Evidence map›Paper›PMID 34956471›Full record

ArticleAmerican journal of translational research2021

Myosin 1b promotes migration, invasion and glycolysis in cervical cancer via ERK/HIF-1α pathway.

Li-Jun Wen, Xiao-Lin Hu, Cui-Ying Li, Jie Liu, Zi-Yang Li, Ya-Zi Li, Jue-Yu Zhou

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

12 citing papers in PubMed, 12 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

7 authors at 1 institution in 1 country.

Li-Jun WenDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Southern Medical University Guangzhou 510515, Guangdong, China.
Xiao-Lin HuDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Southern Medical University Guangzhou 510515, Guangdong, China.
Cui-Ying LiDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Southern Medical University Guangzhou 510515, Guangdong, China.
Jie LiuDepartment of Gynaecology and Obstetrics, Nanfang Hospital, Southern Medical University Guangzhou 510515, Guangdong, China.
Zi-Yang LiDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Southern Medical University Guangzhou 510515, Guangdong, China.
Ya-Zi LiDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Southern Medical University Guangzhou 510515, Guangdong, China.
Jue-Yu ZhouDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Southern Medical University Guangzhou 510515, Guangdong, China.
Southern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIncreasing evidence indicated that metabolic reprograming is essential and has been regarded as a hallmark of cancer. Although the biological functions of Myosin 1b (Myo1b) have been reported in several malignancies, the correlation between Myo1b and cancer metabolism, and its underlying mechanisms remain elusive, particularly in cervical cancer (CC).

methodsMyo1b and other glycolytic enzymes expression levels were examined in CC cells and tumor tissues from xenograft models by quantitative real-time PCR, Western blot and immunohistochemistry. The biological impacts and regulatory mechanisms of Myo1b on cell migration, invasion and glycolysis were explored. Also, the effects of Myo1b on carcinogenesis and metastasis in nude mice were investigated.

resultsUpregulation of Myo1b was found in CC tissues and associated with poor prognosis. Overexpressed Myo1b not only significantly elevated CC cell glycolysis, migration and invasion in vitro, but also promoted tumorigenesis and metastasis in vivo. Conversely, Myo1b knockdown had opposite consequences. Moreover, our study suggested that Myo1b stimulated ERK/HIF-1α pathway and its downstream glycolysis associated genes to modulate the glycolysis, migration and invasion of CC.

conclusionThese findings provide evidence that Myo1b regulates migration, invasion and glycolysis in CC through ERK/HIF-1α pathway, suggesting a promising remedial target in treatment of CC.

Indexed as

cervical cancerERK/HIF-1αglycolysisinvasionmetastasisMyosin 1b

Identifiers

PMID34956471
PMCPMC8661216
OpenAlexW4206850861

What OpenQuestion holds

Textmetadata
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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.