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Objective: To examine the transfection of Homeobox A13 (HOXA13) on epithelial-mesenchymal transition (EMT) and the expression of bone morphogenetic protein-7 (BMP-7) induced by albumin-overload in human kidney tubular epithelial cells (HKCs).
Methods: The cultured HKCs were treated with 20 mg/mL human serum albumin (HSA) for 48 hours. Protein expression of cytokeratin (CK), vimentin and HOXA13 in the HKCs was assessed by Western blot. Protein expression of CK, vimentin, and BMP-7 was also detected in HKCs transfected with lipofectamine contained HOXA13 DNA.
Results: HSA induced EMT in HKCs, presented by decreased CK expression (P<0.01) and increased vimentin expression (P<0.01). The up-regulated expression of HOXA13 transfected by lipofectamine inhibited the level of EMT induced by HSA in HKCs (P<0.05). The decreased rate of BMP-7 protein expression induced by HSA was inhibited by over-expressed HOXA13 in HKCs (P<0.05).
Conclusions: Transfection of HOXA13 in HKCs could inhibit the degree of EMT induced by albumin-overload, possibly by increasing BMP-7 expression.
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Hereditas
August 2025
Department of Obstetrics and Gynecology, Shenzhen Longhua District Maternal and Child Health Hospital, No. 68, Huawang Road, Longhua District, Shenzhen, 570105, China.
Background: Gestational diabetes mellitus (GDM) is considered the most common complication of pregnancy, and is a very dangerous disease for both mother and baby. Homeobox A13 (HOXA13) has been discovered to join into some diseases through exhibiting regulatory functions. Importantly, hypermethylation of HOXA13 has been observed in the placental tissues of preeclampsia.
View Article and Find Full Text PDFHum Immunol
May 2025
DBSBT, IIT Kharagpur, India. Electronic address:
Malfunctions of the complex interactions between embryo and components of decidua lead to recurrent implantation failure (RIF) and pre-eclampsia (PE). Developmental process regulatory HOX proteins (HOXA4,7,10,11) have been extensively studied to chalk reproductive immunology-related diseases with lesser-known effects of HOXA9, HOXA13, and their targets therein. Hence, functional enrichment and differential expression analysis of HOXA9 and HOXA13 targets were conducted to identify immunological markers in RIF and PE.
View Article and Find Full Text PDFFunct Integr Genomics
February 2025
Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, 43400 UPM Serdang, Selangor, Malaysia.
Homebox A13 (HOXA13) and homeobox B13 (HOXB13) expression dysregulation have been previously reported in bladder cancer. However, their roles in bladder carcinogenesis remain unclear. This study characterizes the distinct transcriptomic profile and pathway enrichment of HOXA13 and HOXB13 knockdown in bladder cancer cells.
View Article and Find Full Text PDFJ Biochem Mol Toxicol
February 2025
Department of Pathology, Shanxi Province Cancer Hospital/Shanxi Hospital Affiliated to Cancer Hospital, Chinese Academy of Medical Sciences/Cancer Hospital Affiliated to Shanxi Medical University, Taiyuan, Shanxi, China.
The present work explored the functions of circ_0070934 in regulating malignant phenotype of colorectal cancer (CRC) cells and its underlying mechanisms. Gene expression data set was acquired based on Gene Expression Omnibus (GEO) database for examining circ_0070934 levels within CRC cells and tissues through quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Kaplan-Meier curve and log-rank test were adopted for assessing CRC patient prognosis based on circ_0070934 level.
View Article and Find Full Text PDFJ Biol Chem
November 2024
Department of Biochemistry and Molecular Biology, SUNY Upstate Medical University, Syracuse, New York, United States. Electronic address:
Our understanding of acute leukemia pathology is heavily dependent on 11q23 chromosomal translocations involving the mixed lineage leukemia-1 (MLL1) gene, a key player in histone H3 lysine 4 (H3K4) methylation. These translocations result in MLL1-fusion (MLL1) proteins that are thought to drive leukemogenesis. However, the mechanism behind increased H3K4 trimethylation in MLL1-leukemic stem cells (MLL1-LSCs), following loss of the catalytic SET domain of MLL1 (known for H3K4 monomethylation and dimethylation) remains unclear.
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