Evidence map›Paper›PMID 25603720›Full record

ArticleBMC cancer2015

STK33 overexpression in hypopharyngeal squamous cell carcinoma: possible role in tumorigenesis.

Lingyan Huang, Chen Chen, Guodong Zhang, Yuanrong Ju, Jianzhong Zhang, Haibo Wang, Jianfeng Li

Abstract read
In one paragraph

Article in BMC cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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

15 citing papers in PubMed.

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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.

Lingyan HuangDepartment of Otolaryngology-Head and Neck Surgery, Provincial Hospital Affiliated to Shandong University, Jingwu Street 324, Jinan, 250021, P.R. China. kaixinhly@hotmail.com.
Chen ChenDepartment of Otolaryngology-Head and Neck Surgery, Provincial Hospital Affiliated to Shandong University, Jingwu Street 324, Jinan, 250021, P.R. China. doctorchchen@163.com.
Guodong ZhangDepartment of Otolaryngology-Head and Neck Surgery, Provincial Hospital Affiliated to Shandong University, Jingwu Street 324, Jinan, 250021, P.R. China. doctorzhgdong@163.com.
Yuanrong JuIntensive Care Unit, Provincial Hospital Affiliated to Shandong University, Jinan, 250021, P.R. China. doctorjyrong@163.com.
Jianzhong ZhangDepartment of Pathology, General Hospital of Ningxia Medical University, Yinchuan, 750004, P.R. China. doctorzhjzhong@163.com.
Haibo WangDepartment of Otolaryngology-Head and Neck Surgery, Provincial Hospital Affiliated to Shandong University, Jingwu Street 324, Jinan, 250021, P.R. China. wang.hb7585@hotmail.com.
Jianfeng LiDepartment of Otolaryngology-Head and Neck Surgery, Provincial Hospital Affiliated to Shandong University, Jingwu Street 324, Jinan, 250021, P.R. China. lijianfeng@hotmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe role of serine/threonine kinase 33 (STK33) gene in tumorigenesis is still controversial. This study was aimed to investigate whether STK33 had the effect on hypopharyngeal squamous cell carcinoma (HSCC) and relevant genes, as well as the potential relation to ERK1/2 pathway.

methodsImmunohistochemistry was performed to investigate STK33 expression in human HSCC specimens. MTT, immunofluorescence, clone formation and matrigel invasion assays were employed to detect the effects of STK33 knockdown (STK33-RNAi) and/or PD98059 on major oncogenic properties of a HSCC cell line (Fadu), while, real-time PCR and western blot were used to examine the expressions of relevant genes.

resultsSTK33 was over-expressed in HSCC specimens, which was significantly associated with certain clinicopathological parameters. STK33-RNAi in Fadu cells resulted in inhibition of proliferation, induction of apoptosis, reduction of clone formation, and decline in the migration and invasion. These effects were potentiated by administration of PD98059. Mechanistic studies revealed that STK33-RNAi led to an increase in Caspse-3, Nm-23-H1 and E-Cadherin expressions and a reduction in Bcl-2, Ki-67 and Vimentin expressions. Moreover, PD98059 significantly reduced both ERK1/2 and STK33 expressions in Fadu cells.

conclusionsSTK33 is a potential oncogene and a promising diagnostic marker for HSCC. STK33 may promote tumorigenesis and progression of HSCC, and serve as a valuable molecular target for treatment of HSCC.

Indexed as

ApoptosisCarcinoma, Squamous CellCell Line, TumorCell ProliferationFlavonoidsGene Expression Regulation, NeoplasticHumansHypopharyngeal NeoplasmsProtein Serine-Threonine KinasesUp-Regulation2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-oneFlavonoidsProtein Serine-Threonine KinasesSTK33 protein, human

Identifiers

PMID25603720
PMCPMC4305229

What Socratic holds

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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 Socratic graph.