44 research outputs found

    The supplemental files of 'DNA Methylation Data-based prognosis-subtype distinctions in Patients with Esophageal carcinoma'

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    Our upload is the suplemental files which have been cited in the manuscript 'DNA Methylation Data-based prognosis-subtype distinctions in Patients with Esophageal carcinoma'</p

    MiR-130b-3p promotes colorectal cancer progression by targeting CHD9

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    Colorectal cancer (CRC) is the third most common cancer worldwide. Previous research revealed that microRNA 130b-3p (miR-130b-3p) significantly upregulated in CRC patients can be detected in feces from patients with such a neoplasm. In this study, the biological role and molecular mechanism of miR-130b-3p in CRC were explored. The miR-130b-3p level in CRC tissues, feces and cell lines was measured using RT-qPCR analysis. CCK-8, EdU, TUNEL, flow cytometry, Western blotting, and in vivo experiments were performed to explore the biological function of miR-130b-3p in CRC progression. For this purpose, 16 BALB/c nude mice were assigned to two groups. The experiment lasted for four months. Bioinformatics analysis and luciferase reporter assay were used to investigate the regulatory mechanism related to miR-130b-3p. In our research, miR-130b-3p was upregulated in CRC tissues and cells and it was detected in feces from CRC patients. Moreover, miR-130b-3p inhibition suppressed CRC cell proliferation and promoted cell apoptosis in vitro as well as repressed CRC tumor growth in vivo. Mechanistically, miR-130b-3p directly targeted the 3′untranslated region (UTR) of chromodomain helicase DNA binding protein 9 (CHD9) and negatively regulated CHD9 expression. Furthermore, CHD9 played an anti-oncogenic role in CRC. Inhibition of CHD9 expression was likely to be a key mechanism by which miR-130b-3p increased CRC cell growth, with a target protector experiment revealing miR-130b-3p influenced proliferation via direct inhibition of CHD9. MiR-130b-3p promotes the progression and tumorigenesis of CRC at least partially by targeting CHD9. Abbreviations: CRC: Colorectal cancer; miR-130b-3p: microRNA 130b-3p; CHD9: chromodomain helicase DNA binding protein 9; UTR: untranslated region; FIT: fecal immunochemical test; AAs: advanced adenomas</p

    Table_1_Chemoradiotherapy Is Superior to Radiotherapy Alone in Esophageal Cancer Patients Older Than 65 Years: A Propensity Score-Matched Analysis of the SEER Database.xls

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    IntroductionRadiotherapy (RT) is the main treatment for unoperated esophageal cancer (EC) patients. It is controversial whether adding chemotherapy (CT) to RT is beneficial for elderly EC patients. The purpose of our study was to compare the efficacy of chemoradiotherapy (CRT) with RT alone for non-surgical elderly esophageal cancer patients.MethodsA total of 7,101 eligible EC patients older than 65 years diagnosed between 2000 and 2018 were collected from the Surveillance, Epidemiology, and End Results (SEER) database. All the samples were divided into the radiotherapy group and the chemoradiotherapy group. After being matched by propensity score matching (PSM) at a 1:1 ratio, 3,020 patients were included in our analysis. The Kaplan–Meier method and log-rank test were applied to compare overall survival (OS) and cancer-specific survival (CSS).ResultsAfter PSM, the clinical characteristics of patients between the RT and CRT groups were comparable. For EC patients older than 65 years, the 3-year OS and CSS in the CRT group were 21.8% and 27.4%, and the 5-year OS and CSS in the CRT group were 12.7% and 19.8%, respectively. The 3-year OS and CSS in the RT group were 6.4% and 10.4%, and the 5-year OS and CSS in the RT group were 3.5% and 7.2%, respectively. Next, these patients were divided into five subgroups based on the age stratification (ages 65–69; 70–74; 75–79; 80–84; ≥85). In each subgroup analysis, the 3- and 5-year OS and CSS showed significant benefits in the CRT group rather than in the RT group (all p ConclusionsCRT could improve OS and CSS for non-surgical EC patients older than 65 years. Adding chemotherapy to radiation showed a significant prognostic advantage for elderly esophageal cancer patients.</p

    <i>PARP-1 Val762Ala</i> Polymorphism and Risk of Cancer: A Meta-Analysis Based on 39 Case-Control Studies

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    <div><p>Background</p><p>Poly(ADP-ribose) polymerase-1 (PARP-1) is a nuclear chromatin-associated enzyme involved in several important cellular processes, particularly in the DNA repair system. <i>PARP-1</i> rs1136410: C>T is among the most studied polymorphisms and likely involved in human carcinogenesis. However, results from previous studies are inconclusive. Thus, a meta-analysis was conducted to derive a more precise estimation of the effects of this enzyme.</p><p>Methodology and Principal Findings</p><p>A comprehensive search was conducted in the PubMed and EMBASE databases until December 9, 2013. A total of 39 studies with 16,783 cancer cases and 23,063 control subjects were included in the meta-analysis on the basis of the inclusion and exclusion criteria. No significant association between the <i>PARP-1 Val762Ala</i> polymorphism and cancer risk was found when all of the studies were pooled into the analysis (VA + AA vs. VV: OR = 1.03, 95% CI = 0.95–1.11). The subgroup analysis of cancer types revealed that the –762Ala allele was associated with increased risk of gastric, cervical, and lung cancers and a decreased risk of glioma. In addition, a significantly increased risk of cancer associated with the polymorphism was observed in Asian descendents (VA + AA vs. VV: OR = 1.17, 95% CI = 1.09–1.25; AA vs. VV: OR = 1.28, 95% CI = 1.08–1.51; VA vs. VV: OR = 1.12, 95% CI = 1.04–1.20; AA vs. VA + VV: OR = 1.09, 95% CI = 1.03–1.39). These results also indicated that a joint effect between <i>PARP-1 Val762Ala</i> and <i>XRCC1 Arg399Gln</i> could be involved in the risk of cancer development (OR = 3.53, 95% CI = 1.30–9.59).</p><p>Conclusion</p><p>The present meta-analysis provides evidence that the <i>PARP-1 Val762Ala</i> may be involved in cancer development at least in some ethnic groups (Asian) or some specific cancer types (gastric, cervical, and lung cancers, and glioma).</p></div

    Begger's funnel plot of publication bias for <i>PARP-1 Val762Ala</i> polymorphism with cancer risk under dominant model (VA+AA vs. VV).

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    <p>Each dot represents a separate study for the indicated association. Funnel plot of all 39 eligible studies <i>P</i> = 0.753, Egger's test <i>P</i> = 0.916.</p

    The staining index (SI) of miRNA-148a expressions in FFPE primary lung cancer tissues and their adjacent normal lung tissues.

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    <p>The expression of miRNA-148a in cancer tissues was significantly lower than that in adjacent normal tissues (<i>P</i><0.05) and the median SI of miRNA-148a expressions between the two groups are marked with a red line in the graph.</p

    Inhibition of Wnt1 suppresses migration and invasion of A549 and H1299 cells.

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    <p>(A) Three siRNA were designed and Wnt1 protein level was detected by western blot to select the effective siRNA for the target protein. siRNA#2 exhibited greatest inhibition of Wnt1 protein and was further validated in A549 cells. β-actin was used as a loading control. (B) Both A549 and H1299 cells transfected with siRNA-Wnt1 resulted in inhibition of cell migration using wound-healing assay. (C) Transfection of A549 and H1299 cells with siRNA-Wnt1 inhibited cell invasion using transwell migration assays. Images were captured at 200× optical magnification.</p
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