ArticleInternational journal of molecular medicine2018
Analysis of the oncogene BRAF mutation and the correlation of the expression of wild-type BRAF and CREB1 in endometriosis.
Article in International journal of molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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12 citing papers in PubMed, 18 citations in OpenAlex.
- An Efficient Suppression of EGFR and B-Raf mRNA Overexpression in the Lung of Benzo[a]pyrene-induced mice by Cationic Lipo-ATRA Nanoformulation.Recent patents on nanotechnology · 2025Article
- Immune micro-environment analysis and drug screening for ovarian endometriosis.Genes & genomics · 2024Article
- CREB1 Is Involved in miR-134-5p-Mediated Endometrial Stromal Cell Proliferation, Apoptosis, and Autophagy.Cells · 2023Article
- Remote regulation of rs80245547 and rs72673891 mediated by transcription factors C-Jun and CREB1 affectiScience · 2023Article
- BRAF Modulates Lipid Use and Accumulation.Cancers · 2022Article
- Somatic Genomic Events in Endometriosis: Review of the Literature and Approach to Phenotyping.Reproductive sciences (Thousand Oaks, Calif.) · 2021Review
- [Research progress on the relationship between the Raf murine sarcoma viral oncogene homolog B gene mutation and lymph node metastasis of papillary thyroid carcinoma].Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi · 2021Article
- LncRNA MALAT1 inhibits apoptosis of endometrial stromal cells through miR-126-5p-CREB1 axis by activating PI3K-AKT pathway.Molecular and cellular biochemistry · 2020Article
- Exploring the roles of fecundity-related long non-coding RNAs and mRNAs in the adrenal glands of small-tailed Han Sheep.BMC genetics · 2020Article
- Genes' Interactions: A Major Contributor to the Malignant Transformation of Endometriosis.International journal of molecular sciences · 2019Review
- Endometriosis Knowledgebase: a gene-based resource on endometriosis.Database : the journal of biological databases and curation · 2019Article
- Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
B-Raf proto-oncogene, serine/threonine kinase (BRAF) has previously been identified as a candidate target gene in endometriosis. Wild-type and mutated BRAF serve important roles in different diseases. The aim of the present study was to explore BRAF mutation, the mRNA and protein expression of wild-type BRAF (wtBRAF) in endometriosis, and the association between the expression levels of wtBRAF and the predicted transcription factor cAMP responsive element binding protein 1 (CREB1). In the present study, BRAF mutation was detected using Sanger sequencing among 30 ectopic and matched eutopic endometrium samples of patients with endometriosis as well as 25 normal endometrium samples, and no BRAF mutation was detected in exons 11 or 15. A region of ~2,000 bp upstream of the BRAF gene was then screened using NCBI and UCSC databases, and CREB1 was identified as a potential transcription factor of BRAF by analysis with the JASPAR and the TRANSFAC databases. Quantitative polymerase chain reaction was used to analysis the mRNA expression levels of wtBRAF and CREB1, and the corresponding protein expression levels were evaluated using immunohistochemistry and western blot analysis. The results revealed that the mRNA and protein expression levels of wtBRAF and CREB1 were significantly upregulated in the eutopic endometrial tissues of patients with endometriosis compared with normal endometrial tissues (P<0.05) and no significant difference in wtBRAF and CREB1 levels was detected between the ectopic and eutopic endometrium (P>0.05). In addition, correlation analysis revealed that the protein expression of CREB1 was positively correlated with the transcript level and protein expression of wtBRAF. It is reasonable to speculate that CREB1 may activate the transcription of wtBRAF through directly binding to its promoter, increasing BRAF expression and regulating the cell proliferation, migration and invasion of endometriosis.
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