Evidence map›Paper›PMID 38658569›Full record

ArticleCell death & disease2024

Annexin A2 combined with TTK accelerates esophageal cancer progression via the Akt/mTOR signaling pathway.

Ruiqi Liu, Yanwei Lu, Jing Li, Weiping Yao, Jiajun Wu, Xiaoyan Chen, Luanluan Huang, Ding Nan, Yitian Zhang, Weijun Chen and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
5.6field-weighted citation impact, top 3% 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

20 citing papers in PubMed, 24 citations in OpenAlex.

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  6. Cancer biology & therapy · 2025
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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

15 authors at 5 institutions in 1 country.

Ruiqi Liu *Cancer Center, Department of Radiation Oncology, Zhejiang Provincial People's Hospital (Affiliated People's Hospital), Hangzhou Medical College, Hangzhou, Zhejiang, China.
Yanwei Lu *Cancer Center, Department of Radiation Oncology, Zhejiang Provincial People's Hospital (Affiliated People's Hospital), Hangzhou Medical College, Hangzhou, Zhejiang, China.
Jing Li *The First School of Clinical Medicine, Lanzhou University, Lanzhou, Gansu, China.
Weiping Yao *Cancer Center, Department of Radiation Oncology, Zhejiang Provincial People's Hospital (Affiliated People's Hospital), Hangzhou Medical College, Hangzhou, Zhejiang, China.
Jiajun WuGraduate Department, Bengbu Medical College, Bengbu, Anhui, China.
Xiaoyan ChenCancer Center, Department of Radiation Oncology, Zhejiang Provincial People's Hospital (Affiliated People's Hospital), Hangzhou Medical College, Hangzhou, Zhejiang, China.
Luanluan HuangCancer Center, Department of Radiation Oncology, Zhejiang Provincial People's Hospital (Affiliated People's Hospital), Hangzhou Medical College, Hangzhou, Zhejiang, China.
Ding NanGraduate Department, Hangzhou Normal University, Hangzhou, Zhejiang, China.
Yitian ZhangDepartment of Oncology, Jinxiang People's Hospital, Jining, Shandong, China.
Weijun ChenCancer Center, Department of Radiation Oncology, Zhejiang Provincial People's Hospital (Affiliated People's Hospital), Hangzhou Medical College, Hangzhou, Zhejiang, China.
Ying WangCancer Center, Department of Radiation Oncology, Zhejiang Provincial People's Hospital (Affiliated People's Hospital), Hangzhou Medical College, Hangzhou, Zhejiang, China.
Yongshi JiaCancer Center, Department of Radiation Oncology, Zhejiang Provincial People's Hospital (Affiliated People's Hospital), Hangzhou Medical College, Hangzhou, Zhejiang, China.
Jianming TangDepartment of Radiation Oncology, The First Hospital of Lanzhou University, Lanzhou University, Lanzhou, Gansu, China. 15900792812@163.com.
Xiaodong LiangCancer Center, Department of Radiation Oncology, Zhejiang Provincial People's Hospital (Affiliated People's Hospital), Hangzhou Medical College, Hangzhou, Zhejiang, China. lxdctopone@sina.com.ORCID 0000-0001-9479-0936
Haibo ZhangCancer Center, Department of Radiation Oncology, Zhejiang Provincial People's Hospital (Affiliated People's Hospital), Hangzhou Medical College, Hangzhou, Zhejiang, China. zhbdoctor@163.com.ORCID 0000-0002-5134-4167
Zhejiang Provincial People's Hospital · CNBengbu Medical College · CNFirst Hospital of Lanzhou University · CNHangzhou Normal University · CNLanzhou University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82003236National Natural Science Foundation of China (National Science Foundation of China) 82203377Natural Science Foundation of Zhejiang Province (Zhejiang Provincial Natural Science Foundation) LQ22H160036Natural Science Foundation of Zhejiang Province (Zhejiang Provincial Natural Science Foundation) LY20H160044Natural Science Foundation of Zhejiang Province (Zhejiang Provincial Natural Science Foundation) LY24H160022
6 · The paper itself

Abstract

Annexin A2 (ANXA2) is a widely reported oncogene. However, the mechanism of ANXA2 in esophageal cancer is not fully understood. In this study, we provided evidence that ANXA2 promotes the progression of esophageal squamous cell carcinoma (ESCC) through the downstream target threonine tyrosine kinase (TTK). These results are consistent with the up-regulation of ANXA2 and TTK in ESCC. In vitro experiments by knockdown and overexpression of ANXA2 revealed that ANXA2 promotes the progression of ESCC by enhancing cancer cell proliferation, migration, and invasion. Subsequently, animal models also confirmed the role of ANXA2 in promoting the proliferation and metastasis of ESCC. Mechanistically, the ANXA2/TTK complex activates the Akt/mTOR signaling pathway and accelerates epithelial-mesenchymal transition (EMT), thereby promoting the invasion and metastasis of ESCC. Furthermore, we identified that TTK overexpression can reverse the inhibition of ESCC invasion after ANXA2 knockdown. Overall, these data indicate that the combination of ANXA2 and TTK regulates the activation of the Akt/mTOR pathway and accelerates the progression of ESCC. Therefore, the ANXA2/TTK/Akt/mTOR axis is a potential therapeutic target for ESCC.

Indexed as

Annexin A2Cell ProliferationDisease ProgressionEpithelial-Mesenchymal TransitionEsophageal NeoplasmsProto-Oncogene Proteins c-aktSignal TransductionTOR Serine-Threonine KinasesAnimalsCell Cycle ProteinsCell Line, TumorCell MovementEsophageal Squamous Cell CarcinomaFemaleGene Expression Regulation, NeoplasticHumansAnnexin A2ANXA2 protein, humanCell Cycle ProteinsMTOR protein, humanProto-Oncogene Proteins c-aktTOR Serine-Threonine Kinases

Identifiers

PMID38658569
PMCPMC11043348
OpenAlexW4395071372

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.