ArticleBioengineered2022
Actin-binding Rho activating C-terminal like (ABRACL) transcriptionally regulated by MYB proto-oncogene like 2 (MYBL2) promotes the proliferation, invasion, migration and epithelial-mesenchymal transition of breast cancer cells.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 15 citations in OpenAlex.
- The MYBL2-GTSE1 axis promotes laryngeal squamous cell carcinoma progression by regulating PI3K/AKT-dependent glycolytic reprogramming.Cancer biology & therapy · 2026Article
- MYBL2 promotes malignant phenotypes and M2-like macrophage polarization through CCL2 in non-small cell lung cancer.Molecular and cellular biochemistry · 2026Article
- GAS5 Downregulation Promotes the Progression of Triple-Negative Breast Cancer by Regulating Tumor Cells-MDSCs Crosstalk.Cancers · 2026Article
- FBXW7 Inhibited M2 Macrophage Polarization in Endometrial Cancer by Reducing CCL2 Secretion Through Ubiquitination of MYBL2 Subtitle: The Role of FBXW7 on M2 Macrophage Polarization in EC.Biochemical genetics · 2026Article
- LncRNA DRAIC facilitates the progression of renal cell carcinoma by modulting the microRNA-145-3p/ABRACL pathway signaling.Scientific reports · 2025Article
- ABRACL upregulated by transcription factor CBX4 promotes proliferation and migration and inhibits the apoptosis of gastric cancer cells.Histology and histopathology · 2025Article
- Stemness-Relevant Gene Signature for Chemotherapeutic Response and Prognosis Prediction in Ovarian Cancer.Stem cells international · 2025Article
- Exploring Prognostic Gene Factors in Breast Cancer via Machine Learning.Biochemical genetics · 2024Article
- The tumorigenic effect of the high expression of ABRACL in glioma and its potential as a therapeutic target.Heliyon · 2024Article
- Identification of biomarker associated with Trop2 in breast cancer: implication for targeted therapy.Discover oncology · 2024Article
- The analgesic effects of dezocine in rats with chronic constriction injuries.Experimental animals · 2023Article
- Two-Dimensional Polyacrylamide Gel Electrophoresis Coupled with Nanoliquid Chromatography-Tandem Mass Spectrometry-Based Identification of Differentially Expressed Proteins and Tumorigenic Pathways in the MCF7 Breast Cancer Cell Line Transfected for Jumping Translocation Breakpoint Protein Overexpression.International journal of molecular sciences · 2023Article
- Characterization of the Abracl-Expressing Cell Populations in the Embryonic Mammalian Telencephalon.Biomolecules · 2023Article
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Breast cancer is the most common malignant tumor in females with high incidence and mortality. Actin-binding Rho activating C-terminal like (ABRACL) was highly expressed in several cancers. We aimed to investigate the function and mechanism of ABRACL in breast cancer. In this study, biological information analysis predicted the expression of ABRACL and MYB proto-oncogene-like 2 (MYBL2) in breast cancer tissues and their possible relationship. With the application of RT-qPCR and western blot, the mRNA and protein expression of ABRACL and MYBL2 in breast cancer cell lines were assessed. After ABRACL interference, an assessment of cell proliferation was carried out using cell counting kit (CCK)-8, colony formation, and western blot. The invasive and migratory abilities of cells were determined by transwell and wound healing assays. The epithelial-mesenchymal transition (EMT) process was assayed utilizing western blot. The relationship between ABRACL and MYBL2 was confirmed by luciferase reporter assay and chromatin immunoprecipitation (ChIP). The above experiments were done again after MYBL2 overexpression in breast cancer cells with ABRACL deletion. Results revealed that ABRACL and MYBL2 were highly expressed in breast cancer tissues and cells. ABRACL knockdown suppressed the proliferation, invasion, migration, and EMT of breast cancer cells. MYBL2 transcriptionally activated ABRACL. Besides, MYBL2 overexpression reversed the effects of ABRACL knockdown on cell malignant biological behaviors. To conclude, ABRACL could be transcriptionally regulated by MYBL2 to promote cell malignant biological behaviors in breast cancer cells, implying the potential of ABRACL being a promising target for the improvement of breast cancer therapy.
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