Evidence map›Paper›PMID 35022330›Full record

ArticleAging2022

PSMA3-AS1 induced by transcription factor PAX5 promotes cholangiocarcinoma proliferation, migration and invasion by sponging miR-376a-3p to up-regulate LAMC1.

Dongsheng Sun, Fujun Li, Lang Liu, Shaobo Yu, Haicun Wang, Xin Gao, Guanglin Liu, Yuqiao Zhao, Gongcai Qiu, Xingming Jiang

Open access · hybridAbstract read
In one paragraph

Article in Aging, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 8% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.

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  11. The Expression Patterns and Implications ofInternational journal of molecular 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

10 authors at 3 institutions in 1 country.

Dongsheng SunDepartment of General Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin 150086, China.
Fujun LiDepartment of General Surgery, South China Hospital, Health Science Center, Shenzhen University, Shenzhen 518116, China.
Lang LiuDepartment of General Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin 150086, China.
Shaobo YuDepartment of General Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin 150086, China.
Haicun WangDepartment of General Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin 150086, China.
Xin GaoDepartment of General Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin 150086, China.
Guanglin LiuDepartment of General Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin 150086, China.
Yuqiao ZhaoDepartment of General Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin 150086, China.
Gongcai QiuDepartment of General Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin 150086, China.
Xingming JiangDepartment of General Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin 150086, China.
Second Affiliated Hospital of Harbin Medical University · CNHarbin Medical University · CNShenzhen University Health Science Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long noncoding RNAs (lncRNAs) have been reported to exhibit a crucial regulatory role in tumor progression, including cholangiocarcinoma (CCA). As a promising lncRNA, proteasome 20S subunit alpha 3 antisense RNA 1 (PSMA3-AS1) is involved in development of various tumors. However, the role and function of PSMA3-AS1 in CCA remain unclear. The aim of this study is to examine the expression, function, mechanism, and clinical significance of PSMA3-AS1 in CCA development. By TCGA database analysis, we found that PSMA3-AS1 was overexpressed in CCA. Consistent with the TCGA analysis, PSMA3-AS1 was significantly overexpressed in CCA tissues and cells by RT-qPCR. Upregulated PSMA3-AS1 was related to lymph node invasion, advanced TNM stage and poor survival, and was an independent risk factor of prognosis for CCA patients. Functionally, CCK-8, EdU and colony formation assays confirmed that upregulated PSMA3-AS1 promoted CCA cell proliferation, whereas downregulated PSMA3-AS1 inhibited proliferation. This result was further confirmed by subcutaneous tumor formation in nude mice. Wound healing and transwell assays confirmed that increased PSMA3-AS1 promoted CCA cell migration and invasion, whereas decreased PSMA3-AS1 inhibited these biological phenotypes. In addition, PSMA3-AS1 promoted the EMT process of CCA by downregulating E-cadherin and upregulating N-cadherin and vimentin. Mechanistically, transcription factor PAX5 bound to the promoter region of PSMA3-AS1 and promoted its transcription. Simultaneously, PSMA3-AS1 primarily localized in the cytoplasm could competitively bind miR-376a-3p to upregulate LAMC1, thereby accelerating CCA progression. This study uncovers that PSMA3-AS1 functions as a cancer-promoting gene in CCA, and PAX5/PSMA3-AS1/miR-376a-3p/LAMC1 axis plays a vital role in CCA development.

Indexed as

Bile Duct NeoplasmsCell LineCell MovementCell ProliferationCholangiocarcinomaGene Expression RegulationHumansLamininMicroRNAsPAX5 Transcription FactorRNA, Long NoncodingUp-RegulationLamininlaminin gamma 1MicroRNAsMIRN376C microRNA, humanPAX5 protein, humanPAX5 Transcription FactorRNA, Long NoncodingcholangiocarcinomaLAMC1lncRNAmiR-376a-3pPSMA3-AS1

Identifiers

PMID35022330
PMCPMC8791211
OpenAlexW4206813084

What OpenQuestion holds

Textmetadata
LicenceCC BY
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 OpenQuestion graph.