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ERG the modulates Warburg effect and tumor progression in cervical cancer.

ERG 在宫颈癌中调节 Warburg 效应和肿瘤进展。

  • 影响因子:2.69
  • DOI:10.1016/j.bbrc.2019.11.079
  • 作者列表:"Zhang Z","Chen F","Li S","Guo H","Xi H","Deng J","Han Q","Zhang W
  • 发表时间:2020-01-29
Abstract

:Altered aerobic glycolysis is an important feature of cancer cell energy metabolism, known as the Warburg effect. Cervical cancer is one of the most common causes of cancer death in females. However, the roles of aerobic glycolysis in the development of cervical cancer are still poorly defined. Here, we identified a transcription factor (TF), ETS-related gene (ERG), as a new regulator of cancer progression and the glycolysis process in cervical cancer. In this study, we found that ectopic expression of ERG enhanced the capacity of aerobic glycolysis and increased glucose uptake, lactate production, and ATP generation. ERG overexpression increased and ERG knockdown decreased the anchorage independent cell growth and cell invasion in cervical cancer cells. Mechanistically, we propose that ERG regulates the expression of hexokinase 2 (HK2) and phosphoglycerate kinase 1 (PGK1) in the glycolytic pathway by directly binding to their promoters. A gain-of-function study showed that the knockdown or overexpression of HK2 and PGK1 abolished the increased or decreased aerobic glycolysis and cervical cancer progression induced by stable ectopic expression or depletion of ERG, respectively. Taken together, our findings suggest that ERG plays a potential role in the progression of cervical cancer, and could serve as a novel biomarker and potential therapeutic target in cervical cancer.

摘要

: 有氧糖酵解的改变是癌细胞能量代谢的一个重要特征,被称为 Warburg 效应。宫颈癌是女性癌症死亡的最常见原因之一。然而,有氧糖酵解在宫颈癌发展中的作用仍然知之甚少。在这里,我们鉴定了一个转录因子 (TF),ETS 相关基因 (ERG),作为宫颈癌中癌症进展和糖酵解过程的新调控因子。在这项研究中,我们发现 ERG 的异位表达增强了有氧糖酵解的能力,增加了葡萄糖摄取、乳酸生成和 ATP 生成。ERG 过表达增加,ERG 敲除降低宫颈癌细胞中锚定非依赖性细胞生长和细胞侵袭。从机制上来说,我们提出 ERG 通过直接结合其启动子来调节糖酵解途径中己糖激酶 2 (HK2) 和磷酸甘油酸激酶 1 (PGK1) 的表达。一项功能获得研究表明,HK2 和 PGK1 的敲除或过表达分别消除了 ERG 稳定异位表达或耗竭诱导的有氧糖酵解和宫颈癌进展的增加或减少。总之,我们的研究结果表明,ERG 在宫颈癌的进展中起着潜在的作用,可以作为宫颈癌的新型生物标志物和潜在的治疗靶点。

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影响因子:2.69
发表时间:2020-01-29
DOI:10.1016/j.bbrc.2019.11.079
作者列表:["Zhang Z","Chen F","Li S","Guo H","Xi H","Deng J","Han Q","Zhang W"]

METHODS::Altered aerobic glycolysis is an important feature of cancer cell energy metabolism, known as the Warburg effect. Cervical cancer is one of the most common causes of cancer death in females. However, the roles of aerobic glycolysis in the development of cervical cancer are still poorly defined. Here, we identified a transcription factor (TF), ETS-related gene (ERG), as a new regulator of cancer progression and the glycolysis process in cervical cancer. In this study, we found that ectopic expression of ERG enhanced the capacity of aerobic glycolysis and increased glucose uptake, lactate production, and ATP generation. ERG overexpression increased and ERG knockdown decreased the anchorage independent cell growth and cell invasion in cervical cancer cells. Mechanistically, we propose that ERG regulates the expression of hexokinase 2 (HK2) and phosphoglycerate kinase 1 (PGK1) in the glycolytic pathway by directly binding to their promoters. A gain-of-function study showed that the knockdown or overexpression of HK2 and PGK1 abolished the increased or decreased aerobic glycolysis and cervical cancer progression induced by stable ectopic expression or depletion of ERG, respectively. Taken together, our findings suggest that ERG plays a potential role in the progression of cervical cancer, and could serve as a novel biomarker and potential therapeutic target in cervical cancer.

翻译标题与摘要 下载文献
影响因子:3.18
发表时间:2020-01-29
来源期刊:Vaccine
DOI:10.1016/j.vaccine.2019.11.019
作者列表:["Shilling H","Murray G","Brotherton JML","Hawkes D","Saville M","Sivertsen T","Chambers I","Roberts J","Farnsworth A","Garland SM","Hocking JS","Kaldor J","Guy R","Atchison S","Costa AM","Molano M","Machalek DA"]

METHODS:INTRODUCTION:Australia has recently implemented major changes in cervical cancer prevention policies including introduction of primary human papillomavirus (HPV) screening starting at age 25, and replacement of the quadrivalent HPV vaccine with the nonavalent vaccine in the national school-based program. We assessed the feasibility and utility of conducting HPV testing in residual clinical specimens submitted for routine Chlamydia trachomatis screening, as a means of tracking HPV vaccine program impact among young sexually active women. METHODS:De-identified residual specimens from women aged 16-24 years submitted for chlamydia testing were collected from three pathology laboratories in Victoria and New South Wales. Limited demographic information, and chlamydia test results were also collected. Patient identifiers were sent directly from the laboratories to the National HPV Vaccination Program Register, to obtain HPV vaccination histories. Samples underwent HPV genotyping using Seegene Anyplex II HPV 28 assay. RESULTS:Between April and July 2018, 362 residual samples were collected, the majority (60.2%) of which were cervical swabs. Demographic data and vaccination histories were received for 357 (98.6%) women (mean age 21.8, SD 2.0). Overall, 65.6% of women were fully vaccinated, 9.8% partially, and 24.7% unvaccinated. The majority (86.0%) resided in a major city, 35.9% were classified in the upper quintile of socioeconomic advantage and chlamydia positivity was 7.8%.The prevalence of quadrivalent vaccine-targeted types (HPV6/11/16/18) was 2.8% (1.5-5.1%) overall with no differences by vaccination status (p = 0.729). The prevalence of additional nonavalent vaccine-targeted types (HPV31/33/45/52/58) was 19.3% (15.6-23.8%). One or more oncogenic HPV types were detected in 46.8% (95% CI 41.6-52.0%) of women. CONCLUSIONS:HPV testing of residual chlamydia specimens provides a simple, feasible method for monitoring circulating genotypes. Applied on a larger scale this method can be utilised to obtain a timely assessment of nonavalent vaccine impact among young women not yet eligible for cervical screening.

翻译标题与摘要 下载文献
影响因子:4.02
发表时间:2020-01-29
来源期刊:Journal of virology
DOI:10.1128/JVI.00090-20
作者列表:["Boon SS","Xia C","Lim JY","Chen Z","Law PTY","Yeung ACM","Thomas M","Banks L","Chan PKS"]

METHODS::Human papillomavirus (HPV) type 58 is the third most commonly detected HPV type in cervical cancer among Eastern Asians. Our previous international epidemiological studies revealed that a HPV58E7 natural variant, T20I/G63S (designated as V1), was associated with a higher risk of cervical cancer. We recently showed that V1 possesses a greater ability to immortalise and transform primary cells, as well as degrading pRB more effectively than the prototype and other common variants. In this study, we performed a series of phenotypic and molecular assays using physiologically relevant in vitro and in vivo models to compare the oncogenicity of V1 with that of the prototype and other common natural variants. Through activation of AKT and K-Ras/ERK signalling pathways, V1 consistently showed greater oncogenicity compared with prototype and other variants, as demonstrated by increased cell proliferation, migration and invasion, as well as induction of larger tumours in athymic nude mice. This study complements our previous epidemiological and molecular observations pinpointing the higher oncogenicity of V1 compared with prototype and all other common variants. Since V1 is more commonly found in Eastern Asia, our report provides insight into the design of HPV-screening assays and selection of components for HPV vaccines in this region.IMPORTANCE Epidemiological studies have revealed that a wild type variant of HPV58 carrying an E7 variation, T20I/G63S (V1), is associated with a higher risk of cervical cancer. We previously reported that this increased oncogenicity could be the result of its greater ability to degrade pRB, thereby leading to an increased ability to grow in an anchorage-independent manner. In addition to this, this report further showed that this HPV variant induced activation of AKT and K-Ras/ERK signalling pathways, thereby, explaining its genuine oncogenicity in promoting cell proliferation, migration, invasion, and formation of tumours, all to a greater extent than prototype HPV58 and other common variants.

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