دورية أكاديمية

STAT3-EphA7 axis contributes to the progression of esophageal squamous cell carcinoma.

التفاصيل البيبلوغرافية
العنوان: STAT3-EphA7 axis contributes to the progression of esophageal squamous cell carcinoma.
المؤلفون: Wang L; Department of Obstetrics and Gynecology, Center of Genetics and Prenatal Diagnosis, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, P. R. China., Zhao QF; Department of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, P. R. China.; Collaborative Innovation Center of Henan Province for Cancer Chemoprevention, Zhengzhou University, Zhengzhou, P. R. China., Yang BB; Department of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, P. R. China.; Collaborative Innovation Center of Henan Province for Cancer Chemoprevention, Zhengzhou University, Zhengzhou, P. R. China.; State Key Laboratory of Esophageal Cancer Prevention and Treatment, Zhengzhou University, Zhengzhou, P. R. China., Liang HJ; Department of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, P. R. China.; Collaborative Innovation Center of Henan Province for Cancer Chemoprevention, Zhengzhou University, Zhengzhou, P. R. China., Zhang XE; Department of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, P. R. China.; Collaborative Innovation Center of Henan Province for Cancer Chemoprevention, Zhengzhou University, Zhengzhou, P. R. China.; Second People's Hospital of Henan Province, Zhengzhou, P. R. China., Zhang XY; Department of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, P. R. China.; Collaborative Innovation Center of Henan Province for Cancer Chemoprevention, Zhengzhou University, Zhengzhou, P. R. China., Yang WJ; Department of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, P. R. China.; Collaborative Innovation Center of Henan Province for Cancer Chemoprevention, Zhengzhou University, Zhengzhou, P. R. China., Guo ZY; SanQuan College of XinXiang Medical University, Xinxiang, P. R. China., Xu X; College of Biotechnology, Center for Self-Propelled Nanotechnologies, Suzhou Industrial Park Institute of Services Outsourcing, Suzhou, P. R. China.; Translational Cancer Research Laboratory, Suzhou Acumen Medical Technology, Suzhou, P. R. China., Tian F; Department of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, P. R. China.; Collaborative Innovation Center of Henan Province for Cancer Chemoprevention, Zhengzhou University, Zhengzhou, P. R. China.; State Key Laboratory of Esophageal Cancer Prevention and Treatment, Zhengzhou University, Zhengzhou, P. R. China., Wu QH; Department of Obstetrics and Gynecology, Center of Genetics and Prenatal Diagnosis, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, P. R. China.
المصدر: Acta oncologica (Stockholm, Sweden) [Acta Oncol] 2023 Dec; Vol. 62 (12), pp. 1757-1766. Date of Electronic Publication: 2023 Nov 25.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Medical Journals Sweden AB Country of Publication: England NLM ID: 8709065 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1651-226X (Electronic) Linking ISSN: 0284186X NLM ISO Abbreviation: Acta Oncol Subsets: MEDLINE
أسماء مطبوعة: Publication: 2024- : [Uppsala, Sweden] : Medical Journals Sweden AB
Original Publication: Stockholm, Sweden : Acta Oncologica, [1987-
مواضيع طبية MeSH: Esophageal Neoplasms*/genetics , Esophageal Neoplasms*/pathology , Esophageal Squamous Cell Carcinoma*/genetics , Esophageal Squamous Cell Carcinoma*/pathology , STAT3 Transcription Factor*/genetics , STAT3 Transcription Factor*/metabolism , Receptor, EphA7*/metabolism, Humans ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation/genetics ; Gene Expression Regulation, Neoplastic ; Signal Transduction
مستخلص: Background: Our previous study has revealed that EphA7 was upregulated in patient-derived esophageal squamous cell carcinoma (ESCC) xenografts with hyper-activated STAT3, but its mechanism was still unclear.
Materials and Methods: To assess the association between EphA7 and STAT3, western blotting, immunofluorescence, ChIP assay, and qRT-PCR were conducted. Truncated mutation and luciferase assay were performed to examine the promoter activity of EphA7. CCK-8 assay and colony formation were performed to assess the proliferation of ESCC. Cell-derived xenograft models were established to evaluate the effects of EphA7 on ESCC tumor growth. RNA-seq analyses were used to assess the effects of EphA7 on related signals.
Results: In this study, EphA7 was found upregulated in ESCC cell lines with high STAT3 activation, and immunofluorescence also showed that EphA7 was co-localized with phospho-STAT3 in ESCC cells. Interestingly, suppressing STAT3 activation by the STAT3 inhibitor Stattic markedly inhibited the protein expression of EphA7 in ESCC cells, in contrast, activation of STAT3 by IL-6 obviously upregulated the protein expression of EphA7. Moreover, the transcription of EphA7 was also mediated by the activation of STAT3 in ESCC cells, and the -2000∼-1500 region was identified as the key promoter of EphA7. Our results also indicated that EphA7 enhanced the cell proliferation of ESCC, and silence of EphA7 significantly suppressed ESCC tumor growth. Moreover, EphA7 silence markedly abolished STAT3 activation-derived cell proliferation of ESCC. Additionally, RNA-seq analyses indicated that several tumor-related signaling pathways were significantly changed after EphA7 downregulation in ESCC cells.
Conclusion: Our results showed that the transcriptional expression of EphA7 was increased by activated STAT3, and the STAT3 signaling may act through EphA7 to promote the development of ESCC.
فهرسة مساهمة: Keywords: ESCC; EphA7; STAT3; promoter; transcription
المشرفين على المادة: 0 (STAT3 protein, human)
0 (STAT3 Transcription Factor)
EC 2.7.10.1 (Receptor, EphA7)
تواريخ الأحداث: Date Created: 20230922 Date Completed: 20231219 Latest Revision: 20231219
رمز التحديث: 20231219
DOI: 10.1080/0284186X.2023.2259601
PMID: 37738252
قاعدة البيانات: MEDLINE
الوصف
تدمد:1651-226X
DOI:10.1080/0284186X.2023.2259601