Evidence map›Paper›PMID 32945133›Full record

ArticleThoracic cancer2020

Human papillomavirus 16 (HPV 16) E6 but not E7 inhibits the antitumor activity of LKB1 in lung cancer cells by downregulating the expression of KIF7.

Yue Hu, Ming-Zhe Wu, Na-Jin Gu, Hong-Tao Xu, Qing-Chang Li, Guang-Ping Wu

Open access · goldAbstract read
In one paragraph

Article in Thoracic cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

7 citing papers in PubMed, 8 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

6 authors at 1 institution in 1 country.

Yue HuDepartment of Pathology, The First Affiliated Hospital and College of Basic Medical Sciences, China Medical University, Shenyang, China.
Ming-Zhe WuDepartments of Gynecology, The First Hospital of China Medical University, Shenyang, China.
Na-Jin GuDepartment of Pathology, The First Affiliated Hospital and College of Basic Medical Sciences, China Medical University, Shenyang, China.
Hong-Tao XuDepartment of Pathology, The First Affiliated Hospital and College of Basic Medical Sciences, China Medical University, Shenyang, China.
Qing-Chang LiDepartment of Pathology, The First Affiliated Hospital and College of Basic Medical Sciences, China Medical University, Shenyang, China.
Guang-Ping WuDepartment of Pathology, The First Affiliated Hospital and College of Basic Medical Sciences, China Medical University, Shenyang, China.ORCID 0000-0003-3478-6868
First Hospital of China Medical University · CN

Funding

National Natural Science Foundation of China 81171650 andNational Natural Science Foundation of China 81672082
6 · The paper itself

Abstract

backgroundThe E6 and E7 proteins in human papillomavirus 16 (HPV 16) are the main oncogenes in the occurrence of lung cancer. In recent studies, we found that E6 and E7 downregulated the expression of LKB1 in lung cancer cells. However, it is still unclear how E6 and E7 regulate LKB1 in lung cancer cells.

methodsDouble directional genetic manipulation and nuclear plasma separation technology were performed to explore the molecular mechanism of E6 and E7 inhibiting the antitumor activity of LKB1 in well-established lung cancer cell lines.

resultsE6 but not E7 significantly downregulated the expression of tumor suppressor KIF7 at protein level, and the inhibition of KIF7 further reduced the expression of LKB1 both in the nuclei and in the cytoplasm, whereas reduced the expression of p-LKB1 in the cytoplasm only. This suggested that HPV 16 E6 but not E7 downregulates the antitumor activity of LKB1 by downregulating the expression of p-LKB1 in the cytoplasm only.

conclusionsHere, we demonstrated for the first time that E6 but not E7 inhibits the antitumor activity of LKB1 in lung cancer cells by downregulating the expression of KIF7. Our findings provide new evidence to support the important role of KIF7 in the pathogenesis of lung cancer and suggests new therapeutic targets.

Indexed as

AMP-Activated Protein Kinase KinasesCell Line, TumorDown-RegulationFemaleHuman papillomavirus 16HumansKinesinsLung NeoplasmsMaleOncogene Proteins, ViralPapillomavirus E7 ProteinsProtein Serine-Threonine KinasesRepressor ProteinsTransfectionAMP-Activated Protein Kinase KinasesE6 protein, Human papillomavirus type 16KIF7 protein, humanKinesinsoncogene protein E7, Human papillomavirus type 16Oncogene Proteins, ViralPapillomavirus E7 ProteinsProtein Serine-Threonine KinasesRepressor ProteinsSTK11 protein, humanHuman papillomavirus (HPV)kinesin family member 7 (KIF7)liver kinase B1 (LKB1)lung cancerserine/threonine kinase 11 (STK11)

Identifiers

PMID32945133
PMCPMC7606012
OpenAlexW3087055836

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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.