Evidence map›Paper›PMID 34992689›Full record

ArticleOncology letters2022

LINC01207 promotes prostate cancer progression by sponging miR-1182 to upregulate AKT3.

Daming Qin, Cheng Ni, Biyong Tan, Shengfei Huang, Bingqing Deng, Zhihua Huang

Open access · diamondAbstract read
In one paragraph

Article in Oncology letters, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 55% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. Review
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.

Daming QinDepartment of Radiology, The Central Hospital of Enshi Tujia and Miao Autonomous Prefecture, Enshi Clinical College of Wuhan University, Enshi, Hubei 445000, P.R. China.
Cheng NiDepartment of Radiology, The Central Hospital of Enshi Tujia and Miao Autonomous Prefecture, Enshi Clinical College of Wuhan University, Enshi, Hubei 445000, P.R. China.
Biyong TanDepartment of Radiology, The Central Hospital of Enshi Tujia and Miao Autonomous Prefecture, Enshi Clinical College of Wuhan University, Enshi, Hubei 445000, P.R. China.
Shengfei HuangDepartment of Radiology, The Central Hospital of Enshi Tujia and Miao Autonomous Prefecture, Enshi Clinical College of Wuhan University, Enshi, Hubei 445000, P.R. China.
Bingqing DengDepartment of Ultrasonography, The Central Hospital of Enshi Tujia and Miao Autonomous Prefecture, Enshi Clinical College of Wuhan University, Enshi, Hubei 445000, P.R. China.
Zhihua HuangDepartment of Ultrasonography, The Central Hospital of Enshi Tujia and Miao Autonomous Prefecture, Enshi Clinical College of Wuhan University, Enshi, Hubei 445000, P.R. China.
The Central Hospital of Enshi Tujia and Miao Autonomous Prefecture · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prostate cancer (PC) is recognized as a common malignancy in male patients. Long non-coding RNA (lncRNA) has been implicated in the development of PC. Recently, long intergenic non-protein coding RNA 1207 (LINC01207) has been reported to regulate the carcinogenesis of multiple cancer types. However, its role in the progression of PC remains to be determined. The aim of the present study was to investigate the expression profile, clinicopathological implication and molecular mechanism of action of LINC01207 in the progression of PC. LINC01207 expression levels were compared between PC tumor and paired normal tissue samples from The Cancer Genome Atlas. The expression of LINC01207 was further analyzed in PC cell lines and a normal prostatic cell line. The role of LINC01207 in proliferation, migration and invasion of PC cells was examined using small interfering RNA-mediated silencing. Western blot analysis was used to investigate the changes in protein levels underlying the mechanism of action of LINC01207. The role of LINC01207 in tumorigenesis was evaluated in a xenograft model. LINC01207 was upregulated in PC tumor samples from TCGA data compared with paired normal tissue. LINC01207 expression was significantly increased in PC cells and tumor tissues compared with in normal prostate cells (RWPE1) and normal prostate tissues, respectively. Furthermore, LINC01207 silencing inhibited PC cell proliferation and colony formation and induced apoptosis. Mechanistic experiments showed that LINC01207 promoted carcinogenesis by sponging miR-1182 to regulate the protein levels of AKT3 in PC cell lines. Thus, the findings of the present study indicated that LINC01207 might play a role in the tumorigenesis of PC and may serve as a therapeutic target for PC treatment.

Indexed as

AKT3LINC01207miR-1182prostate cancerThe Cancer Genome Atlas

Identifiers

PMID34992689
PMCPMC8721855
OpenAlexW4200290803

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.