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Mortal Obligate RNA Transcript Inhibits Cancer Cell Invasion and Migration in Lung Adenocarcinoma by Downregulating miRNA-223.

致命的专性 RNA 转录本通过下调 miRNA-223 抑制肺腺癌的癌细胞侵袭和迁移。

  • 影响因子:1.70
  • DOI:10.1089/cbr.2019.3244
  • 作者列表:"Huang Y","Zhuang Q","Zhuang W
  • 发表时间:2020-06-01
Abstract

: Background: Mortal obligate RNA transcript (MORT), a long noncoding RNA, has been reported as a potential tumor suppressor in many types of cancer. The functions of MORT involved in lung adenocarcinoma (LUAD) were investigated in this study. Materials and Methods: A total of 67 patients with LUAD (adenocarcinoma) were recruited in this study. Quantitative reverse transcription-polymerase chain reaction was used to assess gene expression. Cell transfections were used to analyze gene interactions. Transwell migration and invasion assay were carried out to analyze cell migration and invasion. Results: MORT was downregulated, whereas miRNA-223 was upregulated in LUAD. Expression of MORT was significantly affected by tumor metastasis but not by the size of tumors. Expression of miRNA-223 and MORT was inversely correlated in LUAD tissue samples. LUAD cells overexpressing MORT showed downregulated miRNA-223, whereas the expression of MORT was not significantly affected by overexpression of miRNA-223. Besides, overexpression of MORT inhibited, whereas overexpression of miRNA-223 promoted the invasion and migration of LUAD cells. Overexpression of miRNA-223 inhibited the effects of overexpressing MORT on cell invasion and migration. Conclusions: Therefore, MORT may inhibit cancer cell invasion and migration in LUAD by downregulating miRNA-223.

摘要

: 背景: 致命的专性 RNA 转录本 (MORT),一种长链非编码 RNA,已被报道为许多类型癌症的潜在肿瘤抑制因子。本研究探讨了 MORT 参与肺腺癌 (LUAD) 的功能。 材料和方法: 本研究共招募了 67 例 LUAD (腺癌) 患者。定量逆转录-聚合酶链反应用于评估基因表达。细胞转染用于分析基因相互作用。Transwell 迁移和侵袭实验分析细胞迁移和侵袭。 结果: 在 LUAD 中 MORT 下调,而 miRNA-223 上调。MORT 的表达受肿瘤转移的显著影响,而不受肿瘤大小的影响。在 LUAD 组织样本中,miRNA-223 和 MORT 的表达呈负相关。过表达 MORT 的 LUAD 细胞表现出下调的 miRNA-223,而 MORT 的表达不受 miRNA-223 过表达的显著影响。此外,MORT 的过表达抑制,而 miRNA-223 的过表达促进 LUAD 细胞的侵袭和迁移。过表达 miRNA-223 抑制过表达 MORT 对细胞侵袭和迁移的影响。 结论: 因此,MORT 可能通过下调 miRNA-223 抑制 LUAD 中的癌细胞侵袭和迁移。

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发表时间:2020-01-01
DOI:10.1016/j.asjsur.2019.03.008
作者列表:["Esme H","Can A","Şehitogullari A"]

METHODS:BACKGROUND:The objectives of this study are to assess the chest drainage volumes of patients undergoing anatomic resection of non-small cell lung carcinoma and to determine the safety and effectiveness of administering enoxaparin for thromboprophylaxis. METHODS:A total of 77 patients were included in the study. A study was conducted on the first group of 42 patients in which enoxaparin prophylaxis (enoxaparin, 40 mg) was subcutaneously injected once a day for a period of three days after the patients underwent anatomic pulmonary resection between March 2016 and March 2018. An enoxaparin-free group was identified and included 35 patients who received no enoxaparin prophylaxis after undergoing anatomic pulmonary resection between February 2013 and February 2016. We compared the changes in hemoglobin (Hb) levels, postoperative 3-day drainage volume, transfusion volume, pulmonary complications and length of stay between the two groups. RESULTS:No differences in postoperative Hb levels, chest drainage volume, transfusion volume, postoperative complications, and length of stay were observed between the two groups. Deep-vein thrombosis was noted in a patient in the enoxaparin-free group. No major bleeding was noted in either group. CONCLUSION:We found that for patients undergoing anatomic resection of primary lung cancer, the blood transfusion and chest drainage volumes did not differ, regardless of whether the patients were given enoxaparin. To the best of our knowledge, the impact of low-molecular-weight heparin on chest tube drainage volume for patients undergoing anatomic resection of non-small cell lung carcinoma has not been investigated before.

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影响因子:1.84
发表时间:2020-01-01
来源期刊:Oncology letters
DOI:10.3892/ol.2019.11149
作者列表:["Das SK","Huang YY","Li B","Yu XX","Xiao RH","Yang HF"]

METHODS::The aim of the present study was to compare the safety and efficacy of cryoablation (CA) and microwave ablation (MWA) as treatments for non-small cell lung cancer (NSCLC). Patients with stage IIIB or IV NSCLC treated with CA (n=45) or MWA (n=56) were enrolled in the present study. The primary endpoint was progression-free survival (PFS); the secondary endpoints included overall survival (OS) time and adverse events (AEs). The median PFS times between the two groups were not significantly different (P=0.36): CA, 10 months [95% confidence interval (CI), 7.5-12.4] vs. MWA, 11 months (95% CI, 9.5-12.4). The OS times between the two groups were also not significantly different (P=0.07): CA, 27.5 months (95% CI, 22.8-31.2 months) vs. MWA, 18 months (95% CI, 12.5-23.5). For larger tumors (>3 cm), patients treated with MWA had significantly longer median PFS (P=0.04; MWA, 10.5 months vs. CA, 7.0 months) and OS times (P=0.04; MWA, 24.5 months vs. CA, 14.5 months) compared patients treated with CA. However, for smaller tumors (≤3 cm), median PFS (P=0.79; MWA, 11.0 months vs. CA, 13.0 months) and OS times (P=0.39; MWA, 30.0 months vs. CA, 26.5 months) between the two groups did not differ significantly. The incidence rates of AEs were similar in the two groups (P>0.05). The number of applicators, tumor size and length of the lung traversed by applicators were associated with a higher risk of pneumothorax and intra-pulmonary hemorrhage in the two groups. Treatment with CA resulted in significantly less intraprocedural pain compared with treatment with MWA (P=0.001). Overall, the present study demonstrated that CA and MWA were comparably safe and effective procedures for the treatment of small tumors. However, treatment with MWA was superior compared with CA for the treatment of large tumors.

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影响因子:8.44
发表时间:2020-02-01
DOI:10.1016/j.annonc.2019.10.022
作者列表:["Mazieres J","Cropet C","Montané L","Barlesi F","Souquet PJ","Quantin X","Dubos-Arvis C","Otto J","Favier L","Avrillon V","Cadranel J","Moro-Sibilot D","Monnet I","Westeel V","Le Treut J","Brain E","Trédaniel J","Jaffro M","Collot S","Ferretti GR","Tiffon C","Mahier-Ait Oukhatar C","Blay JY"]

METHODS:BACKGROUND:BRAF mutations occurring in 1%-5% of patients with non-small-cell lung cancer (NSCLC) are therapeutic targets for these cancers but the impact of the exact mutation on clinical activity is unclear. The French National Cancer Institute (INCA) launched the AcSé vemurafenib trial to assess the efficacy and safety of vemurafenib in cancers with various BRAF mutations. We herein report the results of the NSCLC cohort. PATIENTS AND METHODS:Tumour samples were screened for BRAF mutations in INCA-certified molecular genetic centres. Patients with BRAF-mutated tumours progressing after ≥1 line of treatment were proposed vemurafenib 960 mg twice daily. Between October 2014 and July 2018, 118 patients were enrolled in the NSCLC cohort. The primary outcome was the objective response rate (ORR) assessed every 8 weeks (RECIST v1.1). A sequential Bayesian approach was planned with an inefficacy bound of 10% for ORR. If no early stopping occurred, the treatment was of interest if the estimated ORR was ≥30% with a 90% probability. Secondary outcomes were tolerance, response duration, progression-free survival (PFS), and overall survival (OS). RESULTS:Of the 118 patients enrolled, 101 presented with a BRAFV600 mutation and 17 with BRAFnonV600 mutations; the median follow-up was 23.9 months. In the BRAFnonV600 cohort, no objective response was observed and this cohort was stopped. In the BRAFV600 cohort, 43/96 patients had objective responses. The mean Bayesian estimated success rate was 44.9% [95% confidence intervals (CI) 35.2%-54.8%]. The ORR had a 99.9% probability of being ≥30%. Median response duration was 6.4 months, median PFS was 5.2 months (95% CI 3.8-6.8), and OS was 10 months (95% CI 6.8-15.7). The vemurafenib safety profile was consistent with previous publications. CONCLUSION:Routine biomarker screening of NSCLC should include BRAFV600 mutations. Vemurafenib monotherapy is effective for treating patients with BRAFV600-mutated NSCLC but not those with BRAFnonV600 mutations. TRIAL REGISTRATION:ClinicalTrials.gov identifier: NCT02304809.

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