Evidence map›Paper›PMID 32436862›Full record

ArticleAging2020

KMT2A regulates cervical cancer cell growth through targeting VDAC1.

Changlin Zhang, Yijun Hua, Huijuan Qiu, Tianze Liu, Qian Long, Wei Liao, Jiehong Qiu, Nang Wang, Miao Chen, Dingbo Shi and 5 more

Open access · greenAbstract read
In one paragraph

Article in Aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.0field-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

17 citing papers in PubMed, 22 citations in OpenAlex.

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  14. The role of KMT2 gene in human tumors.Histology and histopathology · 2022
    Review
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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

15 authors at 5 institutions in 1 country.

Changlin ZhangDepartment of Gynecology, The Seventh Affiliated Hospital of Sun Yat-Sen University, Shenzhen, China.
Yijun HuaSun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, Guangzhou, China.
Huijuan QiuSun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, Guangzhou, China.
Tianze LiuThe Fifth Affiliated Hospital, Sun Yat-Sen University, Zhuhai, China.
Qian LongSun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, Guangzhou, China.
Wei LiaoDepartment of Gynecology, The Seventh Affiliated Hospital of Sun Yat-Sen University, Shenzhen, China.
Jiehong QiuDepartment of Gynecology, The Seventh Affiliated Hospital of Sun Yat-Sen University, Shenzhen, China.
Nang WangCollege of Life Sciences, Jiaying University, Meizhou, Guangdong, China.
Miao ChenSun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, Guangzhou, China.
Dingbo ShiSun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, Guangzhou, China.
Yue YanSun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, Guangzhou, China.
Chuanbo XieSun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, Guangzhou, China.
Wuguo DengSun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, Guangzhou, China.
Tian LiDepartment of Gynecology, The Seventh Affiliated Hospital of Sun Yat-Sen University, Shenzhen, China.
Yizhuo LiSun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, Guangzhou, China.
Sun Yat-sen University Cancer Center · CNSun Yat-sen University · CNThe Seventh Affiliated Hospital of Sun Yat-sen University · CNState Key Laboratory of Oncology in South ChinaJiaying University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cervical cancer is an aggressive cutaneous malignancy, illuminating the molecular mechanisms of tumorigenesis and discovering novel therapeutic targets are urgently needed. KMT2A is a transcriptional co-activator regulating gene expression during early development and hematopoiesis, but the role of KMT2A in cervical cancer remains unknown. Here, we demonstrated that KMT2A regulated cervical cancer growth via targeting VADC1. Knockdown of KMT2A significantly suppressed cell proliferation and migration and induced apoptosis in cervical cancer cells, accompanying with activation of PARP/caspase pathway and inhibition of VADC1. Overexpression of VDAC1 reversed the KMT2A knockdown-mediated regulation of cell proliferation, migration and apoptosis. The

Indexed as

ApoptosisCarcinoma, Squamous CellCell Line, TumorCell MovementCell ProliferationCell Transformation, NeoplasticCervix UteriFemaleHistone-Lysine N-MethyltransferaseHumansMyeloid-Lymphoid Leukemia ProteinSignal TransductionUp-RegulationUterine Cervical NeoplasmsVoltage-Dependent Anion Channel 1Histone-Lysine N-MethyltransferaseKMT2A protein, humanMyeloid-Lymphoid Leukemia ProteinVDAC1 protein, humanVoltage-Dependent Anion Channel 1cervical cancerKMT2AVDAC1

Identifiers

PMID32436862
PMCPMC7288919
OpenAlexW3026589626

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.