Our data reveal that lncRNA-SVUGP2 is under-expressed in NSCLC cells and the reduced expression of lncRNA-SVUGP2 may enhance the development and process of NSCLC by interacting with EZH2 and activating Wnt/β-catenin pathway.
Recently, accumulated evidence indicates that the enhancer of zeste homologue 2 (EZH2) is highly expressed in a wide range of cancer types, including NSCLC.
Increased EZH2 expression predicts for response to HDAC inhibitors and thus could serve as a biomarker for selecting NSCLC patients for treatment with HDAC inhibitors.
Previously we demonstrated that polyphyllin I (PPI), a bioactive component extracted from Paris polyphylla, inhibited the growth of non-small cell lung cancer (NSCLC) cells through the SAPK/JNK-mediated suppressing p65, DNMT1 and EZH2 expressions.
In summary, NEDD4L acted as a tumor suppressor gene in NSCLC and targeting EZH2 could upregulate NEDD4L expression, which might serve as a novel approach for NSCLC.
LATS2 and KLF2 are target genes of LINC00511, which are regulated by LINC00511 through binding to EZH2 and LSD1, thus influencing the progression of NSCLC.
In conclusion, the results in this work confirmed that FOXC2-AS1 could aggravate NSCLC oncogenesis through repressing p15 expression via interacting EZH2, which provide new idea for the NSCLC therapeutic strategy.
In summary, the results indicate an explicit oncogenic role of TP73-AS1 in the NSCLC tumorigenesis, suggesting a TP73-AS1-miR-449a-EZH2 axis and providing new insight for NSCLC tumorigenesis.
In conclusion, the present study demonstrated that FOXN1 served major roles in NSCLC proliferation and invasion by directly repressing EZH2 and β-catenin, which suggested that FOXN1 may function as a tumor suppressor in NSCLC.
Compared with the non-smokers, smokers with NSCLC exhibited a significantly lower apoptotic index (P<0.05), and frequently had a lower level of DNA methylation at CCGG sites, lower H3K27me3 expression and a higher EZH2 expression (P<0.05).
Together, our data uncover that GDF15 is a direct target of EZH2 and, as a regulator of proliferation, might serve as a candidate prognostic biomarker and target for new therapies in human NSCLC.
In conclusion, the hsa_circ_0020123-miR-144-ZEB1/EZH2 axis is critical for NSCLC progression, which indicates that hsa_circ_0020123 is a potential target for NSCLC treatment.
These findings indicated that multifunctional NPs can be utilized as a co-delivery system, and that the combination of EZH2 siRNA and ETP can effectively treat NSCLC.
The mechanistic findings showed demonstrated that HOXA11-AS interacted with EZH2 and DNMT1 and recruited them to the miR-200b promoter regions to repress miR-200b expression in NSCLC cells, which promoted cell EMT in NSCLC.
Furthermore, EZH2 expression rates were higher in NSCLC with moderately and poorly differentiation and nodal disease than in well-differentiated NSCLC without nodal disease.