Evidence map›Paper›PMID 38914958›Full record

ArticleBMC cancer2024

IKBIP promotes tumor development via the akt signaling pathway in esophageal squamous cell carcinoma.

Jiannan Hu, Chuanjing Dai, Zhaoji Ding, Yixiao Pan, Lingxiao Lu, Jiaqian Bao, Jingmin Zheng

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PubMed Full text at PMC Publisher
In one paragraph

Article in BMC cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

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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

6 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.

Jiannan Hu *Department of Public Laboratory, Taizhou Hospital of Zhejiang Province Affiliated to Wenzhou Medical University, 150 Ximenjie, Linhai, Zhejiang Province, 317000, China.
Chuanjing Dai *Department of Public Laboratory, Taizhou Hospital of Zhejiang Province Affiliated to Wenzhou Medical University, 150 Ximenjie, Linhai, Zhejiang Province, 317000, China.
Zhaoji Ding *Department of Public Laboratory, Taizhou Hospital of Zhejiang Province Affiliated to Wenzhou Medical University, 150 Ximenjie, Linhai, Zhejiang Province, 317000, China.
Yixiao PanDepartment of Public Laboratory, Taizhou Hospital of Zhejiang Province Affiliated to Wenzhou Medical University, 150 Ximenjie, Linhai, Zhejiang Province, 317000, China.
Lingxiao LuDepartment of Public Laboratory, Taizhou Hospital of Zhejiang Province Affiliated to Wenzhou Medical University, 150 Ximenjie, Linhai, Zhejiang Province, 317000, China.
Jiaqian BaoDepartment of Public Laboratory, Taizhou Hospital of Zhejiang Province Affiliated to Wenzhou Medical University, 150 Ximenjie, Linhai, Zhejiang Province, 317000, China.
Jingmin ZhengDepartment of Public Laboratory, Taizhou Hospital of Zhejiang Province Affiliated to Wenzhou Medical University, 150 Ximenjie, Linhai, Zhejiang Province, 317000, China. zzjjmm7713@sina.com.

Funding

Key Laboratory of Minimally Invasive Techniques and Rapid Rehabilitation of Digestive System Tumors of Zhejiang Province 21SZDSYS08
6 · The paper itself

Abstract

backgroundEsophageal squamous cell carcinoma (ESCC) is one of the most common cancers worldwide. Inhibitor of kappa B kinase interacting protein (IKBIP) has been reported to promote glioma progression, but its role in other cancers remains unclear. This study aimed to investigate the role of IKBIP and its underlying molecular mechanisms in ESCC.

methodsThe mRNA expression of IKBIP was analyzed using multiple cancer databases. Immunohistochemistry was performed to detect IKBIP protein expression in ESCC tissues and adjacent normal tissues, and Kaplan‒Meier survival and Cox regression analyses were carried out. The effects of IKBIP knockdown (or overexpression) on ESCC cells were detected by cell viability, cell migration, flow cytometry and Western blot assays. LY-294002 was used to validate the activation of the AKT signaling pathway by IKBIP. Finally, the role of IKBIP in ESCC was verified in a xenograft model.

resultsBoth bioinformatics analysis and immunohistochemistry indicated that IKBIP expression in ESCC tissues was significantly increased and was associated with the prognosis of ESCC patients. In vitro experiments revealed that IKBIP knockdown significantly inhibited the proliferation and migration of ESCC cells, and induced cell apoptosis and G1/S phase arrest. Molecular mechanism results showed that the AKT signaling pathway was further activated after IKBIP overexpression, thereby increasing the proliferation and migration abilities of ESCC cells. In vivo study confirmed that IKBIP promoted the initiation and development of ESCC tumors in mice.

conclusionsIKBIP plays a tumor-promoting role in ESCC and may serve as a predictive biomarker and a potential therapeutic target for ESCC.

Indexed as

Cell MovementCell ProliferationEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaProto-Oncogene Proteins c-aktSignal TransductionAdaptor Proteins, Signal TransducingAnimalsApoptosisCell Line, TumorFemaleGene Expression Regulation, NeoplasticHumansMaleMiceMice, NudeAdaptor Proteins, Signal TransducingIKBIP protein, humanProto-Oncogene Proteins c-aktAKTESCCIKBIPPrognosisTumor-promoting

Identifiers

PMID38914958
PMCPMC11197280

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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.