Evidence map›Paper›PMID 34797443›Full record

ArticleDigestive diseases and sciences2022

Troponin C-1 Activated by E2F1 Accelerates Gastric Cancer Progression via Regulating TGF-β/Smad Signaling.

Can Fang, Xinxin Zhang, Chengyan Li, Fang Liu, Hui Liu

Abstract read
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In one paragraph

Article in Digestive diseases and sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

8 citing papers in PubMed, 9 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

5 authors at 1 institution in 1 country.

Can Fang *Department of Gastroenterology, Yantai Affiliated Hospital of Binzhou Medical University, 717 Jinbu Street, Muping District, Yantai, 264100, Shandong, People's Republic of China.
Xinxin Zhang *Department of Gastroenterology, Yantai Affiliated Hospital of Binzhou Medical University, 717 Jinbu Street, Muping District, Yantai, 264100, Shandong, People's Republic of China.
Chengyan LiDepartment of Digestive Endoscopy Room, Yantai Affiliated Hospital of Binzhou Medical University, Yantai, 264100, Shandong, People's Republic of China.
Fang LiuDepartment of Gastroenterology, Yantai Affiliated Hospital of Binzhou Medical University, 717 Jinbu Street, Muping District, Yantai, 264100, Shandong, People's Republic of China.
Hui LiuDepartment of Gastroenterology, Yantai Affiliated Hospital of Binzhou Medical University, 717 Jinbu Street, Muping District, Yantai, 264100, Shandong, People's Republic of China. hui1973l@163.com.ORCID 0000-0003-4275-5383
Binzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTroponin C-1 (TNNC1) has been previously characterized as an oncogenic gene.

aimsThis study aimed to reveal the roles of TNNC1 in gastric cancer and the potential underlying mechanisms.

methodsTNNC1 siRNAs and TNNC1 overexpression plasmid were used to alter its expression in AGS, MKN45, and HGC-27 cells. CCK-8 assay, colony formation, EdU assay, flow cytometry, transwell assay, and scratch test were conducted to measure the phenotype changes. In vivo effects of TNNC1 silence were confirmed by using a xenograft mouse model. Bioinformatics analysis was conducted to screen out the transcription factor and downstream signaling of TNNC1.

resultsTNNC1 was highly expressed in gastric cancer tissues and cell lines, and its expression was associated with poor prognosis. TNNC1 silence suppressed the proliferation, migration, and invasion of AGS and MKN45 cells. However, TNNC1 silence induced apoptosis by mediating the cleavage of caspase-3 and caspase-9. Overexpression of TNNC1 in HGC-27 cells led to the contrary effects. The anti-tumor effects of TNNC1 silence were also confirmed in a xenograft animal model. E2F1 was validated as an upstream transcription factor of TNNC1. Effects of TNNC1 silence on AGS cell migration and invasion were attenuated by E2F1 overexpression. Besides, TGF-β/Smad was a downstream signaling pathway of TNNC1. The anti-tumor impacts of TNNC1 silence were weaken by SB431542 (a specific inhibitor of TGF-β signaling) while accelerated by TGF-β.

conclusionTNNC1 activated by E2F1 functioned as an oncogenic gene through regulating TGF-β/Smad signaling. TNNC1 was suggested as a potential molecular drug target of gastric cancer.

Indexed as

E2F1 Transcription FactorStomach NeoplasmsTroponin CAnimalsCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansMiceSmad ProteinsTransforming Growth Factor betaE2F1 protein, humanE2F1 Transcription FactorSmad ProteinsTransforming Growth Factor betaTroponin CE2F1Gastric cancerSmad signalingTGF-βTroponin C-1

Identifiers

PMID34797443
OpenAlexW3214608023

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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.