Evidence map›Paper›PMID 32195017›Full record

ArticleAmerican journal of cancer research2020

FLNA promotes chemoresistance of colorectal cancer through inducing epithelial-mesenchymal transition and smad2 signaling pathway.

Mengmeng Cheng, Yannan Jiang, Han Yang, Dongyao Zhao, Longyu Li, Xinyu Liu

Open access · greenAbstract read
In one paragraph

Article in American journal of cancer research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.1field-weighted citation impact, top 11% 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

33 citing papers in PubMed, 41 citations in OpenAlex.

  1. Filamin C activates MAPK/ERK signaling to facilitate epithelial-mesenchymal transition in bladder cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 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

6 authors at 1 institution in 1 country.

Mengmeng ChengDivision of Gastroenterology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology Wuhan 430022, China.
Yannan JiangKey Laboratory, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital Suzhou, China.
Han YangDepartment of Hepatobiliary and Pancreatic Surgery, The First Affiliated Hospital of Zhengzhou University No. 1 Jianshe East, Zhengzhou, Henan, China.
Dongyao ZhaoDepartment of Gastroenterology, The First Affiliated Hospital of Zhengzhou University No. 1 Jianshe East, Zhengzhou, Henan, China.
Longyu LiDepartment of Pharmacy, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, Henan Provincial People's Hospital of Henan University Zhengzhou 450003, Henan, China.
Xinyu LiuDepartment of General Surgery, The First Affiliated Hospital of Zhengzhou University No. 1 Jianshe East, Zhengzhou, Henan, China.
Huazhong University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chemoresistance is a leading cause of tumor relapse and treatment failure in colorectal cancer (CRC) patients and is correlated with epithelial-mesenchymal transition (EMT). This study was aimed to explore the mechanism of EMT in chemoresistant CRC. Bioinformatic method was used to screen differentially expressed genes between 5-FU sensitive and resistant CRC cells. Immunohistochemistry staining was utilized to analyze the expression of FLNA in CRC tissues. The roles of FLNA in chemoresistance were validated via loss-of-function and gain-of-function experiments in vitro and in an orthotopic CRC animal model. The regulation of c-Met signaling by FLNA was explored via Co-Immunoprecipitation and luciferase reporter assays. Our results suggested FLNA directly regulated the metastasis and EMT of chemoresistant CRC cells. Moreover, c-Met-AKT mediated ser2152 phosphorylation of FLNA was demonstrated to be correlated with EMT. In turn, FLNA enhanced c-Met promoter activity by its interaction with smad2. Clinically, the expression of FLNA was significantly associated with c-Met protein levels in CRC tissues. These data established that FLNA could be a novel and reliable CRC marker and a potential therapeutic target against CRC.

Indexed as

chemoresistanceColorectal cancerEMTFLNAsmad2

Identifiers

PMID32195017
PMCPMC7061762
OpenAlexW3012863471

What OpenQuestion holds

Textmetadata
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.