Evidence map›Paper›PMID 32110058›Full record

ArticleOncoTargets and therapy2020

FOXC2 Promotes Oxaliplatin Resistance by Inducing Epithelial-Mesenchymal Transition via MAPK/ERK Signaling in Colorectal Cancer.

Yihong Chen, Ganlu Deng, Yaojie Fu, Ying Han, Cao Guo, Ling Yin, Changjing Cai, Hong Shen, Shaobin Wu, Shan Zeng

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

29 citing papers in PubMed, 45 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

10 authors at 2 institutions in 1 country.

Yihong ChenDepartment of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, People's Republic of China.
Ganlu DengDepartment of Oncology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, People's Republic of China.
Yaojie FuDepartment of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, People's Republic of China.
Ying HanDepartment of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, People's Republic of China.
Cao GuoDepartment of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, People's Republic of China.
Ling YinDepartment of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, People's Republic of China.
Changjing CaiDepartment of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, People's Republic of China.
Hong ShenDepartment of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, People's Republic of China.ORCID 0000-0003-0593-7268
Shaobin WuDepartment of Gastrointestinal Surgery, Xiangya Hospital, Central South University, Changsha, Hunan 410008, People's Republic of China.
Shan ZengDepartment of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, People's Republic of China.
Central South University · CNGuangxi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChemoresistance is a major obstacle to improving the survival rate of colorectal cancer (CRC) patients. Forkhead box protein C2 (FOXC2), a member of the forkhead box (Fox) transcription factor family, is reported to be an important regulator of epithelial-to-mesenchymal transition (EMT) and plays a key role in tumor progression. However, little is known about the effects of FOXC2 on oxaliplatin (OXA) resistance in CRC.

methodsOXA-resistant cells were generated from HCT116 cells. CCK-8, colony formation, flow cytometry and Transwell assays were used to compare the characteristics of OXA-resistant HCT116/OXA cells and the corresponding parental HCT116 cells. The expression of FOXC2 was confirmed by qRT-PCR and Western blotting in HCT116/OXA and HCT116 cells. Gain- and loss-of-function assays were performed to evaluate the effects of FOXC2 on OXA sensitivity and EMT in HCT116/OXA and HCT116 cells both in vitro and in vivo, and the possible molecular mechanisms were investigated.

resultsThe relative expression of FOXC2 was significantly increased in HCT116/OXA cells compared with the parental HCT116 cells. Upregulation of FOXC2 in HCT116 cells reduced OXA sensitivity and promoted EMT. However, knockdown of FOXC2 in HCT116/OXA cells markedly increased the in vitro and in vivo sensitivity of HCT116/OXA cells to OXA by regulating EMT progression. Furthermore, FOXC2 activated MAPK/ERK signaling, and blockade of ERK attenuated FOXC2-induced EMT and FOXC2-enhanced OXA resistance.

conclusionFOXC2 induced EMT to promote oxaliplatin resistance by activating the MAPK/ERK signaling pathway. FOXC2 may be a potential therapeutic target for overcoming OXA resistance in human CRC.

Indexed as

colorectal cancerepithelial-mesenchymal transitionforkhead box protein C2MAPK/ERKoxaliplatin resistance

Identifiers

PMID32110058
PMCPMC7041600
OpenAlexW3007064358

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.