Evidence map›Paper›PMID 31126310›Full record

ReviewMolecular cancer2019

Crosstalk between autophagy and epithelial-mesenchymal transition and its application in cancer therapy.

Hong-Tao Chen, Hao Liu, Min-Jie Mao, Yuan Tan, Xiang-Qiong Mo, Xiao-Jun Meng, Meng-Ting Cao, Chu-Yu Zhong, Yan Liu, Hong Shan and 1 more

Abstract readReview
In one paragraph

Review in Molecular cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 180 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
180citing papers in PubMed, 1 pooled it
–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

180 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  7. CHMP4C deletion inhibits the proliferation and metastasis of hypopharyngeal squamous cell carcinoma through the Wnt/β-catenin/EMT signaling pathway.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2026
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120 more citing papers are in PubMed but not listed here.

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.

Hong-Tao ChenDepartment of Clinical Laboratory, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, 2528000, Guangdong, China.
Hao LiuCancer Hospital and Cancer Research Institute, Guangzhou Medical University, Guangzhou, Guangdong, China.
Min-Jie MaoDepartment of Laboratory Medicine, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, Guangdong, China.
Yuan TanDepartment of Clinical Laboratory, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, 2528000, Guangdong, China.
Xiang-Qiong MoDepartment of Gastrointestinal Surgery, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, Guangdong, China.
Xiao-Jun MengDepartment of Endocrinology, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, Guangdong, China.
Meng-Ting CaoDepartment of Clinical Laboratory, The First Affiliated Hospital of University of South China, Hengyang, Hunan, China.
Chu-Yu ZhongDepartment of Geriatrics, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, Guangdong, China.
Yan LiuDepartment of Clinical Laboratory, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, 2528000, Guangdong, China.
Hong ShanGuangdong Provincial Key Laboratory of Biomedical Imaging, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, 2528000, Guangdong, China. shanhong@mail.sysu.edu.cn.
Guan-Min JiangDepartment of Clinical Laboratory, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, 2528000, Guangdong, China. jianggm3@mail.sysu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is a highly conserved catabolic process that mediates degradation of pernicious or dysfunctional cellular components, such as invasive pathogens, senescent proteins, and organelles. It can promote or suppress tumor development, so it is a "double-edged sword" in tumors that depends on the cell and tissue types and the stages of tumor. The epithelial-mesenchymal transition (EMT) is a complex biological trans-differentiation process that allows epithelial cells to transiently obtain mesenchymal features, including motility and metastatic potential. EMT is considered as an important contributor to the invasion and metastasis of cancers. Thus, clarifying the crosstalk between autophagy and EMT will provide novel targets for cancer therapy. It was reported that EMT-related signal pathways have an impact on autophagy; conversely, autophagy activation can suppress or strengthen EMT by regulating various signaling pathways. On one hand, autophagy activation provides energy and basic nutrients for EMT during metastatic spreading, which assists cells to survive in stressful environmental and intracellular conditions. On the other hand, autophagy, acting as a cancer-suppressive function, is inclined to hinder metastasis by selectively down-regulating critical transcription factors of EMT in the early phases. Therefore, the inhibition of EMT by autophagy inhibitors or activators might be a novel strategy that provides thought and enlightenment for the treatment of cancer. In this article, we discuss in detail the role of autophagy and EMT in the development of cancers, the regulatory mechanisms between autophagy and EMT, the effects of autophagy inhibition or activation on EMT, and the potential applications in anticancer therapy.

Indexed as

AutophagyAntineoplastic AgentsEpithelial-Mesenchymal TransitionGene Regulatory NetworksHumansMolecular Targeted TherapyNeoplasm MetastasisNeoplasmsSignal TransductionAntineoplastic AgentsAnticancer therapyAutophagyCancer metastasisEpithelial-mesenchymal transition

Identifiers

PMID31126310
PMCPMC6533683

What OpenQuestion holds

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LicenceCC BY
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.