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Colorectal cancer (CRC) is generally regarded as the third frequent malignancy worldwide, while current diagnosis and treatment of the disease are limited. The previous studies of CRC revealed that epigenetic modification plays a crucial role in the progression of CRC. Epigenetic modification is identified as heritable changes in gene functions that occur without changing the DNA sequence, resulting in cells with similar DNA eventually developing into different types with different functions, which encompasses DNA/RNA methylation, histone modification, and non-coding RNA regulation. Circular RNA (circRNA), a kind of non-coding RNA that forms a covalently closed loop, is widely present in various cells which drive initiation and progression of cancers through multiple pathways. The emerging data show that epigenetic modification may affect the biological functions of circRNA, while circRNA can also participate in the progression of CRC by targeting molecules related to epigenetic modification. N6-methyladenosine (m6A) has been found to directly promote production, translation, and functions of circRNA on the one hand, and interact with circRNA on the other hand, thereby altering onset, progression, and metastasis of the disease. DNA methylation and histone modification have also been observed to have potential interaction with circRNA. This review provides a brief overview about the association between current epigenetic modifications and circRNA, and the significant role they may play in the progression of CRC, and also outlines the potential applications to diagnosis and treatment, and the research direction in the future.

Chronic obstructive pulmonary disease (COPD) induces serious social and economic burdens due to its high disability and mortality, the pathogenesis of which is highly involved with inflammation, oxidative stress (OS), and mechanism of mucin 5AC (MUC5AC) secretion. Lixisenatide is a selective glucagon‐like peptide 1 receptor agonist recently reported to have anti‐inflammatory properties. Our study will focus on the potential impact of lixisenatide on lipopolysaccharide (LPS)‐induced mucin secretion and inflammation in 16 human bronchial epithelial (16HBE) cells to check its potential function in COPD. 16HBE cells were treated with LPS, with or without lixisenatide (10 and 20 nM) for 1 day. Remarkably declined cell viability, enhanced lactate dehydrogenase release, activated OS, and elevated release of inflammatory cytokines were observed in LPS‐treated 16HBE cells, accompanied by the activation of nuclear factor‐κB signaling, all of which were signally reversed by lixisenatide. Moreover, elevated expression and release of MUC5AC were observed in LPS‐treated 16HBE cells but were markedly repressed by lixisenatide. Furthermore, the repressed nuclear factor erythroid 2‐related factor 2 (Nrf2) level in LPS‐treated 16HBE cells was notably rescued by lixisenatide. Lastly, following the knockdown of Nrf2, the protective function of lixisenatide on LPS‐triggered MUC5AC release in 16HBE cells was significantly abrogated. Collectively, lixisenatide ameliorated LPS‐induced expression of mucin and inflammation in bronchial epithelial cells by regulating Nrf2. [ABSTRACT FROM AUTHOR]

Addressing the hot issue of calculation of the oil casing external collapse-resistance, 10 pieces of the 0114.3 mmx8.56 mm MOV casing are selected and subjected to both geometric dimension measurement and mechanical property tests. And the pipes are also subjected to the collapse test to determine their collapse resistance. Meanwhile based on the consideration of the geometric defects and the actual mechanical properties of the pipes, a FEA model for calculating the collapse strength of the casing is set up. After comparing the results of the simulation, the theoretic calculation and the tests, it is demonstrates that the result of the simulation is close to that of the tests, showing a deviation of -0.77% -+7.0%, whereas the theoretic calculation result shows an obvious error, i.e. a deviation of 23.84%-37.56%. Thanks to the above mentioned model, the influence by the wall thickness unevenness and the ovality on the collapse re- sistance of the said oil casing is analyzed. [ABSTRACT FROM AUTHOR]

Xeroderma pigmentosum group C (XPC) is a DNA-damage-recognition gene active at the early stage of DNA repair. XPC also participates in regulation of cell-cycle checkpoint and DNA-damage-induced apoptosis. In the present study, the expression levels of genes involved in nucleotide excision repair (NER) were assessed in human colorectal cancer (CRC) tissue. This analysis revealed that expression of XPC mRNA significantly increased in colorectal carcinoma tissues compared with matched normal controls. Expression of XPC gradually increased along with the degree of progression of CRC. In vitro, an XTT assay demonstrated that small interfering RNA (siRNA) targeting XPC significantly increased the sensitivity of CRC SW480 cells to cisplatin, whereas cells transfected with a XPC-overexpression plasmid became more resistant to cisplatin. Furthermore, flow cytometry revealed that the proportion of apoptotic cells significantly increased in XPC-knockdown cells upon cisplatin treatment. However, the overexpression XPC significantly increased the resistance of cells to cisplatin. In vivo, tumor growth was significantly reduced in tumor-bearing mice when the XPC gene was knocked down. Upregulation of the expression of pro-apoptotic Bcl-associated X and downregulation of the anti-apoptotic B-cell lymphoma 2 proteins was observed in the implanted tumor tissue. In conclusion, XPC serves a key role in chemotherapeutic sensitivity of CRC to cisplatin, meaning that it may be a potential target for chemotherapy of CRC. [ABSTRACT FROM AUTHOR]