have cilia on the surface, acting as cell antenna that receives information from outside the cell. The protein IFT20 is present in most human cells and plays an essential role in the formation and functions of these primary cilia. It acts as a cargo adaptor in healthy cells to transport proteins along microtubules within cilia but many of these cells lose cilia when they become cancerous. For the first time light is being shed from research on the function of IFT20 in non-ciliated cancer cells. That has brought to light that this discovery has potential applications for developing new cancer treatment methods that block invasive cancer cells by targeting the IFT20. The Scientific Reports published the findings online.
An international team including Associate Professor NISHITA Michiru, Professor MINAMI Yasuhiro, Professor Victor W. Hsu and Professor Gregory J. Pazour carried out the research. These professors are affiliated with Kobe University, Harvard Medical School and University of Massachusetts Medical School.
Cell invasion causes most cancer-related deaths and the spread of cancer cells to other parts of the body. Scientists are searching for mechanisms that control the invasive properties of cancer cells to counter this.
It was already known that a cell membrane protein known as Ror2 expresses highly in various cancer cells and promotes cancer cell invasion and metastasis. Various kinds of non-ciliated cancer cells were investigated by the team, and discovered that Ror2 promoted cancer cell invasiveness by inducing the expression of IFT20.
Many tumor cells are able to break through the barrier of the extracellular matrix and infiltrate their surroundings. It was demonstrated that in tumor cells IFT20 induces the Golgi complex to form microtubules by promoting interaction between the Golgi proteins GM130 and AKAP450. They state that this research has clarified a new molecular mechanism related to the formation of Golgi-derived microtubules, and its important role in invasive cancer cells.
It is still unclear about the relationship between loss of cilia and a cell’s cancerous properties. In non-ciliated cancer cells it is clear that IFT20 is responsible for the formation of invadopodia. The line of analyzing the relationship between IFT20 and the loss of cilia could help to shed light on the fundamental question of why many cancer cells lack cilia. If the specific regulatory mechanism of IFT20 in cancer cells is revealed, this could be used to develop treatment that targets IFT20 to block invasive cancer cells.
Dr Fredda Branyon