Evidence map›Paper›PMID 33001583›Full record

ArticleThoracic cancer2020

BCAR1 promotes proliferation and cell growth in lung adenocarcinoma via upregulation of POLR2A.

Chun-Guo Mao, Sha-Sha Jiang, Cheng Shen, Tan Long, Hua Jin, Qun-You Tan, Bo Deng

Open access · goldAbstract read
In one paragraph

Article in Thoracic cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 25% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.

  1. Pooled it
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  12. Novel germline mutation in lung cancer pedigrees establishesAnnals of translational medicine · 2022
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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

7 authors at 1 institution in 2 countries.

Chun-Guo Mao *Thoracic Surgery Department, Institute of Surgery Research, Daping Hospital, Army Medical University, Chongqing, China.
Sha-Sha Jiang *Thoracic Surgery Department, Institute of Surgery Research, Daping Hospital, Army Medical University, Chongqing, China.
Cheng Shen *Thoracic Surgery Department, Institute of Surgery Research, Daping Hospital, Army Medical University, Chongqing, China.
Tan LongThoracic Surgery Department, Institute of Surgery Research, Daping Hospital, Army Medical University, Chongqing, China.
Hua JinThoracic Surgery Department, Institute of Surgery Research, Daping Hospital, Army Medical University, Chongqing, China.
Qun-You TanThoracic Surgery Department, Institute of Surgery Research, Daping Hospital, Army Medical University, Chongqing, China.
Bo DengThoracic Surgery Department, Institute of Surgery Research, Daping Hospital, Army Medical University, Chongqing, China.ORCID 0000-0003-3217-143X
Army Medical University · CN

Funding

National Natural Science Foundation of Chongqing City cstc2018jcyjAX0592National Natural Science Foundations of China (NSFC) 81572285
6 · The paper itself

Abstract

backgroundThis study was designed to investigate the effects of a novel carcinogenetic molecule, p130cas (breast cancer antiestrogen resistance protein 1 or BCAR1) on proliferation and cell growth in lung adenocarcinoma. The study also aimed to identify the possible underlying signal networks of BCAR1.

methodsFirst, we evaluated proliferation, cell colony formation, apoptosis, and cell cycle after BCAR1 was knocked out (KO) using CRISPR-Cas9 technology in H1975 and H1299 human lung adenocarcinoma cells. Subsequently, BCAR1 was upregulated in 293T cells and immunoprecipitation-mass spectrometry (IP-MS) was used with bioinformatics analysis to screen for potential networks of BCAR1 interacting proteins. Ultimately, we validated the correlated expressions of BCAR1 and a selected hub gene, RNA polymerase II subunit A (POLR2A), in 54 lung adenocarcinoma tissues, as well as in H1975 and H1299 cells.

resultsCell proliferation of H1975 and H1299 was significantly inhibited following BCAR1-KO. Colony formation of H1975 cells was also significantly decreased following BCAR1-KO. IP-MS demonstrated 419 potential proteins that may interact with BCAR1. Among them, 68 genes were significantly positively correlated to BCAR1 expression, as verified by TCGA. Six hub genes were revealed by PPI String. High expression of POLR2A, MAPK3, MOV10, and XAB2 predicted poor prognosis in lung adenocarcinoma, as verified by the K-M plotter database. POLR2A and MAPK3 are involved in both catalytic activity and transferase activity. POLR2A and BCAR1 were significantly increased in lung cancer tissues as compared with matched normal tissues. High expression of POLR2A was significantly positively correlated to BCAR1 overexpression and predicted poor prognosis in 54 lung cancer cases. POLR2A expression was significantly decreased following BCAR1-KO in H1975 and H1299 cells.

conclusionsBCAR1 promotes proliferation and cell growth, probably via upregulation of POLR2A and subsequent enhancement of catalytic and transferase activities. However, additional robust studies are required to elucidate the mechanisms involved.

Indexed as

Adenocarcinoma of LungCell Line, TumorCell ProliferationCrk-Associated Substrate ProteinDNA-Directed RNA PolymerasesFemaleHumansMaleMiddle AgedTransfectionUp-RegulationBCAR1 protein, humanCrk-Associated Substrate ProteinDNA-Directed RNA PolymerasesPOLR2A RNA polymerase, humanBCAR1cell growthcell proliferationlung adenocarcinomaPOLR2A

Identifiers

PMID33001583
PMCPMC7606008
OpenAlexW3089577694

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.