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1.  IL-21 polymorphisms rs907715 and rs2221903 are associated with decreased non-small cell lung cancer susceptibility 
The etiology of lung cancer is still incompletely understood. Previous studies have suggested the association between IL-21 polymorphisms and autoimmune diseases, however, little is known about its role in lung cancer susceptibility. Here, we investigated the role of two SNPs of IL-21 gene in a cohort of non-small cell lung cancer (NSCLC) patients. A total of 128 NSCLC patients and 156 healthy controls were genotyped. Multivariate logistic regression was used to analyze the association between IL-21 polymorphisms and NSCLC risk. Our data showed that both rs907715 and rs2221903 were significantly associated with lung cancer susceptibility, and patients carrying rs907715A (P = 0.007, adjusted OR = 0.60, 95% CI = 0.42-0.87) or rs2221903G (P = 0.020, adjusted OR = 0.52, 95% CI = 0.30-0.90) allele had a decreased risk of NSCLC. Further study identified that the association between IL-21 polymorphisms and NSCLC risk was limited to lung adenocarcinoma. Haplotype analysis revealed that the AG (P = 0.006, OR = 0.072 95% CI = 0.011-0.451) and AA (P = 0.022, OR = 0.657, 95% CI = 0.458-0.941) haplotypes of rs907715/rs2221903 were associated with a decreased risk of NSCLC, whereas the GA (P = 0.0001, OR = 1.932, 95% CI = 1.378-2.710) haplotype was associated with an increased risk. In conclusion, our study demonstrates the association between IL-21 polymorphisms (rs907715 and rs2221903) and NSCLC risk in a Chinese Han population, indicating their potential role in lung cancer detection and treatment.
PMCID: PMC4694492  PMID: 26770592
SNP; IL-21; NSCLC; susceptibility
2.  Correlation study and significance of the EGFR expression in serum, lymph nodes and tumor tissue of NSCLC 
Thoracic Cancer  2014;5(1):31-37.
Background
This study was designed to detect the protein expression of epidermal growth factor receptor (EGFR) among serum, lymph node, and tumor tissues, and to discuss their relationship and clinical significance. We investigated whether EGFR levels in serum and lymph nodes could be used as an effective method for non-small cell lung cancer (NSCLC) to diagnose and assess clinical stage.
Methods
In 56 patients with NSCLC and 10 individuals with nonmalignant thoracic disease, we measured EGFR levels in serum using an enzyme immunoassay, and EGFR mRNA levels in lymph node and NSCLC tissues by quantitative real-time-polymerase chain reaction. We examined the correlation between them and with the clinical parameters.
Results
Serum EGFR levels substantially decreased after surgical treatment (P < 0.001). Serum EGFR levels were correlated with smoking, surgery, and pathological type after surgery (all P < 0.05). EGFR mRNA levels in lymph node and tumor tissues were correlated more closely with lymph node metastasis (P = 0.015. EGFR mRNA in tissues was higher than that of benign pulmonary diseases (P = 0.020). There was an obvious positive correlation among EGFR levels of serum and lymph node tissues (r = 0.764; P < 0.001), serum and tumor tissues (r = 0.616; P < 0.001), and lymph node and tumor tissues (r = 0.904; P < 0.001) in NSCLCs.
Conclusion
The data suggest that detecting EGFR levels in serum and lymph node tissues could be a simple and effective method to diagnose and assess the clinical stage in patients with NSCLC.
doi:10.1111/1759-7714.12048
PMCID: PMC4704271  PMID: 26766969
EGFR; enzyme-linked immunosorbent assay; lung neoplasms; polymerase chain reaction
3.  Interplay between the Westerlies and Asian monsoon recorded in Lake Qinghai sediments since 32 ka 
Scientific Reports  2012;2:619.
Two atmospheric circulation systems, the mid-latitude Westerlies and the Asian summer monsoon (ASM), play key roles in northern-hemisphere climatic changes. However, the variability of the Westerlies in Asia and their relationship to the ASM remain unclear. Here, we present the longest and highest-resolution drill core from Lake Qinghai on the northeastern Tibetan Plateau (TP), which uniquely records the variability of both the Westerlies and the ASM since 32 ka, reflecting the interplay of these two systems. These records document the anti-phase relationship of the Westerlies and the ASM for both glacial-interglacial and glacial millennial timescales. During the last glaciation, the influence of the Westerlies dominated; prominent dust-rich intervals, correlated with Heinrich events, reflect intensified Westerlies linked to northern high-latitude climate. During the Holocene, the dominant ASM circulation, punctuated by weak events, indicates linkages of the ASM to orbital forcing, North Atlantic abrupt events, and perhaps solar activity changes.
doi:10.1038/srep00619
PMCID: PMC3431539  PMID: 22943005
4.  LKB1 is Necessary for Akt-mediated Phosphorylation of Pro-apoptotic Proteins 
Cancer research  2008;68(18):7270-7277.
LKB1 plays the role of tumor suppressor, opposite to Akt, by negatively regulating mTOR through the activation of AMPK and TSC signaling. We have discovered a novel, potentially oncogenic role for LKB1, as a supporter of Akt-mediated phosphorylation of pro-apoptotic proteins. We found that Akt activation led to increased phosphorylation of FoxO3a at threonine 32 (Thr32) in LKB1 wild-type cells, but not in LKB1-null cells. Depletion of LKB1 in the cells with wild-type LKB1 resulted in attenuation of that phosphorylation of FoxO3a by activated Akt, while the restoration of LKB1 function in LKB1-null cells re-established Akt-mediated FoxO3a phosphorylation. Upon expanding our analysis to other Akt targets, using isogenic LKB1 knockdown cell line pairs and a phospho-specific antibody microarray, we observed that there was a requirement for LKB1 in the phosphorylation of other Akt down-stream targets, including Ask1 (Ser83), Bad (Ser136), FoxO1 (Ser319), FoxO4 (Ser197) and GSK3β (Ser9). Because the phosphorylation of these sites by Akt suppresses apoptosis, the requirement of LKB1 suggests that LKB1 may have an anti-apoptotic role in tumor cells with constitutively active Akt. Indeed, we found the suppression of LKB1 expression led to apoptosis in three cell lines in which Akt is constitutively active, but not in two cell lines without Akt activation. This observation may explain the lack of LKB1 somatic mutations in brain, breast and colon cancers, where Akt is frequently activated due to mutations in PI3K, PTEN or Akt itself.
doi:10.1158/0008-5472.CAN-08-1484
PMCID: PMC2596073  PMID: 18794113
LKB1; PI3K/Akt signaling; tumor suppressor; apoptosis
5.  Sox7 is an independent checkpoint for β-catenin function in prostate and colon epithelial cells 
Molecular cancer research : MCR  2008;6(9):1421-1430.
The presence of somatic β-catenin mutations in some prostate cancers implies that aberrant WNT signaling is involved in the cancer’s development. Although β-catenin stability is regulated by a multi-component destruction complex, mutational alterations of β-catenin or other components of the destruction complexes are rare in prostate tumors. Therefore, β-catenin may be regulated by another protein in the prostate. In fact, recent linkage and somatic deletion analyses in prostate cancers reveal a 1.4 Mb candidate tumor suppressor locus on 8p23.1, which includes the Sox7 gene. Here we show that Sox7 protein expression was indeed down-regulated in 47% (15/32) of prostate adenocarcinomas. Also, Sox7 mRNA was down-regulated in 60% of snap-frozen tumors. This down-regulation was found to be due to tumor-specific promoter hypermethylation, which was present in 48% (10/21) of primary prostate tumors and 44% (11/25) of prostate cancer cell lines/xenografts. We discovered that Sox7 protein physically interacts with β-catenin and suppresses β-catenin-mediated transcription by depleting active β-catenin. Furthermore, in HCT116 colorectal cancer cell lines with Sox7 inactivation, ectopic Sox7 expression suppressed cell proliferation and inhibited transcription that was activated by an endogenous mutant β-catenin. Even though nearly all colorectal cancers contain mutations in β-catenin or APC/Axin, epigenetic silencing of Sox7 was still observed. These data suggest that Sox7 is a tumor suppressor that functions as an independent checkpoint for β-catenin transcriptional activity. Inactivation of Sox7 could promote the development of a majority of colorectal tumors and approximately half of prostate tumors.
doi:10.1158/1541-7786.MCR-07-2175
PMCID: PMC2652859  PMID: 18819930
WNT signaling; promoter methylation; tumor suppressor; chromosome 8p; Sox7; prostate cancer; colorectal cancer; β-catenin

Results 1-5 (5)