Evidence map›Paper›PMID 33159291›Full record

ArticleReproductive sciences (Thousand Oaks, Calif.)2021

LncRNA BBOX1-AS1 Aggravates the Development of Ovarian Cancer by Sequestering miR-361-3p to Augment PODXL Expression.

Huiping Yao, Rui Chen, Yongxiu Yang, Juan Jiang

Abstract read
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In one paragraph

Article in Reproductive sciences (Thousand Oaks, Calif.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 2 pooled it
2.0field-weighted citation impact, top 12% 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

19 citing papers in PubMed, 2 syntheses or guidelines pooled it, 29 citations in OpenAlex.

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  9. The functional role of circular RNAs in the pathogenesis of retinoblastoma: a new potential biomarker and therapeutic target?Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 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

4 authors at 3 institutions in 1 country.

Huiping YaoDepartment of Gynecology and Obstetrics, Gansu Key Laboratory of Gynecological Oncology, The First Hospital of Lanzhou University, Lanzhou, Gansu, China.
Rui ChenDepartment of Gynecology, East Hospital Affiliated to Tongji University, Shanghai, 200120, China.
Yongxiu YangDepartment of Gynecology and Obstetrics, Gansu Key Laboratory of Gynecological Oncology, The First Hospital of Lanzhou University, Lanzhou, Gansu, China.
Juan JiangDepartment of Gynecology, People's Hospital of Jingjiang, No. 28, Zhongzhou Road, Jingjiang, 214500, Jiangsu, China. taijiang65309@163.com.ORCID 0000-0002-9128-6985
First Hospital of Lanzhou University · CNFirst People's Hospital of Jingzhou · CNShanghai East Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ovarian cancer (OC) is a kind of common gynecological malignancy around the world. Mounting literatures have confirmed the implication of lncRNAs in the development of various cancers. Long non-coding RNA (LncRNA) BBOX1-AS1 has not been reported in most cancer types including OC. Presently, we aimed at exploring the function and regulatory mechanism of BBOX1-AS1 in OC. As a result, we demonstrated the extremely high BBOX1-AS1 expression in OC tissues and cells. BBOX1-AS1 silence inhibited OC progression by suppressing cell proliferation and promoting cell apoptosis. Importantly, BBOX1-AS1 was verified to bind to miR-361-3p, which presented a low expression trend in OC cells. Subsequently, PODXL was testified as the downstream target of miR-361-3p. Of note, BBOX1-AS1 positively regulated PODXL through their competition in binding with miR-361-3p. Furthermore, miR-361-3p inhibition facilitated the growth of BBOX1-AS1-deficient OC cells, while such facilitating effect was then counteracted in response to PODXL depletion. All the results above explained that BBOX1-AS1 was overexpressed in OC and that BBOX1-AS1 caused carcinogenic influences on OC cell growth via miR-361-3p/PODXL pathway, highlighting BBOX1-AS1 as a novel potential target for OC treatment.

Indexed as

Cell ProliferationCell Line, TumorDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansMicroRNAsOvarian NeoplasmsRNA, Long NoncodingSialoglycoproteinsMicroRNAsMIRN361 microRNA, humanpodocalyxinRNA, Long NoncodingSialoglycoproteinsBBOX1-AS1miR-361-3pOvarian cancerPODXL

Identifiers

PMID33159291
OpenAlexW3095580630

What OpenQuestion holds

Textmetadata
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.