Evidence map›Paper›PMID 24413079›Full record

ArticleOncogene2015

Overexpression of AKIP1 promotes angiogenesis and lymphangiogenesis in human esophageal squamous cell carcinoma.

C Lin, L Song, A Liu, H Gong, X Lin, J Wu, M Li, J Li

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

41 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Lymphangiogenesis in gastric cancer: function and mechanism.European journal of medical research · 2023
    Review
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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

8 authors at 2 institutions in 1 country.

C Lin1] Department of Experimental Research, State Key Laboratory of Oncology in Southern China, Cancer Center, Sun Yat-sen University, Guangdong, China [2] Department of Biochemistry, Zhongshan School of Medicine, Sun Yat-sen University, Guangdong, China.
L SongDepartment of Experimental Research, State Key Laboratory of Oncology in Southern China, Cancer Center, Sun Yat-sen University, Guangdong, China.
A LiuDepartment of Biochemistry, Zhongshan School of Medicine, Sun Yat-sen University, Guangdong, China.
H GongDepartment of Biochemistry, Zhongshan School of Medicine, Sun Yat-sen University, Guangdong, China.
X LinDepartment of Experimental Research, State Key Laboratory of Oncology in Southern China, Cancer Center, Sun Yat-sen University, Guangdong, China.
J Wu1] Department of Microbiology, Zhongshan School of Medicine, Sun Yat-sen University, Guangdong, China [2] Key Laboratory of Tropical Disease Control, Ministry of Education, Sun Yat-sen University, Guangdong, China.
M Li1] Department of Microbiology, Zhongshan School of Medicine, Sun Yat-sen University, Guangdong, China [2] Key Laboratory of Tropical Disease Control, Ministry of Education, Sun Yat-sen University, Guangdong, China.
J Li1] Department of Biochemistry, Zhongshan School of Medicine, Sun Yat-sen University, Guangdong, China [2] Key Laboratory of Tropical Disease Control, Ministry of Education, Sun Yat-sen University, Guangdong, China.
Sun Yat-sen University · CNSun Yat-sen University Cancer Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A-kinase-interacting protein 1 (AKIP1) is found to be overexpressed in breast and prostate cancers, suggesting that AKIP1 might act as a potent oncogenic protein. However, the clinical significance and biological role of AKIP1 in cancer progression remain largely unknown. Herein, we report that AKIP1 is markedly overexpressed in esophageal squamous cell carcinoma (ESCC) cell lines and clinical ESCC samples. AKIP1 expression significantly correlates with ESCC progression and patients' shorter survival time. Furthermore, we find that overexpressing AKIP1 induces, whereas silencing AKIP1 reduces, ESCC angiogenesis and lymphangiogenesis both in vitro and in vivo. Moreover, we demonstrate that AKIP1 transcriptionally upregulates vascular endothelial growth factor-C (VEGF-C) via interaction with its promoter through cooperation with multiple transcriptional factors, including SP1, AP2 and nuclear factor-κB (NF-κB). Importantly, significant correlation between levels of AKIP1 and VEGF-C is observed in a cohort of human ESCC, as well as in non-small cell lung cancer, hepatocellular carcinoma and ovarian cancer. Hence, these findings indicate an important role for AKIP1 in ESCC angiogenesis and lymphangiogenesis, and uncover a novel mechanism for the upregulation of VEGF-C in cancers.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsBlotting, WesternCarcinoma, Squamous CellCell Line, TumorChick EmbryoEsophageal NeoplasmsFemaleGene Expression Regulation, NeoplasticHumansKaplan-Meier EstimateLymphangiogenesisMaleMice, Inbred BALB CMice, NudeMiddle AgedAdaptor Proteins, Signal TransducingAKIP1 protein, humanNuclear ProteinsVascular Endothelial Growth Factor C

Identifiers

PMID24413079
OpenAlexW2056831929

What OpenQuestion holds

Textmetadata
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.