Evidence map›Paper›PMID 34853810›Full record

ArticleMolecular therapy oncolytics2021

RUNX1/EGFR pathway contributes to STAT3 activation and tumor growth caused by hyperactivated mTORC1.

Wei Lin, Xiaofeng Wan, Anjiang Sun, Meng Zhou, Xu Chen, Yanling Li, Zixi Wang, Hailiang Huang, Hongwu Li, Xianguo Chen and 2 more

Open access · goldAbstract read
In one paragraph

Article in Molecular therapy oncolytics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
6.2field-weighted citation impact, top 2% 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

15 citing papers in PubMed, 47 citations in OpenAlex.

  1. Targeting Runx1 Slows Cyst Growth in Autosomal Dominant Polycystic Kidney Disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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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

12 authors at 1 institution in 1 country.

Wei LinDepartment of Stomatology, The First Affiliated Hospital of Anhui Medical University, Hefei 230031, China.
Xiaofeng WanDepartment of Biochemistry & Molecular Biology, School of Basic Medicine, Anhui Medical University, Hefei 230031, China.
Anjiang SunDepartment of Biochemistry & Molecular Biology, School of Basic Medicine, Anhui Medical University, Hefei 230031, China.
Meng ZhouDepartment of Biochemistry & Molecular Biology, School of Basic Medicine, Anhui Medical University, Hefei 230031, China.
Xu ChenDepartment of Biochemistry & Molecular Biology, School of Basic Medicine, Anhui Medical University, Hefei 230031, China.
Yanling LiDepartment of Biochemistry & Molecular Biology, School of Basic Medicine, Anhui Medical University, Hefei 230031, China.
Zixi WangDepartment of Biochemistry & Molecular Biology, School of Basic Medicine, Anhui Medical University, Hefei 230031, China.
Hailiang HuangDepartment of Biochemistry & Molecular Biology, School of Basic Medicine, Anhui Medical University, Hefei 230031, China.
Hongwu LiDepartment of Otorhinolaryngology, Head & Neck Surgery, The Fourth Affiliated Hospital of Anhui Medical University, Hefei 230031, China.
Xianguo ChenDepartment of Urology, The First Affiliated Hospital of Anhui Medical University, Hefei 230031, China.
Juan HuaDepartment of Biochemistry & Molecular Biology, School of Basic Medicine, Anhui Medical University, Hefei 230031, China.
Xiaojun ZhaDepartment of Biochemistry & Molecular Biology, School of Basic Medicine, Anhui Medical University, Hefei 230031, China.
Anhui Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Loss of function of tuberous sclerosis complex 1 or 2 (TSC1 or TSC2) leads to the activation of mammalian target of rapamycin complex 1 (mTORC1). Hyperactivated mTORC1 plays a critical role in tumor growth, but the underlying mechanism is still not completely elucidated. Here, by analyzing Tsc1- or Tsc2-null mouse embryonic fibroblasts, rat Tsc2-null ELT3 cells, and human cancer cells, we present evidence for the involvement of epidermal growth factor receptor (EGFR) as a downstream target of mTORC1 in tumor growth. We show that mTORC1 leads to increased EGFR expression through upregulation of runt-related transcriptional factor 1 (RUNX1). Knockdown of EGFR impairs proliferation and tumoral growth of Tsc-deficient cells, while overexpression of EGFR promotes the proliferation of the control cells. Moreover, the mTOR signaling pathway has been shown to be positively correlated with EGFR in human cancers. In addition, we demonstrated that EGFR enhances cell growth through activation of signal transducer and activator of transcription 3 (STAT3). We conclude that activation of the RUNX1/EGFR/STAT3 signaling pathway contributes to tumorigenesis caused by hyperactivated mTORC1 and should be targeted for the treatment of mTORC1-related tumors, particularly TSC.

Indexed as

EGFRmTORRUNX1STAT3tuberous sclerosis complextumorigenesis

Identifiers

PMID34853810
PMCPMC8605091
OpenAlexW3211142434

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.