Cell Death Dis:lncRNA CASC9: Triggers of gyfygenic resistance in non-small cell lung cancer

Non-small cell lung cancer (NSCLC) is one of the most common malignancies in the world.
Although treatment strategies for surgery, radiotherapy and drug therapy for the disease, including chemotherapy, targeted therapy and immunotherapy, are evolving, the prognostics for patients with advanced NSCLC remain poor.
Current studies have shown that the first generation of EGFR-TKI (the methotrexel growth factor-subject tyrosine kinase inhibitor), represented by gefitinib, significantly prolongs the median survival of patients with advanced lung cancer with EGFR-sensitive mutations and significantly improves the quality of life of patients.
, however, due to the inevitable resistance, greatly affects the clinical outcomes of NSCLC patients.
, the in-depth study of EGFR-TKIs drug resistance mechanism, as well as the search for drug resistance-related genes and reversal of drug resistance has become an important topic in lung cancer treatment research in recent years.
CASC9 expresses elevated long-chain non-coding RNA (lncRNA) as a non-coding RNA that regulates gene expression at a variety of levels, including post-esoteric, transcriptional, and post-transcriptional levels.
previous studies have shown that lncRNA can regulate tumor development, little is known about its contribution to NSCLC's gyfetinib resistance.
CASC9 expression reduction reduces gyfythinib resistance The study identified lncRNA expressed in different expressions in Gyfetinib-resistant cells and gyfeitinib-sensitive cells by analyzing the GEO database of the National Institutes of Health.
researchers found that lncRNA CASC9 expression levels increased in drug-resistant cells and were also validated in drug-resistant tissue.
the obtaining and loss of functionality showed that inhibiting the expression of CASC9 restored gyfetinib sensitivity, while over-expression of CASC9 in contrast promoted the production of gyfynagosin resistance.
CASC9 regulation in NSCLC Gifetinib resistance schematic mechanism study found that CASC9 can inhibit the tumor inhibitor DUSP1 by collecting histone methyl metastase EZH2, and ultimately improve the resistance of gyfrotein.
addition, the iso-expression DUSP1 can improve gaffetinib sensitivity by insensitive ERK signaling path.
, the results reveal the important role of CASC9 in Gifetinib resistance, suggesting that the CASC9/EZH2/DUSP1 path is likely to be a new target for inhibiting EGFR-TKI resistance in NSCLC.