ABLIM3

Last update 08 May 2025

Basic Info

Synonyms

abLIM-3, ABLIM3, actin binding LIM protein family member 3

+ [3]

Introduction

May act as scaffold protein. May stimulate ABRA activity and ABRA-dependent SRF transcriptional activity.

100 Clinical Results associated with ABLIM3

100 Translational Medicine associated with ABLIM3

0 Patents (Medical) associated with ABLIM3

Literatures (Medical) associated with ABLIM3

01 Dec 2024·Computational and Structural Biotechnology Journal

Corrigendum to 'Downregulation of ABLIM3 confers to the metastasis of neuroblastoma via regulating the cell adhesion molecules pathway' [Comput. Struct. Biotechnol. J., Vol. 23 (2024) 1547–1561]

Author: Zhao, Qiang ; Wang, Chaoyu ; Zhang, Jiaojiao ; Qu, Tongyuan ; Jin, Yan ; Chen, Chong ; Song, Zian ; Yang, Jiaxing ; Gong, Baocheng ; Liu, Yun ; Cao, Wenfeng ; Jia, Yubin

[This corrects the article DOI: 10.1016/j.csbj.2024.04.024.].

01 Dec 2024·Computational and Structural Biotechnology Journal

Downregulation of ABLIM3 confers to the metastasis of neuroblastoma via regulating the cell adhesion molecules pathway

Article

Author: Zhao, Qiang ; Wang, Chaoyu ; Qu, Tongyuan ; Zhang, Jiaojiao ; Jin, Yan ; Chen, Chong ; Song, Zian ; Gong, Baocheng ; Yang, Jiaxing ; Liu, Yun ; Cao, Wenfeng ; Jia, Yubin

Neuroblastoma (NB) is the most prevalent extracranial solid tumor in pediatric patients, and its treatment failure often associated with metastasis. In this study, LASSO, SVM-RFE, and random forest tree algorithms, was used to identify the pivotal gene involved in NB metastasis. NB cell lines (SK-N-AS and SK-N-BE2), in conjunction with NB tissue were used for further study. ABLIM3 was identified as the hub gene and can be an independent prognostic factor for patients with NB. The immunohistochemical analysis revealed that ABLIM3 is negatively correlated with the metastasis of NB. Patients with low expression of ABLIM3 had a poor prognosis. High ABLIM3 expression correlated with APC co-stimulation and Type1 IFN response, and TIDE analysis indicated that patients with low ABLIM3 expression exhibited enhanced responses to immunotherapy. Downregulation of ABLIM3 by shRNA transfection increased the migration and invasion ability of NB cells. Gene Set Enrichment Analysis (GSEA) revealed that genes associated with ABLIM3 were primarily enriched in the cell adhesion molecules (CAMs) pathway. RT-qPCR and western blot analyses demonstrated that downregulation of ABLIM3 led to decreased expression of ITGA3, ITGA8, and KRT19, the key components of CAMs. This study indicated that ABLIM3 can be an independent prognostic factor for NB patients, and CAMs may mediate the effect of ABLIM3 on the metastasis of NB, suggesting that ABLIM3 is a potential therapeutic target for NB metastasis, which provides a novel strategy for future research and treatment strategies for NB patients.

01 Aug 2024·International Journal of Experimental Pathology

GABRP inhibits the progression of oesophageal cancer by regulating CFTR: Integrating bioinformatics analysis and experimental validation

Article

Author: Zeng, Ling ; Liu, Xue ; Zhang, Jingzhi ; Hu, Ying

AbstractOesophageal cancer (EC) is a malignancy which accounts for a substantial number of cancer‐related deaths worldwide. The molecular mechanisms underlying the pathogenesis of EC have not been fully elucidated. GSE17351 and GSE20347 data sets from the Gene Expression Omnibus (GEO) database were employed to screen differentially expressed genes (DEGs). Reverse transcription quantitative PCR (RT‐qPCR) was used to examine hub gene expression. ECA‐109 and TE‐12 cells were transfected using the pcDNA3.1 expression vector encoding GABRP. The cell counting kit‐8 (CCK‐8), cell scratch and Transwell assays were performed to assess the effect of GABRP on EC cell proliferation, migration and invasion. Epithelial‐mesenchymal transition (EMT)‐associated protein levels were measured by Western blotting. Subsequently, CFTR was knocked down to verify whether GABRP affected biological events in EC cells by targeting CFTR. Seven hub genes were identified, including GABRP, FLG, ENAH, KLF4, CD24, ABLIM3 and ABLIM1, which all could be used as diagnostic biomarkers for EC. The RT‐qPCR results indicated that the expression levels of GABRP, FLG, KLF4, CD24, ABLIM3 and ABLIM1 were downregulated, whereas the expression level of ENAH was upregulated. In vitro functional assays demonstrated that GABRP overexpression suppressed the proliferation, migration, invasion and EMT of EC cells. Mechanistically, GABRP promoted the expression of CFTR, and CFTR knockdown significantly counteracted the influence of GABRP overexpression on biological events in EC cells. Overexpression of GABRP inhibited EC progression by increasing CFTR expression, which might be a new target for EC treatment.

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ABLIM3

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