Lung cancer is known as one of the deadliest forms of cancer as it spreads rapidly making the chances of survival extremely low.
In this study scientists identified a new pathway through which they could explain the reason for which some tumors are more prone to spreading than others.
This work has been published in Molecular Cell.
"Lung cancer, even when it's discovered early, is often able to metastasize almost immediately and take hold throughout the body," The reason behind why some tumors do that and others don't has not been very well understood. Now, through this work, we are beginning to understand why some subsets of lung cancer are so invasive says Reuben J. Shaw, Salk professor of molecular and cell biology and a Howard Hughes Medical Institute early career scientist.
Lung cancer which doesn’t spare even non smokers is extremely difficult to treat because of the extensive spreading nature of the tumours, 80 percent of the patients do not survive more than five years after the first diagnosis.
It is an established concept that in a fifth of lung cancer cases, an anti-cancer gene called LKB1 (also known as STK11) is absent. Cancers with missing LKB1 are more aggressive, reports suggest.
This particular research has established the much needed connection and a new target for therapy: a lesser talked about gene known as DIXDC1. The researchers discovered that DIXDC1 receives instructions from LKB1 to go to focal adhesions and change their size and number.
If DIXDC1 is "switched on," half a dozen or so focal adhesions grow large and sticky, anchoring cells to their specific spots.
"The communication between LKB1 and DIXDC1 is responsible for a 'stay-put' signal in cells," says first author Jonathan Goodwin. "DIXDC1, which no one knew much about, turns out to be inhibited in cancer and metastasis."
The team used metastatic cell with lower expression of DIXDC1, and over-expressed the gene. The over expression of DIXDC1 could successfully reduce the ability of these cells to be metastatic in vitro and in vivo.
"The good news is that this finding predicts that patients missing either gene should be sensitive to new therapies targeting focal adhesion enzymes, which are currently being tested in early-stage clinical trials," Shaw was quoted saying.
So if everything goes fine, in near future, fighting the battle against lung cancer will be less difficult that it is at this moment.