Aim: Ovarian cancer (OC) is a fatal female malignant tumor that severely impacts the health of women worldwide. Due to the lack of diagnostic biomarkers, 70% of OC patients are considered in the advanced stage at the first diagnosis. Exploring novel biomarkers for OC diagnosis has become an urgent clinical need to address. TRIB1 is a newly discovered oncogene in several malignant tumors, including acute myeloid leukemia, prostate cancer, and breast cancer. However, the biological function of TRIB1 in OC remains uncertain and, therefore, was explored in the present study.
Methods: Levels of TRIB1 in OC and normal tissues were evaluated in the GEPIA database. TRIB1-KD was constructed in ES-2 cells and TRIB1-OE was constructed in OVCAR3 cells using a siRNA and OE vector, respectively. The proliferation ability was determined using the CCK-8 and clone formation assays. The migration ability was detected using the wound healing and Transwell assays. The expression of epithelial-mesenchymal transition (EMT) biomarkers was determined using western blotting.
Results: TRIB1 was markedly upregulated in OC tissues compared with normal ovarian tissues in the GEPIA database. The TRIB1 level was slightly altered among ES-2, CAOV3, and SKOV3 cells, with the highest expression in ES-2 cells, which was greatly reduced in OVCAR3 cells. In TRIB1-KD ES-2 cells, a remarkably reduced proliferation ability was observed with the CCK-8 and clone formation assays, accompanied by a reduction in migration distance in the Wound healing assay and the number of migrated cells in the Transwell assay. In contrast, in TRIB1-OE OVCAR3 cells, increased proliferation ability was observed, accompanied by increased migration distance and number of migrated cells. Furthermore, EMT progression was markedly repressed in TRIB1-KD ES-2 cells and remarkably enhanced in TRIB1-OE OVCAR3 cells.
Conclusion: TRIB1 facilitated the proliferation and migration of OC cells by enhancing EMT progression.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.14670/HH-18-868 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
TRIB1 facilitates the proliferation and migration of ovarian cancer cells by inducing EMT progression.
Histol Histopathol
December 2024
Department of Microbiology, Tumor and Cell Biology, Karolinska Institute, Solna, Sweden.
Aim: Ovarian cancer (OC) is a fatal female malignant tumor that severely impacts the health of women worldwide. Due to the lack of diagnostic biomarkers, 70% of OC patients are considered in the advanced stage at the first diagnosis. Exploring novel biomarkers for OC diagnosis has become an urgent clinical need to address.
View Article and Find Full Text PDFHDC downregulation induced by chronic stress promotes ovarian cancer progression via the IL-6/STAT3/S100A9 pathway.
Front Pharmacol
December 2024
Fengxian Hospital, School of Pharmaceutical Sciences, Southern Medical University, Shanghai, China.
Objective: This study aimed to investigate the underlying mechanism of chronic stress promoting ovarian cancer growth comorbid with depression and evaluate the potential role of histamine (HIS) in treating this comorbidity.
Methods: Chronic unpredictable mild stress (CUMS) was used to establish a comorbid mouse model of ovarian cancer and depression. The behavioral phenotypes were assessed using the sucrose preference test (SPT), tail suspension test (TST), forced swimming test (FST), and open field test (OFT).
Collective total synthesis of chartreusin derivatives and bioactivity investigations.
Chem Sci
December 2024
National Research Center for Carbohydrate Synthesis, Jiangxi Normal University 99 Ziyang Avenue Nanchang 330022 China
Capitalizing on Hauser annulation and Yu glycosylation, the chemical synthesis of chartreusin-type aromatic polycyclic polyketide glycosides has been investigated, culminating in the successful establishment of chemical approaches toward chartreusin derivatives with intricate chemical structures but promising bioactivities. Based on the chemical synthesis strategy, the first and collective chemical syntheses of chartreusin, D329C, and elsamicins A and B have been accomplished. The chemical strategy was featured by two complementary routes to secure chartarin 10--monosaccharide glycosides, the key intermediates in chartreusin derivative synthesis, as well as the highly stereoselective construction of the difficult glycosidic linkages.
View Article and Find Full Text PDFThe YAP1-MAML2 fusion drives tumorigenesis and sustains tumor growth.
Mol Ther Oncol
December 2024
Department of Molecular Genetics and Microbiology, University of Florida, Gainesville, FL 32610, USA.
The Yes1-associated transcriptional regulator-mastermind-like transcriptional co-activator 2 (YAP1-MAML2 [YM]) fusion protein arises from an intrachromosomal inversion and is implicated in various cancers. However, the oncogenic role of the endogenous YM fusion protein remained undefined. In this study, we employed YM-positive ES-2 ovarian cancer cells as a model to explore the roles of the YM fusion in cancer initiation and maintenance.
View Article and Find Full Text PDFTissue factor pathway inhibitor-2 inhibits integrin β1 activation and focal adhesion formation and suppresses peritoneal ovarian cancer dissemination in mice.
Biochem Biophys Res Commun
December 2024
Molecular Pathology and Genetics Division, Kanagawa Cancer Center Research Institute, 2-3-2 Nakao, Asahi Ward, Yokohama, Kanagawa, 241-8515, Japan. Electronic address:
Tissue factor pathway inhibitor-2 (TFPI2) is a Kunitz-type serine protease inhibitor and an ovarian clear cell carcinoma (CCC) biomarker. TFPI2 is expressed in several cancers and exerts tumor-suppressive effects; however, the role of TFPI2 in the CCC cell phenotype remains unclear. Therefore, in this study, we investigated the function of TFPI2 by establishing a gene knockout (KO) in ES-2 CCC cells and observed the change in phenotypes in vitro and in vivo.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!