Recently, Chinese scientists reported the major role of histone-acetylation controlled noncoding RNA for tumor survival. This provides a potential diagnostic and line of therapy for lung cancer.
The researchers involved in the study revealed that destroying of lysosome cell death regulator (LCDR) in lung cancer cells could accelerate apoptosis.
Physiologically, lysosome is involved in cellular homeostasis. The deregulation of lysosome is associated with various human diseases such as cancer. Lysosome cell death regulator are noncoding RNAs that are more than 200 nucleotides in length, and its dysregulation is linked with cancer hallmarks. They drive cancer growth and assist in survival by interacting with RNA, DNA, and protein assemblies.
However, if lysosome cell death regulator are involved in lysosome-assisted cancer survival is not explained.
During the course of the study, LCDR combines with heterogeneous nuclear ribonucleoprotein to control the stability of lysosomal-linked protein transmembrane 5 that maintains the virtues of lysosomal membrane.
The knockdown of hnRNPK, LCDT, or LAPTM5 accentuated lysosomal cell death and lysosomal membrane permeabilization to result in apoptosis, find researchers.
The overexpression of LAPTM5 or cathepsin B inhibotors partially revived the effects on lysosomal cell both in in vivo and in vitro.
In the same way, targeting LCDR decreased tumor growth of xenografts obtained from patients of lung adenocarcinoma significantly, and led to significant cell death using nanoparticle-assisted systematic siRNA delivery.
Furthermore, upregulation of LCDR/hnRNP K/LAPTM5 occurred in LUAD tissues, and their co-expression demonstrated elevated diagnostic value for LUAD.
Following this, the findings show how LCDR/hnRNP K/LAPTM5 can be potential therapeutic targets and thus indicating targeting lysosome as a promising technique in cancer treatment.