Evidence map›Paper›PMID 39535578›Full record

ArticleMolecular biology reports2024

GPD1L may inhibit the development of esophageal squamous cell carcinoma through the PI3K/AKT signaling pathway: bioinformatics analysis and experimental exploration.

LanLan Gan, Lu Zhou, ALan Chu, Chen Sun, YongTai Wang, MengLin Yang, ZongWen Liu

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Article in Molecular biology reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

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3citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

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3 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

LanLan Gan *Tumor Radiotherapy Department, The Second Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 450000, P.R. China.
Lu Zhou *Tumor Radiotherapy Department, The Second Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 450000, P.R. China.
ALan ChuTumor Radiotherapy Department, The Second Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 450000, P.R. China.
Chen SunTumor Radiotherapy Department, The Second Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 450000, P.R. China.
YongTai WangTumor Radiotherapy Department, The Second Clinical Medical School of Zhengzhou University, Zhengzhou, Henan, 450000, P.R. China.
MengLin YangTumor Radiotherapy Department, The Second Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 450000, P.R. China.
ZongWen LiuTumor Radiotherapy Department, The Second Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 450000, P.R. China. liuzwhh@sina.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEsophageal squamous carcinoma (ESCC) is the most prevalent pathological subtype of esophageal cancer (EC). It has the characteristics of significant local invasion, quick disease progression, high recurrence rates, and a dismal prognosis for survival. Phosphatidylinositol 3-kinase/serine-threonine kinase (PI3K/AKT) is a signaling system whose aberrant activation regulates downstream factors, leading to the promotion of cancer development. This study looks at a protein called Glycerol-3-phosphate dehydrogenase 1-like (GPD1L), which strongly affects the development of several cancers. However, its association with ESCC development and its underlying mechanisms are not clear.

methodsIn this paper, we analyzed six ESCC transcriptome data obtained from the GEO database. We utilized bioinformatics technology and immunohistochemistry to differentially analyze GPD1L levels of mRNA and protein expression in ESCC and normal adjacent tissues. Furthermore, we conducted survival, co-expression, enrichment, immune infiltration and drug sensitivity analysis. Moreover, we further investigated the role and mechanism of GPD1L by Western Blot (WB), Cell Counting Kit-8 (CCK8), wound healing assay, Transwell assay, and flow cytometry. Finally, the addition of IGF-1, the activator of PI3K/AKT, could rescue the inhibitory effect of GPD1L on ESCC.

resultsThe findings manifest that the expression of GPD1L was low in ESCC, and functional experiments showed that GPD1L promoted apoptosis in vitro while blocking cell migration, invasion, and proliferation. Based on mechanism research, GPD1L's impact on ESCC could be explained by its suppression of the PI3K/AKT signaling pathway's activation.

conclusionTo sum up, our findings imply that GPD1L may impede the initiation and advancement of ESCC via modulating the PI3K/AKT signaling pathway. GPD1L is considered to be a promising therapeutic target and biomarker to diagnose and treat ESCC.

Indexed as

Computational BiologyEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaGene Expression Regulation, NeoplasticPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionApoptosisCell Line, TumorCell MovementCell ProliferationGlycerolphosphate DehydrogenaseHumansPrognosisGlycerolphosphate DehydrogenasePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktBioinformaticsBiological behaviorESCCGPD1LPI3K/AKT

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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.