Evidence map›Paper›PMID 35090377›Full record

ArticleCell cycle (Georgetown, Tex.)

Long non-coding RNA tumor protein 53 target gene 1 promotes cervical cancer development via regulating microRNA-33a-5p to target forkhead box K2.

Dan Liao, Xiaomei Liu, Xiuying Yuan, Poling Feng, Zhiwei Ouyang, Yanyan Liu, Cuifen Li

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

14 citing papers in PubMed, 13 citations in OpenAlex.

  1. AKT Phosphorylation of FOXK2 at Ser398 Impacts Breast Cancer Cell Growth and Viability.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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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 2 institutions in 1 country.

Dan LiaoDepartment of Gynaecology, SSL Central Hospital of Dongguan, Affiliated Dongguan Shilong People's Hospital of Southern Medical University, Dongguan, Guangdong, China.
Xiaomei LiuDepartment of Gynaecology, SSL Central Hospital of Dongguan, Affiliated Dongguan Shilong People's Hospital of Southern Medical University, Dongguan, Guangdong, China.
Xiuying YuanDepartment of Gynaecology, SSL Central Hospital of Dongguan, Affiliated Dongguan Shilong People's Hospital of Southern Medical University, Dongguan, Guangdong, China.
Poling FengDepartment of Gynaecology, SSL Central Hospital of Dongguan, Affiliated Dongguan Shilong People's Hospital of Southern Medical University, Dongguan, Guangdong, China.
Zhiwei OuyangDepartment of Gynaecology, SSL Central Hospital of Dongguan, Affiliated Dongguan Shilong People's Hospital of Southern Medical University, Dongguan, Guangdong, China.
Yanyan LiuDepartment of Gynaecology, SSL Central Hospital of Dongguan, Affiliated Dongguan Shilong People's Hospital of Southern Medical University, Dongguan, Guangdong, China.
Cuifen LiDepartment of Gynaecology, SSL Central Hospital of Dongguan, Affiliated Dongguan Shilong People's Hospital of Southern Medical University, Dongguan, Guangdong, China.
Southern Medical University · CNDongguan People’s Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long non-coding RNA tumor protein 53 target gene 1 (TP53TG1) has been unraveled to exert regulatory effects on cancer progression, while the regulatory function of TP53TG1 on cervical cancer (CC) via regulating microRNA (miR)-33a-5p/Forkhead box K2 (FOXK2) axis remains rarely explored. This study aims to unearth the regulatory mechanism of TP53TG1/miR-33a-5p/FOXK2 axis in CC. The CC clinical samples were collected, and CC cells were cultured. TP53TG1, miR-33a-5p and FOXK2 levels were examined in CC tissues and cells. The CC cells were transfected with high- or low-expressed TP53TG1, FOXK2 or miR-33a-5p to determine the changes of CC cell biological activities and the status of phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) pathway. The tumorigenesis in nude mice was conducted. The relationship among TP53TG1, miR-33a-5p and FOXK2 was validated. TP53TG1 and FOXK2 expression levels were increased and miR-33a-5p expression level was reduced in CC cells and tissues. The silenced TP53TG1 or FOXK2, or elevated miR-33a-5p decelerated the CC cell development and restrained the activation of PI3K/AKT/mTOR signaling pathway. The depleted FOXK2 or elevated miR-33a-5p reversed the effects of decreased TP53TG1 on CC cell progression. TP53TG1 sponged miR-33a-5p, which targeted FOXK2. The experiment

Indexed as

DNA-Binding ProteinsForkhead Transcription FactorsMicroRNAsRNA, Long NoncodingUterine Cervical NeoplasmsAnimalsCell Line, TumorCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansMammalsMiceMice, NudePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktDNA-Binding ProteinsForkhead Transcription Factorsinterleukin binding factorMicroRNAsMIRN33a microRNA, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA, Long NoncodingTOR Serine-Threonine KinasesTP53TG1 protein, humanbiological developmentCervical cancerforkhead box K2long non-coding RNA tumor protein 53 target gene 1MicroRNA-33a-5pphosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin signaling pathway

Identifiers

PMID35090377
PMCPMC8942495
OpenAlexW4210440748

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.