Evidence map›Paper›PMID 33247506›Full record

ArticleCancer science2021

c-KIT-ERK1/2 signaling activated ELK1 and upregulated carcinoembryonic antigen expression to promote colorectal cancer progression.

Jian Ma, Xiaohui Liu, Hong Chen, Muhammad Khawar Abbas, Liu Yang, Haimei Sun, Tingyi Sun, Bo Wu, Shu Yang, Deshan Zhou

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 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
2.5field-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

15 citing papers in PubMed, 27 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 1 institution in 1 country.

Jian MaDepartment of Histology and Embryology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.ORCID https://orcid.org/0000-0001-6921-5278
Xiaohui LiuDepartment of Histology and Embryology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Hong ChenDepartment of Histology and Embryology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Muhammad Khawar AbbasDepartment of Histology and Embryology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Liu YangDepartment of Histology and Embryology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Haimei SunDepartment of Histology and Embryology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Tingyi SunDepartment of Histology and Embryology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Bo WuDepartment of Histology and Embryology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Shu YangDepartment of Histology and Embryology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Deshan ZhouDepartment of Histology and Embryology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Capital Medical University · CN

Funding

Beijing Natural Science Foundation 5172008Beijing Natural Science Foundation 7172021National Natural Science Foundation of China 31771332National Natural Science Foundation of China 81572322Natural Science Foundation of Capital Medical University PYZ19069Support Project of High-level Teachers in Beijing Municipal Universities in the Period of 13th Five-year plan IDHT20170516
6 · The paper itself

Abstract

Carcinoembryonic antigen (CEA) is highly expressed in embryo and colorectal cancer (CRC) and has been widely used as a marker for CRC. Emerging evidence has demonstrated that elevated CEA levels promote CRC progression. However, the mechanism of the increased CEA expression in patients with primary and recurrent CRC is still an open question. In this study, we showed that c-KIT, ELK1, and CEA were hyperexpressed in patients with CRC, especially patients with recurrent disease. From bioinformatics analysis, we picked ELK1 as a candidate transcription factor (TF) for CEA; the binding site of ELK1 within the CEA promoter was confirmed by chromatin immunoprecipitation and dual luciferase reporter assays. Overexpression of ELK1 increased CEA expression in vitro, while knockdown of ELK1 decreased CEA. Upregulated ELK1 promoted the adhesion, migration, and invasion of CRC cells, however knockdown of CEA blocked the activities of ELK1-overexpressed CRC cells. Furthermore, we explored the role of c-KIT-ERK1/2 signaling in activation of ELK1. Blocking c-KIT signaling using Imatinib or ISCK03 reduced p-ELK1 expression and consequently decreased CEA levels in CRC cells, as did blocking the ERK1/2 pathway by U0126. Compared with wild type littermates, the c-kit loss-of-functional Wads

Indexed as

AnimalsCarcinoembryonic AntigenColorectal NeoplasmsDisease Progressionets-Domain Protein Elk-1Gene Expression Regulation, NeoplasticHumansMAP Kinase Signaling SystemMiceMice, Inbred C57BLMice, Mutant StrainsProto-Oncogene Proteins c-kitUp-RegulationCarcinoembryonic AntigenELK1 protein, humanets-Domain Protein Elk-1KIT protein, humanProto-Oncogene Proteins c-kitCEAc-KITcolorectal cancerELK1targeted therapy

Identifiers

PMID33247506
PMCPMC7894012
OpenAlexW3107681451

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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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.