Evidence map›Paper›PMID 32038723›Full record

ArticleFrontiers in genetics2019

Linc00662 Promotes Tumorigenesis and Progression by Regulating miR-497-5p/AVL9 Axis in Colorectal Cancer.

Huaiming Wang, Mengya Yu, Weixian Hu, Xin Chen, Yuwen Luo, Xiaosheng Lin, Yongming Zeng, Xueqing Yao

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Frontiers in genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
4.0field-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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 1 country.

Huaiming WangThe Second School of Clinical Medicine, Southern Medical University, Guangzhou, China.
Mengya YuThe Second School of Clinical Medicine, Southern Medical University, Guangzhou, China.
Weixian HuThe Second School of Clinical Medicine, Southern Medical University, Guangzhou, China.
Xin ChenThe Second School of Clinical Medicine, Southern Medical University, Guangzhou, China.
Yuwen LuoThe Second School of Clinical Medicine, Southern Medical University, Guangzhou, China.
Xiaosheng LinDepartment of Gastrointestinal Surgery, The First Affiliated Hospital of Shantou University Medical College, Shantou, China.
Yongming ZengDepartment of Gastrointestinal Surgery, The First Affiliated Hospital of Shantou University Medical College, Shantou, China.
Xueqing YaoThe Second School of Clinical Medicine, Southern Medical University, Guangzhou, China.
Guangdong Provincial People's Hospital · CNFirst Affiliated Hospital of Shantou University Medical College · CNGuangdong Academy of Medical Sciences · CNSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRecently, multiple lines of evidence have demonstrated that linc00662 serves as an oncogene in various cancers. However, the exact mechanism of oncogenesis mediated by linc00662 in colorectal cancer (CRC) remains unknown. In this study, we aimed to explore the biological role of linc00662 in the regulation of CRC progression.

methodsBoth gene expression omnibus (GEO) and the cancer genome atlas (TCGA) datasets were used to evaluate the expression of linc00662. RT-qPCR was used to analyze the expression of linc00662, miR-497-5p, and

resultsIn this study, we found that the expression of linc00662 was significantly upregulated in CRC tissues compared to normal tissues and positively correlated with tissue differentiation, T stage, and lymphatic metastasis. Further, our data showed that the expression of linc00662 was positively associated with lymph node metastasis, TMN stage, and poor-moderate differentiation. Patients with higher linc00662 expression level were more likely to have poorer overall survival. Knockdown of linc00662 inhibited CRC cell growth, induced cell apoptosis, triggered cell cycle arrest at G2/M phase, and suppressed cell migration and invasion through regulating the EMT pathway. Further, mechanistic studies revealed that knockdown of linc00662 significantly reduced the expression of

conclusionsLinc00662 was significantly upregulated in CRC, and mediated CRC progression and metastasis by competing with miR-497-5p to modulate the expression of

Indexed as

biomarkercolorectal cancer (CRC)linc00662prognosisproliferation

Identifiers

PMID32038723
PMCPMC6993758
OpenAlexW3000927381

What Socratic holds

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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 Socratic graph.