Taken together, our study suggests that miR-590-5p acts as a tumor-suppressor in NSCLC through regulating the STAT3 pathway, and may serve as a useful biomarker for the diagnosis/prognosis of NSCLC, and as a potential therapeutic target for the treatment of NSCLC.
Consistently, immunohistochemistry staining showed that activated STAT3 correlated with repressed infiltration CD8+ T cells in non-small cell lung cancer.
An enhancement of PD-L1 antibody by niclosamide was observed in inhibition of NSCLC growth in vitro and in vivo, which was involved in blockage of p-STAT3 binding to promoter of PD-L1 and finally downregulation of PD-L1 expression.
These results indicated that the combination of SSD with gefitinib had an increased antitumor effect in NSCLC cells and that the molecular mechanisms were associated with the inhibition of STAT3/Bcl-2 signaling pathway.
Taken together, LINC81507 is decreased in NSCLC and functions as a sponge to miR-199b-5p to regulate CAV1/STAT3 pathway, which suggests that LINC81507 serve as a tumor suppressor and potential therapeutic target and biomarker for metastasis and prognosis in NSCLC.
In summary, EP inhibited NSCLC cell growth, invasion and migration and induced apoptosis by suppressing the HMGB1/RAGE axis and the NF‑κB/STAT3 pathway, thus suggesting that EP may be a valuable therapeutic agent for NSCLC.
In this study, the potential role of TP in the proliferation, apoptosis, and migration of non‑small cell lung cancer cell lines was investigated and evaluated the impact of TP on the interleukin‑6 (IL‑6)/STAT3 axis.
Moreover, it inhibits the invasion and metastasis capacities through targeting STAT3, which can serve as a therapeutic target for cisplatin-based chemotherapy resistance of NSCLC.
Persistently activated IL-6/STAT3 pathway promotes acquired resistance to targeted therapy with epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) in non-small-cell lung cancer (NSCLC) treatment. miR-206 has been verified to be dysregulated and plays as a negative regulator in lung cancer.
In the present study, it was reported that signal transducer and activator of transcription 3 (STAT3) may function as a novel target gene for miR‑4500 in NSCLC.
The present study reported that signal transducer and activator of transcription 3 is not the only target of cryptotanshinone during the inhibition of human NSCLCs.
We report frequent hypermethylation of the PTPRT promoter which correlates with transcriptional silencing of PTPRT and increased STAT3 phosphorylation (Y705) as determined by methylation-specific PCR (MSP) and real time quantitative reverse transcription (RT)-PCR in NSCLC cell lines.
Our findings suggested that STAT3-induced LINC00668 contributed to NSCLC progression through upregulating KLF7 expression by sponging miR-193a, and may serve as a prognostic biomarker and a potential target for NSCLC.
In conclusion, these findings suggest that FXT could be a promising lead compound to be used as a novel STAT3 inhibitor and potential antitumor agent for the treatment of NSCLC.