Evidence map›Paper›PMID 35570225›Full record

ArticleMedical oncology (Northwood, London, England)2022

Long non-coding RNA AC245100.4 contributes to prostate cancer migration via regulating PAR2 and activating p38-MAPK pathway.

Chi Liu, Shan Jiang, Hui Xie, Huizhen Jia, Rou Li, Ke Zhang, Nan Wang, Ping Lin, Xiaoguang Yu

Abstract read
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In one paragraph

Article in Medical oncology (Northwood, London, England), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

6 citing papers in PubMed, 22 citations in OpenAlex.

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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

9 authors at 1 institution in 1 country.

Chi Liu *Department of Biochemistry & Molecular Biology, Harbin Medical University, Harbin, 150086, Heilongjiang, China.
Shan Jiang *Department of Biochemistry & Molecular Biology, Harbin Medical University, Harbin, 150086, Heilongjiang, China.
Hui XieTeaching Experiment Center of Biotechnology, Harbin Medical University, Harbin, 150086, Heilongjiang, China.
Huizhen JiaDepartment of Biochemistry & Molecular Biology, Harbin Medical University, Harbin, 150086, Heilongjiang, China.
Rou LiDepartment of Biochemistry & Molecular Biology, Harbin Medical University, Harbin, 150086, Heilongjiang, China.
Ke ZhangDepartment of Biochemistry & Molecular Biology, Harbin Medical University, Harbin, 150086, Heilongjiang, China.
Nan WangDepartment of Biochemistry & Molecular Biology, Harbin Medical University, Harbin, 150086, Heilongjiang, China.
Ping LinDepartment of Biochemistry & Molecular Biology, Harbin Medical University, Harbin, 150086, Heilongjiang, China. linp@hrbmu.edu.cn.
Xiaoguang YuDepartment of Biochemistry & Molecular Biology, Harbin Medical University, Harbin, 150086, Heilongjiang, China. yuxg@hrbmu.edu.cn.ORCID http://orcid.org/0000-0002-6293-4285
Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prostate cancer (PCa) is the second most common cause of cancer-related mortality in men. Prostate cancer metastasis usually observed at the last stage is the major cause of prostate cancer-related death. Long non-coding RNAs were reported to be involved in tumorigenesis and progression of prostate cancer. This study aimed to investigate the effects and related mechanisms of AC245100.4 in prostate cancer. Knockdown and overexpression of AC245100.4 was used to detect the effect of AC245100.4 on cell migration. qRT-PCR was used to confirm the downstream target of AC245100.4. RAP-MS was used to find pathways related to AC245100.4. Western blot was performed to detect the expression of p-p38 and p38. We found that AC245100.4 promoted the migration of prostate cancer cells via regulating PAR2. The AC245100.4 or PAR2 knockdown resulted in a decrease in Vimentin but an increase in E-cadherin protein levels, while the AC245100.4 or PAR2 overexpression got the opposite results. Moreover, we discovered that AC245100.4 activated the p38-MAPK via regulating PAR2. In brief, these results have suggested that AC245100.4 and PAR2 served as oncogenic factors in cellular migration in PCa cells.

Indexed as

Prostatic NeoplasmsRNA, Long NoncodingCarcinogenesisCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansMalep38 Mitogen-Activated Protein Kinasesp38 Mitogen-Activated Protein KinasesRNA, Long NoncodingAC245100.4Migrationp38-MAPKPAR2Prostate cancer

Identifiers

PMID35570225
OpenAlexW4280492199

What Socratic holds

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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 Socratic graph.