Epithelium-specific ETS transcription factor 1 (ESE1) has been implicated in epithelial homeostasis, inflammation, as well as tumorigenesis, and cancer progression. However, numerous studies have reported contradictory roles-as an oncogene or a tumor suppressor of ESE1 in different cancers, and its function in the development and progression of pancreatic ductal adenocarcinoma (PDAC) has remained largely unexplored. Herein, we report that ESE1 was found upregulated in primary PDAC compared to normal pancreatic tissue, but high expression of ESE1 correlated to better relapse-free survival in patients with PDAC. Interestingly, ESE1 was found to exhibit dual roles in regulation of malignant properties of PDAC cells in that its overexpression promoted cell proliferation, whereas its downregulation enhanced epithelial-mesenchymal transition (EMT) phenotype. In the context of TGF-β-induced EMT, ESE1 is markedly downregulated at post-transcriptional level, and reconstituted ESE1 expression partially reversed TGF-β-induced EMT marker expression. Furthermore, we identify AGR2 as a novel transcriptional target of ESE1 that participates in TGF-β-induced EMT in PDAC. Collectively, our findings reveal an ESE1/AGR2 axis that interacts with TGF-β signaling to modulate EMT phenotype in PDAC.
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http://dx.doi.org/10.1002/cam4.5397 | DOI Listing |
ACS Omega
December 2024
Department of Gastroenterology, The Affiliated Changzhou Second People's Hospital of Nanjing Medical University, Changzhou, Jiangsu 213003, China.
Disulfidptosis, a recently identified pathway of cellular demise, served as the focal point of this research, aiming to pinpoint relevant lncRNAs that differentiate between hepatocellular carcinoma (HCC) with and without vascular invasion while also forecasting survival rates and responses to immunotherapy in patients with vascular invasion (VI+). First, we identified 300 DRLRs in the TCGA database. Subsequently, utilizing univariate analysis, LASSO-Cox proportional hazards modeling, and multivariate analytical approaches, we selected three DRLRs (AC009779.
View Article and Find Full Text PDFWorld J Gastroenterol
December 2024
Department of General Surgery, Guangdong Provincial Key Laboratory of Precision Medicine for Gastrointestinal Tumor, Nanfang Hospital, Southern Medical University, Guangzhou 510515, Guangdong Province, China.
Background: Advanced gastric tumors are extremely prone to metastasize the in 20%-30% of gastric cancer, and patients have a poor prognosis despite systemic chemotherapy. Peritoneal metastases from gastric cancer usually indicate the end stage of the disease without curative treatment.
Aim: To peritoneal metastasis for facilitating clinical therapy are urgently needed.
J Cell Commun Signal
March 2025
Papillary thyroid carcinoma (PTC), the most common thyroid cancer, has been linked to various molecular alterations. This study focuses on microRNA-223-3p, whose upregulated expression in PTC tissues appears to enhance tumor growth and cellular dysfunctions. Our findings demonstrate that microRNA-223-3p significantly promotes cell proliferation, invasion, and migration and induces epithelial-mesenchymal transition (EMT).
View Article and Find Full Text PDFOpen Life Sci
December 2024
Department of Gastroenterology, The Ninth People's Hospital of Chongqing, No. 69, Jialing Village, Beibei District, Chognqing, 400700, China.
Colorectal cancer (CRC) is a common malignant tumor characterized by a high degree of invasiveness, and since zinc-α2 glycoprotein (ZAG) has been implicated in the progression of several malignancies, this study was designed to investigate the role of ZAG in CRC. Its expression was assessed using the GEPIA database, and short hairpin RNA (shRNA) interference was conducted to create ZAG knockdown in CRC cell lines. We also conducted lipid synthesis, cell proliferation, apoptosis, and epithelial-mesenchymal transition (EMT) experiments to elucidate the effects of ZAG expression on CRC, as well as explored the potential underlying mechanistic pathways.
View Article and Find Full Text PDFJ Med Chem
December 2024
School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China.
In this study, we discovered and identified a novel AXL/triple angiokinase inhibitor by rational structural modification based on the structure of triple angiokinase inhibitor Nintedanib. We found that potently inhibited AXL expression with the IC value of 3.75 nM and possessed similar inhibitory activity on KDR as Nintedanib.
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