Recent studies have reported the anticancer activity of huaier extract in various human malignancies. However, little is known about the effect of huaier extract in non‐small cell lung cancer (NSCLC) and its underlying mechanism. The current study aimed to investigate whether huaier extract affects the progression of NSCLC. mRNA and proteins expression of pyroptotic‐related genes (NLRP3, caspase‐1, IL‐1β, and IL‐18) in NSCLC tissues and cells were, respectively, detected by qRT‐PCR and western blot. The effects of huaier extract on NSCLC cell viability and cytotoxicity were evaluated by CCK‐8 assay, colony formation assay, and LDH detection kit. Besides, we established a xenograft model to assess the antitumor effect of huaier extract on tumor growth in vivo. Our results showed that the expression of pyroptotic‐related genes was downregulated in NSCLC tissues and cell lines. Huaier extract pretreatment inhibited cell viability and the percentage of colony formation of H520 and H358 cells, and upregulated the expression of pyroptotic‐related genes. Mechanistically, huaier extract exhibited antitumor effect in NSCLC via inducing NLRP3‐dependent pyroptosis in vitro and in vivo. In conclusion, our finding confirmed that huaier extract played an antitumor role in NSCLC progression through promoting pyroptotic cell death, which provided a new potential strategy for NSCLC clinical treatment.
Aim
The aim of this study was to explore the role and molecular basis of the long noncoding RNA (lncRNA) TRHDE‐AS1 in lung cancer.
Methods
We used real‐time polymerase chain reaction to analyze the messenger RNA expression levels of TRHDE‐AS1, miR‐103, and KLF4. The cell viability, proliferation, and invasion rates were assessed via 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide, Cell Counting Kit‐8, and Transwell assays to elucidate the role of TRHDE‐AS1.
Results
Our results demonstrated that the lncRNA TRHDE‐AS1 is mainly located in the cytoplasm and that the cell proliferation and invasion were suppressed in the group of overexpressed TRHDE‐AS1. We also showed that miR‐103 could directly bind to TRHDE‐AS1 and provided evidence of the oncogenic function of miR‐103. Besides, we proved that miR‐103 exerted its function by adjusting the expression level of the tumor‐suppressor gene KLF4, and the expression level was negatively associated with miR‐103.
Conclusion
In summary, we determined that the effects of TRHDE‐AS1 on proliferation, invasion, and cell death could be rescued by the overexpression of miR‐103. Our experiments demonstrate that the TRHDE‐AS1/miR‐103/KLF4 axis may provide new evidence for understanding the molecular basis of lung cancer.
BackgroundAlthough numerous efforts have been made, the pathogenesis underlying lung squamous-cell carcinoma (SCC) remains unclear. This study aimed to identify the CNV-driven genes by an integrated analysis of both the gene differential expression and copy number variation (CNV).ResultsA higher burden of the CNVs was found in 10–50 kb length. The 16 CNV-driven genes mainly located in chr 1 and chr 3 were enriched in immune response [e.g. complement factor H (CFH) and Fc fragment of IgG, low affinity IIIa, receptor (FCGR3A)], starch and sucrose metabolism [e.g. amylase alpha 2A (AMY2A)]. Furthermore, 38 TFs were screened for the 9 CNV-driven genes and then the regulatory network was constructed, in which the GATA-binding factor 1, 2, and 3 (GATA1, GATA2, GATA3) jointly regulated the expression of TP63.ConclusionsThe above CNV-driven genes might be potential contributors to the development of lung SCC.
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