Evidence map›Paper›PMID 34983878›Full record

ArticleAging2022

Deglycosylated EpCAM regulates proliferation by enhancing autophagy of breast cancer cells via PI3K/Akt/mTOR pathway.

Liu Yang, Qijun Wang, Qian Zhao, Fan Yang, Tingjiao Liu, Xiaohua Huang, Qiu Yan, Xuesong Yang

Open access · hybridAbstract read
In one paragraph

Article in Aging, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

12 citing papers in PubMed, 17 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

8 authors at 1 institution in 1 country.

Liu YangDepartment of Biochemistry and Molecular Biology, College of Basic Medicine Sciences, Dalian Medical University, Dalian, China.
Qijun WangDepartment of Biochemistry and Molecular Biology, College of Basic Medicine Sciences, Dalian Medical University, Dalian, China.
Qian ZhaoDepartment of Biochemistry and Molecular Biology, College of Basic Medicine Sciences, Dalian Medical University, Dalian, China.
Fan YangDepartment of Biochemistry and Molecular Biology, College of Basic Medicine Sciences, Dalian Medical University, Dalian, China.
Tingjiao LiuSection of Oral Pathology, College of Stomatology, Dalian Medical University, Dalian, China.
Xiaohua HuangDepartment of Clinical Biochemistry, College of Laboratory Science, Dalian Medical University, Dalian, China.
Qiu YanDepartment of Biochemistry and Molecular Biology, College of Basic Medicine Sciences, Dalian Medical University, Dalian, China.
Xuesong YangDepartment of Biochemistry and Molecular Biology, College of Basic Medicine Sciences, Dalian Medical University, Dalian, China.
Dalian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is an important regulator of cellular homeostasis and its dysregulation often results in cancer. Aberrant glycosylation induced by oncogenic transformation contributes to tumor invasion and metastasis. In a previous study, we have demonstrated that EpCAM, a glycosylation protein, is associated with cell growth and metastasis in breast cancer. But the effect of EpCAM glycosylation on autophagy is not clear. the precise mechanism of regulation remains largely unknown. In this study, breast cancer cells were transfected with N-glycosylation mutation EpCAM plasmid to express deglycosylated EpCAM. The result showed that deglycosylated EpCAM promoted autophagy in breast cancer cells. We further confirmed this conclusion with the activator (Rapamycin, RAP) and inhibitor (Wortmannin) of autophagy. We also found that deglycosylated EpCAM promoted apoptosis and inhibited proliferation through activating autophagy by suppressing Akt/mTOR signaling pathway in breast cancer cells. These findings represent a novel mechanism by which deglycosylated EpCAM inhibits proliferation by enhancing autophagy of breast cancer cells via PI3K/Akt/mTOR pathway. In conclusion, the combination of autophagy modulation and EpCAM targeted therapy is a promising therapeutic strategy in the treatment of breast cancer.

Indexed as

Breast NeoplasmsAntifungal AgentsAutophagyBiomarkersCell Line, TumorCell ProliferationEpithelial Cell Adhesion MoleculeFemaleGene Expression Regulation, NeoplasticGene SilencingHeterocyclic Compounds, 3-RingHumansPhosphatidylinositol 3-KinasesProtein Kinase InhibitorsProto-Oncogene Proteins c-aktSirolimusAntifungal AgentsBiomarkersEpithelial Cell Adhesion MoleculeHeterocyclic Compounds, 3-RingMK 2206MTOR protein, humanPhosphatidylinositol 3-KinasesProtein Kinase InhibitorsProto-Oncogene Proteins c-aktSirolimusTOR Serine-Threonine KinasesWortmanninautophagybreast cancerEpCAMglycosylationPI3K/Akt/mTOR

Identifiers

PMID34983878
PMCPMC8791205
OpenAlexW4205629565

What OpenQuestion holds

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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.