Epidemiology of Lung Cancer : Diagnosis and Management of Lung Cancer, 3rd ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines

Every year more than 13 million deaths worldwide are due to environmental pollutants, and approximately 24% of diseases are caused by environmental exposures that might be averted through preventive measures. Rapidly growing evidence has linked environmental pollutants with epigenetic variations, including changes in DNA methylation, histone modifications and microRNAs.

Environ mental chemicals and epigenetic changes All of these mechanisms are likely to play important roles in disease aetiology, and their modifications due to environmental pollutants might provide further understanding of disease aetiology, as well as biomarkers reflecting exposures to environmental pollutants and/or predicting the risk of future disease. We summarize the findings on epigenetic alterations related to environmental chemical exposures, and propose mechanisms of action by means of which the exposures may cause such epigenetic changes. We discuss opportunities, challenges and future directions for future epidemiology research in environmental epigenomics. Future investigations are needed to solve methodological and practical challenges, including uncertainties about stability over time of epigenomic changes induced by the environment, tissue specificity of epigenetic alterations, validation of laboratory methods, and adaptation of bioinformatic and biostatistical methods to high-throughput epigenomics. In addition, there are numerous reports of epigenetic modifications arising following exposure to environmental toxicants, but most have not been directly linked to disease endpoints. To complete our discussion, we also briefly summarize the diseases that have been linked to environmental chemicals-related epigenetic changes.

https://www.mtpinnacle.com/pdfs/Environmental-chemical-exposures-and-human-epigenetics.pdf

Environmental chemical exposures and human epigenetics

Circular (circ)RNAs, a newly recognized class of noncoding RNA, have been implicated in the occurrence and development of several diseases, including neurological and cardiovascular diseases. Studies of human tumors, including those of liver cancer, gastric cancer, lung cancer and colorectal cancer, have shown differential expression profiles of circRNAs, suggesting regulatory roles in cancer pathogenesis and metastasis. In this review, we discuss the most recent research into tumor-related circRNAs, providing a comprehensive summary of the expression or/and function of these circRNAs and proposing rational perspectives on the potential clinical application of circRNAs as helpful biomarkers or therapeutic targets in human tumors.

/pdf/circular-rna-a-novel-biomarker-and-therapeutic-target-for-1on6ln13z9.pdf

Circular RNA: a novel biomarker and therapeutic target for human cancers.

Although CircRNA_100269 is a biomarker used to predict cancer recurrence, its expression and function in gastric cancer (GC) remain unknown. In this study, the expression of circRNA_100269 and its potential downstream miRNA targets were investigated. The molecular function and regulatory mechanism of circRNA_100269 in GC cell lines were also elucidated. The expression levels of circRNA_100269 and its linear isomer LPHN2 mRNA were found to be downregulated (p<0.01) in GC tissues. The target miRNA was predicted to be miR-630, whose expression was upregulated (p<0.01) and found to be negatively correlated with that of circRNA_100269 (r = -0.688) in GC tissues. Moreover, direct interaction of circRNA_100269 and miR-630 was confirmed through dual-luciferase assays. Overexpressing the circRNA_100269 plasmid inhibited cell proliferation (p<0.05). Furthermore, transfection of miR-630 mimics into cell lines overexpressing circRNA_100269 blocked the function of circRNA_100269 (p<0.05). Thus, circRNA_100269 level was downregulated in GC and correlated negatively with that of miR-630. Taken together, our results suggest that circRNA_100269 and miR-630 comprise a novel pathway that regulates proliferation of GC cells.

/pdf/circrna-100269-is-downregulated-in-gastric-cancer-and-34cmrilxx8.pdf

CircRNA_100269 is downregulated in gastric cancer and suppresses tumor cell growth by targeting miR-630.

Lung cancer epigenetics: From knowledge to applications.

Methylation of multiple genes as a candidate biomarker in non-small cell lung cancer.

Esophageal squamous cell carcinoma (ESCC) is the most common histological type in China. MicroRNAs are endogenously expressed in mammals and play a significant role in tumor invasion and metastasis by targeting potential downstream genes. In the present study, microarray analysis showed that miR-375 expression was distinctly downregulated in ESCC compared with that in normal esophageal epithelium tissues. Then, luciferase reporter assay showed that SHOX2 was the direct downstream target of miR-375 and this interaction was confirmed by the rescue experiments. Quantitative polymerase chain reaction results also showed that SHOX2 expression was upregulated in ESCC cells and tissues. Further analysis showed that SHOX2 induced proliferation, invasion, and metastasis of ESCC both in vivo and in vitro. Moreover, the interaction between miR-375 and SHOX2 affected the epithelial-to-mesenchymal transition. We conclude that miR-375 may suppress invasion and metastasis of ESCC by directly targeting SHOX2. The miR-375/SHOX2 axis may be a novel therapeutic target for ESCC.

/pdf/mir-375-suppresses-invasion-and-metastasis-by-direct-bsu9g7j4mb.pdf

MiR-375 suppresses invasion and metastasis by direct targeting of SHOX2 in esophageal squamous cell carcinoma.

Background and objective DNA methylation is one of the mechanisms of epigenetics. Allelic loss located on chromosome 3p happen frequently and early in non-small cell lung cancer (NSCLC). The aim of this study is to detect the promoter methylation status of tumor suppressor genes (TSGs) located on chromosome 3p in NSCLC and to evaluate its correlation with clinicopathological features. Methods A total of 78 paired NSCLC specimens and their adjacent normal tissues were collected in the study. Promoter methylation status was determined by methylation-specific polymerase chain reaction (MSP). DLEC1 gene expression was determined by RT-PCR and immunohistochemistry. Results Aberrant methylation frequency of DLEC1, RASSF1A, hMLH1, RARβ and FHIT genes detected in 78 NSCLC tissues were 41.03%, 39.74%, 30.77% and 16.67%, respectively, which were all significantly higher than that in adjacent normal tissues. However, FHIT gene was not detected methylation in both cancerous and non-cancerous tissues. DLEC1 hypermethylation was associated with advanced stage (P=0.011) and lymph metastasis (P=0.019), while RASSF1A, RARβ, hMLH1 and mean methylation index (MI) were not correlated with any clinicopathological parameters. Moreover, DLEC1 gene downregulation was detected in 56.41% (44/78) NSCLC tissues and correlated with promoter hypermethylation. Conclusion Frequent hypermethylation of TSGs located on chromosome 3p was a common event contributing to NSCLC pathogenesis and DLEC1 methylation was closely correlated with loss of expression.

DOI: 10.3779/j.issn.1009-3419.2011.03.09

[DNA methylation of tumor suppressor genes located on chromosome 3p in non-small cell lung cancer].

Overexpression of epidermal growth factor receptor (EGFR) is common in non-small-cell lung cancer (NSCLC) and has been recently shown to contribute to cancer chemoresistance. It has been reported that the EGFR antibodies such as cetuximab in combination with chemotherapy could lead to an absolute benefit of overall survival (OS) compared with chemotherapy alone. In this study, we investigated the effects of nimotuzumab (h-R3), a humanized anti-EGFR antibody, in combination with docetaxel (DTX), on DTX-resistant human lung adenocarcinoma cell line SPC-A1 (SPC-A1/DTX) both in vitro and in vivo. Immunohistochemistry and FCM assays demonstrated that SPC-A1/DTX cells had a relatively higher rate of EGFR overexpression than SPC-A1 cells. Accordingly, SPC-A1/DTX cells were approximately 13.7 times resistant to DTX than SPC-A1 cells. The combined therapy of h-R3 and DTX showed strong synergistic suppressive effect on cell proliferation of SPC-A1/DTX cells in vitro. The synergistic antitumor effect was also observed in SPC-A1/DTX xenograft-bearing nude mice. Further study showed that h-R3 could lead to a significant cell arrest at G1 phase of cell cycle in both SPC-A1DTX and SPC-A1 cells. A dramatic increase of apoptosis rate was detected in h-R3-treated SPC-A1/DTX but not SPC-A1 cells. Moreover, when combined with DTX, h-R3 brought higher apoptosis rate in SPC-A1/DTX cells rather than in SPC-A1 cells. In conclusion, our results suggested that h-R3 could significantly enhance chemosensitivity of human lung adenocarcinoma cells to DTX, at least partially by induction of G1 phase arrest and cell apoptosis.

Nimotuzumab increases chemosensitivity of human lung adenocarcinoma cell lines to docetaxel.

Frequent Epigenetic Inactivation of Deleted in Lung and Esophageal Cancer 1 Gene by Promoter Methylation in Non–Small-Cell Lung Cancer

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