Evidence map›Paper›PMID 30962766›Full record

ArticleCancer cell international2019

LncRNA BCAR4, targeting to miR-665/STAT3 signaling, maintains cancer stem cells stemness and promotes tumorigenicity in colorectal cancer.

Shurui Ouyang, Xin Zhou, Zhengquan Chen, Maijian Wang, Xinbin Zheng, Ming Xie

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
4.4field-weighted citation impact, top 4% 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

54 citing papers in PubMed, 81 citations in OpenAlex.

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  11. Inhibiting MEK1 R189 citrullination enhances the chemosensitivity of docetaxel to multiple tumour cells.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023
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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.

Shurui OuyangDepartment of Gastrointestinal, The Affiliated Hospital of Zunyi Medical College, Huichuan Area, Dalian Road 149, Zunyi, 563000 Guizhou Province China.
Xin ZhouDepartment of Gastrointestinal, The Affiliated Hospital of Zunyi Medical College, Huichuan Area, Dalian Road 149, Zunyi, 563000 Guizhou Province China.
Zhengquan ChenDepartment of Gastrointestinal, The Affiliated Hospital of Zunyi Medical College, Huichuan Area, Dalian Road 149, Zunyi, 563000 Guizhou Province China.
Maijian WangDepartment of Gastrointestinal, The Affiliated Hospital of Zunyi Medical College, Huichuan Area, Dalian Road 149, Zunyi, 563000 Guizhou Province China.
Xinbin ZhengDepartment of Gastrointestinal, The Affiliated Hospital of Zunyi Medical College, Huichuan Area, Dalian Road 149, Zunyi, 563000 Guizhou Province China.
Ming XieDepartment of Gastrointestinal, The Affiliated Hospital of Zunyi Medical College, Huichuan Area, Dalian Road 149, Zunyi, 563000 Guizhou Province China.ORCID 0000-0002-2072-5549
Affiliated Hospital of Zunyi Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBreast cancer anti-estrogen resistance 4 (BCAR4) is closely associated with colorectal cancer (CRC) initiation and propagation. However, the mechanisms underlying BCAR4 function in colon cancer remains largely unknown. In this study, we hypothesized that BCAR4 could regulate colon cancer stem/initiating cells (CSC) function and further facilitates the colon cancer progression.

methodsqRT-PCR was used to examine the expression of BCAR4 and various CSC markers. FACS, acetaldehyde dehydrogenase (ALDH) activity and western blot assays were applicable to test the expression of CSC markers. CCK8, tumorsphere formation and transwell assays were adopted to examine the capacity of CRC cells proliferation, self-renewal and migration. Pull down assay was used to test the interaction between BCAR4 and miR-665. Luciferase reporter assay was used to examine the interaction of miR-665 and activators of transcription (STAT3). In vivo tumor xenograft study was used to verify the malignancy of CRC cells with inhibition of BCAR4.

resultsBreast cancer anti-estrogen resistance 4 was highly expressed in both CRC cells and stem/initiating cells. In addition, overexpression of BCAR4 facilitated the maintenance of ALDH positive cells (a type of cancer stem/initiating cells) stemness and promoted ALDH+ cells proliferation and migration. Inhibition of BCAR4 restricted ALDH+ cells proliferation and migration. We further proved that miR-665 was the target of BCAR4 and subsequently activated signal transducers and STAT3 signaling which is an important pathway in cancer stem cells self-renewal.

conclusionsBreast cancer anti-estrogen resistance 4 promotes the CRC cells stemness through targeting to miR-665/STAT3 signaling and identification of the BCAR4 in CRC stem cells provides a new insight into CRC diagnosis, treatment, prognosis and next-step translational investigations.

Indexed as

ALDH+ cancer stem/initiating cellsBreast cancer anti-estrogen resistance 4 (BCAR4)Colorectal cancer (CRC)LncRNAmiR-665

Identifiers

PMID30962766
PMCPMC6438025
OpenAlexW2940568549

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LicenceCC BY
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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.