Evidence map›Paper›PMID 34210956›Full record

ArticleCell death & disease2021

ALPK2 acts as tumor promotor in development of bladder cancer through targeting DEPDC1A.

Yuchen Wang, Jie Wu, Wenjie Luo, Hailiang Zhang, Guohai Shi, Yijun Shen, Yao Zhu, Chunguang Ma, Bo Dai, Dingwei Ye and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 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
2.7field-weighted citation impact, top 9% 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, 16 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

11 authors at 1 institution in 1 country.

Yuchen Wang *Department of Urology, Fundan University Shanghai Cancer Center, No. 270 Dongan Road, 200032, Shanghai, People's Republic of China.ORCID 0000-0003-2338-6893
Jie Wu *Department of Urology, Fundan University Shanghai Cancer Center, No. 270 Dongan Road, 200032, Shanghai, People's Republic of China.
Wenjie Luo *Department of Urology, Fundan University Shanghai Cancer Center, No. 270 Dongan Road, 200032, Shanghai, People's Republic of China.
Hailiang ZhangDepartment of Urology, Fundan University Shanghai Cancer Center, No. 270 Dongan Road, 200032, Shanghai, People's Republic of China.
Guohai ShiDepartment of Urology, Fundan University Shanghai Cancer Center, No. 270 Dongan Road, 200032, Shanghai, People's Republic of China.
Yijun ShenDepartment of Urology, Fundan University Shanghai Cancer Center, No. 270 Dongan Road, 200032, Shanghai, People's Republic of China.
Yao ZhuDepartment of Urology, Fundan University Shanghai Cancer Center, No. 270 Dongan Road, 200032, Shanghai, People's Republic of China.
Chunguang MaDepartment of Urology, Fundan University Shanghai Cancer Center, No. 270 Dongan Road, 200032, Shanghai, People's Republic of China.
Bo DaiDepartment of Urology, Fundan University Shanghai Cancer Center, No. 270 Dongan Road, 200032, Shanghai, People's Republic of China.
Dingwei YeDepartment of Urology, Fundan University Shanghai Cancer Center, No. 270 Dongan Road, 200032, Shanghai, People's Republic of China. dwyeli@163.com.
Yiping ZhuDepartment of Urology, Fundan University Shanghai Cancer Center, No. 270 Dongan Road, 200032, Shanghai, People's Republic of China. qdzhuyiping@aliyun.com.ORCID 0000-0001-8015-420X
Shanghai Medical College of Fudan University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81772706
6 · The paper itself

Abstract

Bladder cancer is one of the most common malignant tumors in the urinary system. The development and improvement of treatment efficiency require the deepening of the understanding of its molecular mechanism. This study investigated the role of ALPK2, which is rarely studied in malignant tumors, in the development of bladder cancer. Our results showed the upregulation of ALPK2 in bladder cancer, and data mining of TCGA database showed the association between ALPK2 and pathological parameters of patients with bladder cancer. In vitro and in vivo experiments demonstrated that knockdown of ALPK2 could inhibit bladder cancer development through regulating cell proliferation, cell apoptosis, and cell migration. Additionally, DEPDC1A is identified as a potential downstream of ALPK2 with direct interaction, whose overexpression/downregulation can inhibit/promote the malignant behavioral of bladder cancer cells. Moreover, the overexpression of DEPDC1A can rescue the inhibitory effects of ALPK2 knockdown on bladder cancer. In conclusion, ALPK2 exerts a cancer-promoting role in the development of bladder cancer by regulating DEPDC1A, which may become a promising target to improve the treatment strategy of bladder cancer.

Indexed as

AnimalsApoptosisCell Line, TumorCell MovementCell ProliferationDatabases, GeneticGene Expression Regulation, NeoplasticGTPase-Activating ProteinsHumansMiceMice, Inbred BALB CMice, NudeNeoplasm InvasivenessNeoplasm ProteinsProtein KinasesSignal TransductionALPK2 protein, humanDEPDC1 protein, humanGTPase-Activating ProteinsNeoplasm ProteinsProtein Kinases

Identifiers

PMID34210956
PMCPMC8249393
OpenAlexW3174612049

What Socratic 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 Socratic graph.