Evidence map›Paper›PMID 33767988›Full record

ArticleFrontiers in oncology2021

Overexpression of RhoV Promotes the Progression and EGFR-TKI Resistance of Lung Adenocarcinoma.

Hongjin Chen, Ruixue Xia, Long Jiang, Yong Zhou, Haojun Xu, Weiwei Peng, Chengyun Yao, Guoren Zhou, Yijie Zhang, Hongping Xia and 1 more

Abstract read
In one paragraph

Article in Frontiers in oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
–field-weighted citation impact
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

23 citing papers in PubMed.

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  12. Atypical RhoUV GTPases in development and disease.Biochemical Society transactions · 2024
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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

11 authors.

Hongjin ChenDepartment of Pathology, School of Basic Medical Sciences & Sir Run Run Hospital & Key Laboratory of Antibody Technique of National Health Commission, Nanjing Medical University, Nanjing, China.
Ruixue XiaDepartment of Respiratory and Critical Care Medicine, Henan University Huaihe Hospital, Kaifeng, China.
Long JiangShanghai Lung Cancer Center, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai, China.
Yong ZhouNanjing Drum Tower Hospital Affiliated to Medical School of Nanjing University, Nanjing, China.
Haojun XuDepartment of Pathology, School of Basic Medical Sciences & Sir Run Run Hospital & Key Laboratory of Antibody Technique of National Health Commission, Nanjing Medical University, Nanjing, China.
Weiwei PengJiangsu Cancer Hospital & The Affiliated Cancer Hospital of Nanjing Medical University & Jiangsu Institute of Cancer Research, Nanjing, China.
Chengyun YaoJiangsu Cancer Hospital & The Affiliated Cancer Hospital of Nanjing Medical University & Jiangsu Institute of Cancer Research, Nanjing, China.
Guoren ZhouJiangsu Cancer Hospital & The Affiliated Cancer Hospital of Nanjing Medical University & Jiangsu Institute of Cancer Research, Nanjing, China.
Yijie ZhangDepartment of Respiratory and Critical Care Medicine, Henan University Huaihe Hospital, Kaifeng, China.
Hongping XiaDepartment of Pathology, School of Basic Medical Sciences & Sir Run Run Hospital & Key Laboratory of Antibody Technique of National Health Commission, Nanjing Medical University, Nanjing, China.
Yongsheng WangNanjing Drum Tower Hospital Affiliated to Medical School of Nanjing University, Nanjing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe Rho GTPase family with ~20 member genes play central roles in a wide variety of cellular processes and tumor cell migration and metastasis. Different Rho GTPase may play different roles in the progression of lung adenocarcinoma.

methodsWe comprehensively examined the expression of all Rho GTPase family member genes in a panel of lung adenocarcinoma patient's tumors and matched normal tissues. We next investigated the critical role of RhoV in different lung adenocarcinoma cells and animal models.

resultsRhoV was identified as one of the most significantly overexpressed Rho GTPases in lung adenocarcinoma and associated with patients' survival. Silencing RhoV expression inhibits proliferation, migration and invasion, and tumorigenicity capacities of lung adenocarcinoma cells. Moreover, knockdown RhoV promoted the sensitivity of EGFR-TKI in the gefitinib resistant PC9 cells (PC9-GR) and aggravated gefitinib-induced lung cancer cell apoptosis both in PC9 and PC9-GR cells. Our data also indicated that RhoV induced progression and EGFR-TKI resistance of lung adenocarcinoma may be related to the activation of the AKT/ERK pathway.

conclusionOverexpression of RhoV in lung adenocarcinoma promotes the progression and EGFR-TKI resistance, suggesting RhoV is a promising prognosis and therapeutic target of lung adenocarcinoma.

Indexed as

AKTERKgefitiniblung adenocarcinomaRhoV

Identifiers

PMID33767988
PMCPMC7986718

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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.