The mRNA level of UBC12 in lung cancer tissues was much higher than that in normal lung tissues, increased with disease deterioration, and positively correlated with NEDD8 expression.
The aim of this study was to characterize the role of Alport syndrome, mental retardation, midface hypoplasia, and elliptocytosis chromosomal region gene 1 (AMMECR1) in human lung cancer cell lines.
Further, clinical analysis showed that STC2 expression was increased after the development of EGFR TKI resistance and that higher levels were correlated with shorter progression-free survival in EGFR TKI-treated lung cancer patients.
By analyzing the correlation between gene markers and clinicopathological parameters of lung cancer and its effect on prognosis, the TPBG gene was selected to analyze differential expression, its possible pathways and functions were predicted using gene set enrichment analysis (GSEA), and its protein interaction network was constructed using the Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) database; then, quantitative PCR and the Oncomine database were used to verify the expression differences of TPBG in lung cancer cells and tissues.
Here we unexpectedly found that two understudied kinases, SIK1 and SIK3, are critical targets in lung cancer.<i>This article is highlighted in the In This Issue feature, p. 1469</i>.
In addition, SOX9 was identified as a transcription factor of FOXA1 in lung cancer and involved in affecting the expression of FOXA1 targeted genes-Bcl2, CDKN1B, RPRM and NKX2.
To conclude, our study discovered the role of lncRNA GATA2-AS1 in human non-small cell lung cancer growth thus providing a potential target for lung cancer drugs.
The aim of this study was to investigate the association between purinergic receptor P2X7 (P2RX7) gene rs1718125 polymorphism and analgesic effect of fentanyl after surgery among patients with lung cancer in a Chinese Han population.A total of 238 patients with lung cancer who received resection were enrolled in our study.
This study investigates the functions and molecular mechanisms of circNOL10 in the development of lung cancer and reveals its involvement in the transcriptional regulation of the HN polypeptide family by SCML1.
Our primary focus was on the expression of immune checkpoint (IC)-molecules, such as programmed death (PD)-1, T-cell immunoglobulin and mucin-domain containing (TIM)-3, T cell Ig and ITIM domain (TIGIT), and cytotoxic T lymphocyte antigen (CTLA)-4, on T<sub>reg</sub> cells in paired lymphocytes from blood, peritumoral tissue, and tumors of 12 patients with lung cancer.
At the same time, EZH2 expression in LCa tissues was also remarkably up-regulated relative to adjacent tissues, and it was positively correlated with the expression of MSTO2P.
In this study, we demonstrated that CC chemokine ligand 7 (CCL7) and its receptors CCR1, CCR2 and CCR3 were up-regulated markedly in lung cancer bone metastasis.
Multiple blinded raters validated CLE videos of lung tumours and mediastinal nodes twice.EUS-nCLE-FNA was performed in 22 patients with suspected or proven lung cancer in whom 27 lesions (six tumours, 21 mediastinal nodes) were evaluated without complications.
Our findings demonstrate that the miR-148a-3p may play a significant role in NSCLC including the kind of lung cancer with K-Ras gene mutation, and it exerted the tumor inhibitor function by targeting SOS2.
This study investigates the functions and molecular mechanisms of circNOL10 in the development of lung cancer and reveals its involvement in the transcriptional regulation of the HN polypeptide family by SCML1.
CONCLUSIONS: The high frequency of both MUC1 and MUC5AC cytoplasmic expression, coupled with a lack of MUC2 and MUC6 expression in ALK + lung cancer may contribute to the biologically aggressive behavior of ALK + cancer.
After GWA filtration, two mRNAs (Myo7a and Zfp874a) and two lncRNAs (n290048 and n271850) were highlighted as the candidates responsible for genetic susceptibility to lung cancer.
The molecular docking was further performed to study the binding mode of the final product into the active site of human Caprin-2 C1q domain (4OUM, cause gastric cancer protein), liver cancer protein (1UV0) and lung cancer protein (3B9S).