Evidence map›Paper›PMID 37160815›Full record

ArticleDiscover oncology2023

Targeting EFNA1 suppresses tumor progression via the cMYC-modulated cell cycle and autophagy in esophageal squamous cell carcinoma.

Houxiang Jiang, Shaoxiang Wang, Ying Liu, Chaopan Zheng, Lipeng Chen, Kai Zheng, Zhenyu Xu, Yong Dai, Hongtao Jin, Zhiqiang Cheng and 4 more

Open access · goldAbstract read
In one paragraph

Article in Discover oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

9 citing papers in PubMed, 10 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

14 authors at 6 institutions in 1 country.

Houxiang Jiang *Department of Gastrointestinal Surgery, The First Affiliated Hospital of Wannan Medical College (Yijishan Hospital of Wannan Medical College), Wuhu, 241001, Anhui, China.
Shaoxiang Wang *School of Pharmaceutical Sciences, Health Science Center, Shenzhen University, Shenzhen, 518060, China.
Ying Liu *Guangdong Provincial Clinical Research Center for Geriatrics, Shenzhen Clinical Research Center for Geriatrics, Shenzhen People's Hospital (The Second Clinical Medical College of Jinan University), Shenzhen, 518020, Guangdong, China.
Chaopan Zheng *Department of Otolaryngology, Shenzhen People's Hospital (The Second Clinical Medical College of Jinan University), Shenzhen, 518020, Guangdong, China.
Lipeng ChenGuangdong Provincial Clinical Research Center for Geriatrics, Shenzhen Clinical Research Center for Geriatrics, Shenzhen People's Hospital (The Second Clinical Medical College of Jinan University), Shenzhen, 518020, Guangdong, China.
Kai ZhengSchool of Pharmaceutical Sciences, Health Science Center, Shenzhen University, Shenzhen, 518060, China.
Zhenyu XuPrecision Medicine Center, The First Affiliated Hospital of Wannan Medical College (Yijishan Hospital of Wannan Medical College), Wuhu, 241001, Anhui, China.
Yong DaiGuangdong Provincial Clinical Research Center for Geriatrics, Shenzhen Clinical Research Center for Geriatrics, Shenzhen People's Hospital (The Second Clinical Medical College of Jinan University), Shenzhen, 518020, Guangdong, China.
Hongtao JinDepartment of Pathology, Shenzhen People's Hospital (The Second Clinical Medical College of Jinan University), Shenzhen, 518020, Guangdong, China.
Zhiqiang ChengDepartment of Pathology, Shenzhen People's Hospital (The Second Clinical Medical College of Jinan University), Shenzhen, 518020, Guangdong, China.
Chang ZouGuangdong Provincial Clinical Research Center for Geriatrics, Shenzhen Clinical Research Center for Geriatrics, Shenzhen People's Hospital (The Second Clinical Medical College of Jinan University), Shenzhen, 518020, Guangdong, China.
Li FuDepartment of Pharmacology, Shenzhen University School of Medicine, Shenzhen, 518060, Guangdong, China. gracelfu@szu.edu.cn.
Kaisheng LiuGuangdong Provincial Clinical Research Center for Geriatrics, Shenzhen Clinical Research Center for Geriatrics, Shenzhen People's Hospital (The Second Clinical Medical College of Jinan University), Shenzhen, 518020, Guangdong, China. liukaisheng@szhospital.com.
Xiaoshi MaDepartment of Urology, Shenzhen People's Hospital (The Second Clinical Medical College of Jinan University), Shenzhen, 518020, Guangdong, China. ma.xiaoshi@szhospital.com.
Jinan University · CNFirst Affiliated Hospital of Wannan Medical College · CNShenzhen University Health Science Center · CNShenZhen People’s Hospital · CNShenzhen Second People's Hospital · CNShenzhen University · CN

Funding

Basic and Applied Basic Research Foundation of Guangdong Province 2021A1515111144National Natural Science Foundation of China 82273040University Natural Science Research Project of Anhui Province gzyqZD2021143
6 · The paper itself

Abstract

purposeEsophageal squamous cell carcinoma (ESCC) remains one of the most common causes of cancer death due to the lack of effective therapeutic options. New targets and the targeted drugs are required to be identified and developed.

methodsHighly expressed genes in ESCA were identified using the edgeR package from public datasets. Immunostaining assay verified the high expression level of EFNA1 in ESCC. CCK-8, colony formation and wound healing assays were performed to examine the role of EFNA1 and EPHA2 in ESCC progression. Cell cycle was analyzed by flow cytometry and autophagy activation was determined by autophagolysosome formation using transmission electron microscopy. The small molecule targeting to EFNA1 was identified by molecular docking and the anti-tumor effects were verified by in vitro and in vivo models with radiation treatment.

resultsEFNA1 was highly expressed in esophageal cancer and significantly associated with poor prognosis. Downregulation of EFNA1 remarkably inhibited cell proliferation and migration. Furthermore, decreased EFNA1 significantly suppressed the expression of cMYC along with its representative downstream genes involved in cell cycle, and activated autophagy. Similar effects on ESCC progression were obtained from knockdown of the corresponding receptor, EPHA2. The potential small molecule targeting to EFNA1, salvianolic acid A (SAA), could significantly suppress ESCC progression and increase the sensitivity to radiotherapy.

conclusionWe revealed that EFNA1 facilitated the ESCC progression via the possible mechanism of activating cMYC-modulated cell proliferation and suppressing autophagy, and identified SAA as a potential drug targeting EFNA1, providing new options for the future treatments for ESCC patients.

Indexed as

AutophagycMYCEFNA1Esophageal squamous cell carcinomaSalvianolic acid A

Identifiers

PMID37160815
PMCPMC10169935
OpenAlexW4376122054

What OpenQuestion holds

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Registered trials

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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.