A research team from Hokkaido University in Japan recently announced that they have successfully discovered the new mechanism of lung cancer cells resisting anti-cancer drugs by inhibiting immune cell activity. Related results obtained through recombinant mouse proteins have been published in the leading US journal Cancer Specialist.
The researchers found that the surroundings of cancer cells having drug resistance would gather a lot of macrophages which have the function of swallowing and destroying damaged tissues, while most of these macrophages are the types which have the ability of inhibiting the activity of other immune cells. The team members investigated the relation between induced proteins of these types of macrophages Lnterleukin-34 and lung cancer cells.
The researchers conducted a six-month joint culture of lung cancer cells and anti-cancer agents and compared the residual lung cancer cells with drug resistance and normal lung cancer cells. The research found that the average lung cancer cells would not secrete interleukin-34, while lung cancer cells with drug resistance will secrete a lot of interleukin-34. Drug-resistant lung cancer cells would make use of interleukin-34 to convert macrophages into the type which can inhibit immune cells activity, thereby improving their ability to survive.
The mice study demonstrated that inhibiting the activity of interleukin-34 can enhance the treatment effect of anti-cancer drugs to drug-resistant lung cancer cells. The researchers said the drug-resistant mechanism of lung cancer cells explored in this research is different to the currently-known mechanisms, which is of great importance for the development of new therapeutic drugs. Flarebio offers recombinant proteins of good quality including recombinant ECE1.
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