Evidence map›Paper›PMID 31289493›Full record

ArticleOncology letters2019

ERCC6L promotes cell growth and invasion in human colorectal cancer.

Yang Xie, Jun Yu, Feng Wang, Mengying Li, Xiao Qiu, Yuting Liu, Jian Qi

Open access · diamondAbstract read
In one paragraph

Article in Oncology letters, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.1field-weighted citation impact, top 23% 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, 21 citations in OpenAlex.

  1. Review
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  6. Expression profiling of luminal B breast tumor in Indian women.Journal of cancer research and clinical oncology · 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

7 authors at 2 institutions in 1 country.

Yang XieDepartment of Gastroenterology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei 430071, P.R. China.
Jun YuDepartment of Gastroenterology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei 430071, P.R. China.
Feng WangDepartment of Gastroenterology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei 430071, P.R. China.
Mengying LiDepartment of Gastroenterology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei 430071, P.R. China.
Xiao QiuDepartment of Gastroenterology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei 430071, P.R. China.
Yuting LiuDepartment of Gastroenterology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei 430071, P.R. China.
Jian QiDepartment of Gastroenterology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei 430071, P.R. China.
Wuhan University · CNZhongnan Hospital of Wuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Excision repair cross-complementation group 6 like (ERCC6L), a recently discovered DNA helicase, has been demonstrated to be highly expressed in a variety of human cancer types. However, the precise role of ERCC6L in colorectal cancer (CRC) remains unclear. The current study aimed to investigate the potential role of ERCC6L in the development and progression of CRC. Reverse transcription-quantitative polymerase chain reaction, western blot analysis and immunohistochemistry were used to detect the expression level of ERCC6L in 30 matched pairs of CRC and adjacent noncancerous tissues. The function of ERCC6L in cell proliferation, cycle, apoptosis, invasion and colony formation was examined in CRC cell lines. ERCC6L was revealed to be highly expressed in CRC tissues and cell lines compared with normal controls (P<0.05). The expression level of ERCC6L was significantly associated with tumor size (P<0.05), but not with other clinical features, including age, gender, differentiation and clinical stage. It was identified that reducing ERCC6L expression using small interfering RNA significantly inhibited the proliferation and colony-forming ability of CRC cell lines. Flow cytometric analysis demonstrated that ERCC6L knockdown in CRC cells inhibited cell cycle progression and increased the number of cells in the G0/G1 phase without affecting apoptosis. Furthermore, ERCC6L knockdown markedly decreased the number of invading CRC cells compared with control cells. These results suggest that ERCC6L promotes the growth and invasion of CRC cells, and ERCC6L may be a potential new target for cancer therapy.

Indexed as

colorectal cancerexcision repair cross-complementation group 6 likeimmunohistochemistryproliferationsRNA interference

Identifiers

PMID31289493
PMCPMC6540252
OpenAlexW2942759342

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.