Overexpression of LINC00852 promotes prostate cancer cell proliferation and metastasis.

AIM: Long noncoding RNAs play a key role in the development and progression of various human cancers. Recently, LINC00852 has been reported to be associated with spinal metastasis lung adenocarcinoma. However, the role and potential mechanisms of LINC00852 in prostate cancer cells remain largely unknown. METHODS: LINC00852 expression in prostate cancer cells was examined by quantitative real-time polymerase chain reaction. Western blotting was used to detect protein expressions in prostate cancer cells. Cell cycle was analyzed by flow cytometric analysis. Cell proliferation was measured by cck-8 assay. The migration and invasion capabilities were determined using transwell assays. RESULTS: In this study, we found that LINC00852 was highly expressed in prostate cancer tissues based on the TCGA database. Overexpression of LINC00852 mediated by lentivirus significantly reinforced the proliferation and colony formation abilities of prostate cancer cell linePC3. The migration and invasion capabilities were also augmented by overexpression of LINC00852. Flow cytometric analysis revealed that LINC00852 overexpression resulted in a decrease of cells in G0/G1 phase. Moreover, overexpression of LINC00852 affected the expression of epithelial-mesenchymal transition-related proteins. CONCLUSIONS: Our data collectively demonstrate that LINC00852 contributes to prostate cancer proliferation and metastasis, indicating that LINC00852is a new promising diagnostic and therapeutic target for treatment of prostate cancer.

Efficacy and safety of radiofrequency ablation for lung cancers: A systematic review and meta-analysis.

OBJECTIVE: To evaluate the efficacy and safety of radiofrequency ablation(RFA) for patients with lung cancers using meta-analysis. METHODS AND MATERIALS: A literature search (PubMed, Embase, Web of science and China National Knowledge Infrastructure) was undertaken until August 2017 to identify sufficient studies evaluating the efficacy and safety of RFA. Pooled proportions of estimates were calculated by performing the random effect model, including technical success rate, recurrence rate, local tumor progression rate and complications. RESULTS: A total of 25 eligible studies were collected, giving a sample size of 1989 patients with 3025 lung tumors. In the present series, the pooled technical success rate was 96%(95%CIs: 93%-100%). Further, we observed pooled recurrence rate of 35%(95%CIs: 12%-59%) following RFA. Additionally, the pooled rate of local tumor progression was 26%(95%CIs: 20%-32%). One hundred and ninety major complications of RFA were reported in 20 studies, giving a pooled proportion of 6% (95%CIs: 3%-8%) for major RFA complications. Pooled rate of minor complications was 27% (95%CIs:14%-41%). CONCLUSION: In this meta-analysis, RFA was found to be a safe and efficient treatment for the patients with lung cancers. The efficacy and safety of RFA for lung cancer deserve future investigation in further well-designed randomized controlled trials.

Identification of genome variations in patients with lung adenocarcinoma using whole genome re­sequencing.

Lung adenocarcinoma is one of the types of non­small cell lung carcinoma, which tends to be treated with surgical therapy rather than radiation therapy. It occurs in smokers and non­smokers, and is the most common form of lung cancer among non­smokers and women. Gene rearrangements, including ALK, ROS1 and RET, and gene mutations, including epidermal growth factor receptor (EGFR), HER2, Kristen rat sarcoma viral oncogene homolog, BRAF, phosphoinositide­3­kinase, catalytic, α polypeptide and MET, have been identified in lung adenocarcinoma, which enable targeted therapy in lung adenocarcinoma, for example erlotinib, gefitinib and afatinib, which are EGFR inhibitors. The aim of the present study was to further investigate genome variations in lung adenocarcinoma. Single nucleotide polymorphisms (SNPs), insertions and deletions (InDels), structural variations (SVs) and copy number variations (CNVs) were identified in the whole genome from four patients with adenocarcinoma using a whole genome re­sequencing method performed on the Illumina HiSeq Xten platform. In total, ~415 GB of clean reads were obtained, the average sequencing depth was 31.10­fold, and 99.29% of the reference genome was covered by the clean reads. An average of 3,364,270 SNPs was identified, 98.76% of which were matched to the SNP database (dbSNP), and an average of 453,547 InDels were identified, 28.28% of which were in the dbSNP. The present study also identified a total of 13,050 SVs and 886 CNVs. The majority of the SVs were deletions (74.25%) and the major CNVs were in intergenic regions and coding sequence regions. In conclusion, the results of the present study generated an output of the genome alterations in lung adenocarcinoma, and provided a foundation for further investigation of the pathogenesis of lung adenocarcinoma.

The association of SIPA1 gene polymorphisms with breast cancer risk: evidence from published studies.

Previous studies have focused on the association of signal-induced proliferation associated 1 gene (SIPA1) with carcinogenesis of many cancers, including breast cancer. It has been suggested that SIPA1 polymorphisms are associated with susceptibility to breast cancer. In the present study, we performed a meta-analysis to systematically summarize the possible association between SIPA1 and the risk for breast cancer. We conducted a search of case-control studies on the associations of SPIA1 with susceptibility to breast cancer in PubMed, Embase, International Statistical Institute Web of Science, Wanfang Database in China, and Chinese National Knowledge Infrastructure databases. Data from eligible studies were extracted for meta-analysis. Breast cancer risk associated with SIPA1 was estimated by pooled odds ratios and 95% confidence intervals. Four studies on SIPA1 and breast cancer were included in our meta-analysis. Our results showed that rs746429 was associated with the risk of breast cancer. However, rs931127 and rs3741378 were not found to be associated with breast cancer in our analysis. This meta-analysis suggests that rs746429 is associated with the risk of breast cancer. Well-designed studies with larger sample size and more ethnic groups are required to further validate the results.

Identification of mutant genes with high-frequency, high-risk, and high-expression in lung adenocarcinoma.

BACKGROUND: To identify mutant genes with high-frequency-risk-expression between lung adenocarcinoma and normal samples. METHODS: The ribonucleic acid RNA-Seq data GSE34914 and GSE37765 were downloaded from the Gene Expression Omnibus database, including 12 lung adenocarcinoma samples and six controls. All RNA-Seq reads were processed and the gene-expression level was calculated. Single nucleotide variation (SNV) was analyzed and the locations of mutant sites were recorded. In addition, the frequency and risk-level of mutant genes were calculated. Gene Ontology (GO) functional analysis was performed. The reported cancer genes were searched in tumor suppressor genes, Cancer Genes, and the Catalogue of Somatic Mutations in Cancer (COSMIC) database. RESULTS: The SNV annotations of somatic mutation sites showed that 70% of mutation sites in the exon region occurred in the coding sequence (CDS). Thyroid hormone receptor interactor (TRIP)12 was identified with the highest frequency. A total of 118 mutant genes with high frequency and high-risk were selected and significantly enriched into several GO terms. No base mutation of cyclin C (CCNC) or RAB11A was recorded. At fragments per kilobase per million reads (FPKM) ≥ 56.5, reported tumor suppressor genes catenin (cadherin-associated protein), delta (CTNND)1, dual specificity phosphatase (DUSP)6, malate dehydrogenase (MDH)1 and RNA binding motif protein (RBM)5, were identified. Notably, signal transducer and activator of transcription 2 (STAT2) was the only transcription factor (TF) with high-risk mutation and its expression was detected. CONCLUSION: For the mutant genes with high-frequency-risk-expression, CTNND1, DUSP6, MDH1 and RBM5 were identified. TRIP12 might be a potential cancer-related gene, and expression of TF STAT2 with high-risk was detected. These mutant gene candidates might promote the development of lung adenocarcinoma and provide new diagnostic potential targets for treatment.

Null genotype of GSTT1 contributes to esophageal cancer risk in Asian populations: evidence from a meta-analysis.

BACKGROUND/AIMS: Glutathione S-transferase T1 (GSTT1), a phase-II enzyme, plays an important role in detoxification of carcinogen electrophiles. Many studies have investigated the association between GSTT1 polymorphism and esophageal cancer risk in Asian populations, but its actual impact is not clear owing to apparent inconsistencies among those studies. Thus, a meta-analysis was performed to explore the effect of GSTT1 polymorphism on the risk of developing esophageal cancer. METHODS: A literature search of PubMed, Embase, and Wanfang databases up to August 2012 was conducted and 15 eligible papers were finally selected, involving a total of 1,626 esophageal cancer cases and 2,216 controls. We used the pooled odds ratio (OR) with its corresponding 95% confidence interval (95%CI) to estimate the association of GSTT1 polymorphism with esophageal cancer risk. Subgroup analyses and sensitivity analyses were performed to further identify the association. RESULTS: Meta-analysis of total studies showed the null genotype of GSTT1 was significantly associated with an increased risk of esophageal cancer in Asians (OR=1.26, 95%CI=1.05-1.52, POR=0.015, I2=42.7%). Subgroup analyses by sample size and countries also identified a significant association. Sensitivity analysis further demonstrated a relationship of GSTT1 polymorphism to esophageal cancer risk in Asians. CONCLUSIONS: The present meta-analysis of available data showed a significant association between the null genotype of GSTT1 and an increased risk of esophageal cancer in Asians, particularly in China.