Evidence map›Paper›PMID 27725900›Full record

ArticleAmerican journal of cancer research2016

Identification of HRAS as cancer-promoting gene in gastric carcinoma cell aggressiveness.

Xiao Yu Wu, Wen Tao Liu, Zhen Feng Wu, Che Chen, Jia Yun Liu, Guan Nan Wu, Xue Quan Yao, Fu Kun Liu, Gang Li

Open access · greenAbstract read
In one paragraph

Article in American journal of cancer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

32 citing papers in PubMed, 49 citations in OpenAlex.

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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

9 authors at 3 institutions in 1 country.

Xiao Yu WuDepartment of Surgical Oncology, Affiliated Hospital of Nanjing University of Traditional Chinese Medicine No. 155 Hanzhong Road, Nanjing 210029, Jiangsu, China.
Wen Tao LiuDepartment of Surgery, Ruijin Hospital, Shanghai Jiaotong University, Shanghai Institute of Digestive Surgery 197 Ruijin 2 Road, Shanghai 200025, China.
Zhen Feng WuDepartment of Surgical Oncology, Affiliated Hospital of Nanjing University of Traditional Chinese Medicine No. 155 Hanzhong Road, Nanjing 210029, Jiangsu, China.
Che ChenDepartment of Surgical Oncology, Affiliated Hospital of Nanjing University of Traditional Chinese Medicine No. 155 Hanzhong Road, Nanjing 210029, Jiangsu, China.
Jia Yun LiuDepartment of Surgical Oncology, Affiliated Hospital of Nanjing University of Traditional Chinese Medicine No. 155 Hanzhong Road, Nanjing 210029, Jiangsu, China.
Guan Nan WuDepartment of Surgical Oncology, Affiliated Hospital of Nanjing University of Traditional Chinese Medicine No. 155 Hanzhong Road, Nanjing 210029, Jiangsu, China.
Xue Quan YaoDepartment of Surgical Oncology, Affiliated Hospital of Nanjing University of Traditional Chinese Medicine No. 155 Hanzhong Road, Nanjing 210029, Jiangsu, China.
Fu Kun LiuDepartment of Surgical Oncology, Affiliated Hospital of Nanjing University of Traditional Chinese Medicine No. 155 Hanzhong Road, Nanjing 210029, Jiangsu, China.
Gang LiDepartment of General Surgery, Jiangsu Cancer Hospital, The Affiliated Cancer Hospital of Nanjing Medical University No. 42 Baiziting, Nanjing 210009, Jiangsu, China.
Nanjing University of Chinese Medicine · CNJiangsu Cancer Hospital · CNRuijin Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gastric carcinoma is one of the most lethal malignancies of cancers and its prognosis remains dismal due to the paucity of effective therapeutic targets. Herein, we showed that HRAS is markedly up-regulated in gastric carcinoma. Prognostic analysis indicated that HRAS expression might be a prognostic indicator for the survival of patients with gastric carcinoma. Ectopic expression of HRAS in gastric carcinoma cells accelerated proliferation, migration, invasion, angiogenesis, and clone formation ability of gastric carcinoma cells in vitro. Furthermore, HRAS over-expressing significantly promoted the tumorigenicity of gastric carcinoma cells in vivo whereas silencing endogenous HRAS caused opposite outcomes. Moreover, we demonstrated that HRAS enhanced gastric carcinoma aggressiveness by activating VEGFA/PI3K/AKT pathway and Raf-1 signaling. Together, our results provide new evidence that HRAS overexpression promotes the progression of gastric carcinoma and might represent a novel therapeutic target for its treatment.

Indexed as

angiogenesisgastric carcinomagrowthHRAS

Identifiers

PMID27725900
PMCPMC5043104
OpenAlexW2562221651

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.