Lung microbiome mediates the progression from chronic obstructive pulmonary disease to lung cancer through inflammation.

Lung microbiome exists in the respiratory tract and parenchymal tissues. It mediates lung injury through a variety of mechanisms, including bacterial disturbance, metabolites, inflammatory response, immune response, and genotoxicity. Accumulating evidences suggest that changes in lung microbiome correlates with chronic obstructive pulmonary disease (COPD) and lung cancer, and the microbiome promotes the progression from COPD to lung cancer. In this review, we mainly introduce the impairment of the homeostasis of the lung microbiome and its inflammation that leads to COPD and lung cancer, then focus on how the microbiome mediates the progression from COPD to lung cancer through inflammatory response. The review may provide a new theoretical basis for clinical prevention, optimal treatment strategy and design of new drugs for COPD and lung cancer.

Oral exposure of low-dose bisphenol A promotes proliferation of dorsolateral prostate and induces epithelial-mesenchymal transition in aged rats.

Bisphenol A (BPA) is a well-known endocrine disruptor compound reported to have prostate toxicity. This study aimed to assess the effect of BPA on the proliferation of dorsolateral prostate (DLP) and the expression of epithelial-mesenchymal transition (EMT)-related genes in aged rats. Male aged SD rats were treated with BPA (10.0, 30.0, and 90.0 µg/kg i.g., daily) or vehicle (i.g., daily) for 3 months. Treatment with BPA resulted in increased the expression of PCNA, DLP weight and DLP epithelial height compared with the control group (P < 0.01); such effects were more obvious at higher BPA doses. 90 µg/kg BPA significantly increased the estrogen to androgen ratio (P < 0.05). The EMT chip showed the BPA induced upregulation of vimentin, Snail, Twist1, and transforming growth factor beta 1, as well as the downregulation of E-cadherin in the DLP. Immunohistochemical data showed that the expression of vimentin, estrogen receptor subtypes, and androgen receptor increased and the expression of E-cadherin decreased in 30 and 90 µg/kg BPA groups. It was concluded that environmental exposure to low doses of BPA might promote the proliferation of DLP in aged rats by increasing the estrogen to androgen ratio and inducing EMT.

[Gene regulation of prostaglandin synthase and prostate diseases].

Prostaglandin synthase (PGS) can catalyze the production of various types of prostaglandins and regulate the expression levels of related substances. The regulation mechanisms of the PGS gene are closely related with the occurrence and development of prostate diseases. However, few studies are reported on the regulation mechanisms of PGS in prostatic diseases, such as benign prostatic hyperplasia (BPH) and prostate cancer (PCa), or on the relationship between PGS gene regulation and prostate diseases. This review aims to analyze their correlation and provide some ideas for the prevention and control of BPH and PCa by intervention of the prostaglandin synthase regulatory pathway.

[Surgical resection versus radiofrequency ablation for primary hepatocellular carcinoma of 3-5 cm in diameter: a meta-analysis].

OBJECTIVE: To compare the therapeutic effects of surgical hepatic resection (HR) and radiofrequency ablation (RFA) in treatment of primary hepatocellular carcinoma of 3-5 cm in diameter. METHODS: The databases PubMed, CBMdisc, CNKI, WanFang Data and VIP databases were searched for controlled clinical trials on evaluating the efficacy between RFA and HR in treatment of primary hepatocellular carcinoma of 3-5 cm in diameter published from January 1990 to February 2014. Two reviewers independently screened the literature, extracted the data and assessed the methodological quality of the studies included. Then the meta-analysis was performed by using RevMan5.0 software. RESULTS: Eleven controlled clinical trials were included, including one randomized controlled trial and 10 non-randomized controlled trials. A total of 811 patients were involved: 404 patients were treated with RFA as the initial treatment and 407 patients with surgical resection. Meta-analysis showed that for a single lesion with diameter of 3-5 cm of primary hepatocellular carcinoma, the 3-， 5-year disease-free survival rates in HR group was significantly higher than those in RFA group (all P<0.05). There were no significant difference in the 1-， 3-， 5-year overall survival rates and 1-year disease-free survival rate between RFA group and HR group (P>0.05). For 1-2 nodules with diameters of 3-5 cm of primary hepatocellular carcinoma, the 3-， 5-year disease-free survival rates and 5-year overall survival rates in HR group was significantly higher than those in RFA group (all P<0.05). No significant difference in 1-， 3-year overall survival rates and 1-year disease-free survival rate was found between RFA group and HR group (P>0.05). For maximum nodule of 3-5 cm of multiple primary hepatocellular carcinoma, the 5-year overall survival rates in HR group was significantly higher than that in RFA group (all P<0.05). No significant difference in 1-， 5-year overall survival rates was noted between RFA group and HR group (P>0.05). CONCLUSION: For primary hepatocellular carcinoma of 3-5 cm in diameter, HR is better than RFA. For the limitation of quality and quantity of included studies, this conclusion needs to be confirmed by more high quality studies.

Down-regulation of ALKBH2 increases cisplatin sensitivity in H1299 lung cancer cells.

AIM: To elucidate the combined effect of alkylated DNA repair protein alkB homolog 2 (ALKBH2)-targeting gene therapy and cisplatin (cDDP) chemotherapy on the non-small cell lung cancer (NSCLC) H1299 cell line. METHODS: ALKBH2 was down-regulated in H1299 cells by lentivirus-mediated RNA interference (RNAi). Changes in ALKBH2 expression were determined using real-time RT-PCR and Western blotting. Cell viability was evaluated using MTT assay. DNA synthesis in proliferating cells was determined using BrdU incorporation assay. Cell apoptosis was determined using flow cytometry. RESULTS: Lentivirus-mediated ALKBH2 silencing alone did not induce apoptosis or attenuate the growth potential of H1299 cells within five days post-infection. Combined treatment modalities with lentivirus-mediated ALKBH2 down-regulation and cDDP (333 µmol/L) were significantly more potent in inhibiting cell growth and inducing apoptosis than mono-chemotherapy. CONCLUSION: Combined treatment modalities of ALKBH2 knockdown and cDDP chemotherapy have the potential to improve the efficacy in the treatment of NSCLC.