Evidence map›Paper›PMID 30103827›Full record

ArticleCancer communications (London, England)2018

Overexpression of amplified in breast cancer 1 (AIB1) gene promotes lung adenocarcinoma aggressiveness in vitro and in vivo by upregulating C-X-C motif chemokine receptor 4.

Liru He, Haixia Deng, Shiliang Liu, Jiewei Chen, Binkui Li, Chenyuan Wang, Xin Wang, Yiguo Jiang, Ningfang Ma, Mengzhong Liu and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cancer communications (London, England), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed, 1 pooled it
0.5field-weighted citation impact, top 31% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed, 1 synthesis or guideline pooled it, 7 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. SRC-3, a Steroid Receptor Coactivator: Implication in Cancer.International journal of molecular sciences · 2021
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 1 country.

Liru HeThe State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, No. 651, Dongfeng Road East, Guangzhou, 510060, China.
Haixia DengThe State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, No. 651, Dongfeng Road East, Guangzhou, 510060, China.
Shiliang LiuThe State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, No. 651, Dongfeng Road East, Guangzhou, 510060, China.
Jiewei ChenThe State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, No. 651, Dongfeng Road East, Guangzhou, 510060, China.
Binkui LiThe State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, No. 651, Dongfeng Road East, Guangzhou, 510060, China.
Chenyuan WangThe State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, No. 651, Dongfeng Road East, Guangzhou, 510060, China.
Xin WangThe State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, No. 651, Dongfeng Road East, Guangzhou, 510060, China.
Yiguo JiangThe State Key Laboratory of Respiratory Disease, Guangzhou Medical University, Guangzhou, China.
Ningfang MaKey Laboratory of Protein Modification and Degradation, School of Basic Medical Sciences, Affiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou, China.
Mengzhong LiuThe State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, No. 651, Dongfeng Road East, Guangzhou, 510060, China. liumzh@sysucc.org.cn.
Dan XieThe State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, No. 651, Dongfeng Road East, Guangzhou, 510060, China. xiedan@sysucc.org.cn.
Sun Yat-sen University · CNGuangzhou Medical University · CNState Key Laboratory of Respiratory Disease · CN

Funding

National Key R&D Program of China 2017YFC1309001Nature Science Foundation of China 81201842Nature Science Foundation of China 81772483Open Project of State Key Laboratory of Respiratory Disease of China 2007DA80154F1108Open Project of State Key Laboratory of Respiratory Disease of China SKLRD2016OP004
6 · The paper itself

Abstract

backgroundWe previously found that overexpression of the gene known as amplified in breast cancer 1 (AIB1) was associated with lymph node metastasis and poor prognosis in patients with lung adenocarcinoma. However, the role of AIB1 in that malignancy remains unknown. The present study aimed to investigate the function of AIB1 in the process of lung adenocarcinoma cell metastasis.

methodsA series of in vivo and in vitro assays were performed to elucidate the function of AIB1, while real-time PCR and Western blotting were utilized to identify the potential downstream targets of AIB1 in the process of lung adenocarcinoma metastasis. Rescue experiments and in vitro assays were performed to investigate whether the invasiveness of AIB1-induced lung adenocarcinoma was mediated by C-X-C motif chemokine receptor 4 (CXCR4).

resultsThe ectopic overexpression of AIB1 in lung adenocarcinoma cells substantially enhanced cell migration and invasive abilities in vitro and tumor metastasis in vivo, whereas the depletion of AIB1 expression substantially inhibited lung adenocarcinoma cell migration and invasion. CXCR4 was identified as a potential downstream target of AIB1 in lung adenocarcinoma. The knockdown of AIB1 greatly reduced CXCR4 gene expression at both the transcription and protein levels, whereas the knockdown of CXCR4 in cells with AIB1 ectopic overexpression diminished AIB1-induced migration and invasion in vitro and tumor metastasis in vivo. Furthermore, we found a significant positive association between the expression of AIB1 and CXCR4 in lung adenocarcinoma patients (183 cases), and the co-overexpression of AIB1 and CXCR4 predicted the poorest prognosis.

conclusionsThese findings suggest that AIB1 promotes the aggressiveness of lung adenocarcinoma in vitro and in vivo by upregulating CXCR4 and that it might be usable as a novel prognostic marker and/or therapeutic target for this disease.

Indexed as

Gene Expression Regulation, NeoplasticA549 CellsAdenocarcinomaAnimalsCell Line, TumorFemaleHumansKaplan-Meier EstimateLung NeoplasmsMaleMice, Inbred BALB CMice, NudeMiddle AgedNuclear Receptor Coactivator 3Receptors, CXCR4RNA InterferenceCXCR4 protein, humanNCOA3 protein, humanNuclear Receptor Coactivator 3Receptors, CXCR4Amplified in breast cancer 1C-X-C motif chemokine receptor 4Lung adenocarcinomaMetastasisPrognosis

Identifiers

PMID30103827
PMCPMC6090807
OpenAlexW2887309074

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.