Evidence map›Paper›PMID 36700980›Full record

ArticleJournal of cancer research and clinical oncology2023

hnRNP K induces HPV16 oncogene expression and promotes cervical cancerization.

Yuanjing Lyu, Li Song, Rui Mao, Chunliang Liu, Meijuan Feng, Caihong Wu, Ruixin Pei, Ling Ding, Jintao Wang

Open access · greenAbstract read
In one paragraph

Article in Journal of cancer research and clinical oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.5field-weighted citation impact, top 29% 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

0 citing papers in PubMed, 2 citations in OpenAlex.

No citing paper in PubMed yet.

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 3 institutions in 2 countries.

Yuanjing Lyu *Department of Epidemiology, School of Public Health, Shanxi Medical University, Taiyuan, China.
Li Song *Department of Epidemiology, School of Public Health, Shanxi Medical University, Taiyuan, China.
Rui MaoQuestrom School of Business, Boston University, Boston, MA, USA.
Chunliang LiuDepartment of Gastroenterology, Second Hospital of Shanxi Medical University, Taiyuan, China.
Meijuan FengDepartment of Epidemiology, School of Public Health, Shanxi Medical University, Taiyuan, China.
Caihong WuDepartment of Epidemiology, School of Public Health, Shanxi Medical University, Taiyuan, China.
Ruixin PeiDepartment of Epidemiology, School of Public Health, Shanxi Medical University, Taiyuan, China.
Ling DingDepartment of Epidemiology, School of Public Health, Shanxi Medical University, Taiyuan, China.
Jintao WangDepartment of Epidemiology, School of Public Health, Shanxi Medical University, Taiyuan, China. wangjt59@163.com.
Shanxi Medical University · CNBoston University · USSecond Hospital of Shanxi Medical University · CN

Funding

National Health and Family Planning Commission of the People's Republic of China 201402010National Natural Science Foundation of China 81473060
6 · The paper itself

Abstract

purposeThis study aims to explore the expression of hnRNP K in cervical carcinogenesis and to investigate the regulatory role of hnRNP K on HPV16 oncogene expression as well as biological changes in cervical cancer cells.

methodsIn total 1042 subjects, including 573 with the normal cervix and 469 with different grades of cervical lesions were enrolled in this study to explore the association between hnRNP K and HPV16 oncogene expression in cervical carcinogenesis. Additionally, the Gene Omnibus (GEO) database was used to analyze hnRNP K mRNA expression in cervical cancerization. Meanwhile, the effects of hnRNP K on cell biological functions and HPV16 oncogene expression were investigated in Siha cells. Moreover, Function analyses were conducted using Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) databases after ChIP-seq.

resultshnRNP K was highly expressed in cervical cancer and precancerous lesions, and positively correlated with HPV16 E6, but negatively correlated with HPV16 E2 and HPV16 E2/E6 ratio. hnRNP K induced cell proliferation, inhibited apoptosis and caused cell cycle arrest in the S phase, and particularly increased HPV16 E6 protein expression.

conclusionThis study revealed that hnRNP K overexpression has important warning significance for the malignant transformation of cervical lesions, and could be used as a potential therapeutic target for inhibiting the carcinogenicity of HPV16 and prevention of cervical carcinogenesis.

Indexed as

Oncogene Proteins, ViralPapillomavirus InfectionsUterine Cervical NeoplasmsCarcinogenesisCervix UteriFemaleHeterogeneous-Nuclear Ribonucleoprotein KHuman papillomavirus 16HumansOncogenesHeterogeneous-Nuclear Ribonucleoprotein KOncogene Proteins, ViralCervical cancerizationhnRNP KHPV16 E2HPV16 E2/E6 ratioHPV16 E6

Identifiers

PMID36700980
PMCPMC11797120
OpenAlexW4318067187

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Registered trials

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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.