Evidence map›Paper›PMID 33163274›Full record

ArticleAmerican journal of cancer research2020

Ubiquitin ligase KLHL2 promotes the degradation and ubiquitination of ARHGEF7 protein to suppress renal cell carcinoma progression.

Encheng Zhang, Xiao Dong, Siteng Chen, Jialiang Shao, Pingzhao Zhang, Yuqi Wang, Xiang Wang

Open access · greenAbstract read
In one paragraph

Article in American journal of cancer research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

8 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
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  6. The roles of KLHL family members in human cancers.American journal of cancer research · 2022
    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

7 authors at 2 institutions in 1 country.

Encheng ZhangDepartment of Urology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine Shanghai, China.
Xiao DongDepartment of Oncology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine Shanghai, China.
Siteng ChenDepartment of Urology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine Shanghai, China.
Jialiang ShaoDepartment of Urology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine Shanghai, China.
Pingzhao ZhangState Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences, Fudan University Shanghai, China.
Yuqi WangState Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences, Fudan University Shanghai, China.
Xiang WangDepartment of Urology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine Shanghai, China.
Shanghai Jiao Tong University · CNFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies have revealed that ARHGEF7 is upregulated in many malignant tumors, but the underlying molecular mechanisms to this response remain to be fully elucidated. In this study, we confirm that ARHGEF7 physically interacts with KLHL2, which was previously identified to be an E3 ubiquitin ligase. KLHL2 is capable of promoting ARHGEF7 degradation via the ubiquitin-proteasome pathway. We identify that the Kelch domain of KLHL2 is necessary for binding with ARHGEF7 and downstream activities. In addition, we find that ARHGEF7 is overexpressed in clear cell renal cell carcinoma (ccRCC) specimens, and that the level of expression negatively correlates with that of KLHL2. Moreover, we utilize knockdown loss-of-function assays to demonstrate that ARHGEF7 in 786-O and A498 cell lines can act as a regulator of cell proliferation, migration and invasion, and that these effects can be reversed by KLHL2 inactivation. Taken together, our data suggest that ARHGEF7 is a putative oncogene that functions via an interaction with KLHL2, and control of ARHGEF7 can be a potential future target to inhibit tumor progression.

Indexed as

ARHGEF7KLHL2protein degradationrenal cell carcinomaubiquitination

Identifiers

PMID33163274
PMCPMC7642650
OpenAlexW3102962262

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.