CHINESE JOURNAL OF MEDICINAL GUIDE >
Advances in the Study of E-cadherin′s Role in Esophageal Cancer
Received date: 2025-01-09
Revised date: 2025-02-06
Accepted date: 2025-02-17
Online published: 2025-07-23
Esophageal cancer is a highly lethal malignancy characterized by strong invasiveness and low early detection rates. Studying its molecular mechanisms and potential therapeutic targets is of utmost importance. E-cadherin， a cal-cium-dependent cell adhesion molecule， plays a critical role in maintaining epithelial cell polarity and the integrity of tissue structure. In esophageal cancer， the loss of E-cadherin is often accompanied by the initiation of epitheli-al-mesenchymal transition （EMT）， a process associated with the invasiveness and metastasis of the tumor. Down-regulation of E-cadherin disrupts intercellular adhesion junctions， promotes cancer cell detachment， and facilitates their invasion into surrounding tissues， thereby accelerating tumor infiltration and metastasis. Clinically， the expression level of E-cadherin serves as a potential biomarker for predicting tumor invasiveness and patient prognosis. Effective regulation of E-cadherin expression can inhibit tumor cell migration and invasion. Fur-thermore， the loss of E-cadherin is closely associated with increased tumor cell resistance to chemotherapy and targeted therapy， suggesting that modulating E-cadherin expression may be an effective strategy to overcome drug resistance. Future research should further explore the regulatory mechanisms of E-cadherin in esophageal cancer and its potential clinical applications， providing new theoretical foundations and therapeutic strategies for precision medicine in esophageal cancer treatment. This paper reviews the role of E-cadherin in esophageal cancer and its related research progress.
贵堂 周
.
Advances in the Study of E-cadherin′s Role in Esophageal Cancer
［1］ Morgan E， Soerjomataram I， Rumgay H， et al. The global landscape of esophageal squamous cell carcinoma and esophageal adenocarcinoma incidence and mortality in 2020 and projections to 2040： new estimates from GLOBOCAN 2020［J］.Gastroenterology，2022，163（3）：649-658.e2.
［2］ He S， Xu J， Liu X， et al. Advances and challenges in the treatment of esophageal cancer［J］.Acta Pharm Sin B，2021，11（11）：3379-3392.
［3］ Huang J， Koulaouzidis A， Marlicz W， et al. Global burden， risk factors， and trends of esophageal cancer： an analysis of cancer registries from 48 countries［J］.Cancers （Basel），2021，13（1）：141.
［4］ 付神波，龚拓拓，郭俊俊.LncRNA PTENP1在TGF-β诱导的食管鳞状细胞癌上皮间质转化中的作用［J］. 肿瘤防治研究，2023，50（9）：847-853.
［5］ 曹飞，俞文豪，唐晓男.LINC01410促进食管鳞状细胞癌细胞增殖和迁移的作用及其机制研究［J］.中国癌症杂志，2024，34（8）：753-762.
［6］ 王冬杨，吴玉青，应方莉，等.E-Cadherin的表达调控及对细胞增殖的影响［J］.生物过程，2022，12（1）：10-19.
［7］ Farokhi E， Alaofi AL， Prasasty VD， et al. Mechanism of the blood-brain barrier modulation by cadherin peptides［J］.Explor Drug Sci，2024，2（28）：322-338.
［8］ Mendonsa AM， Na TY， Gumbiner BM. E-cadherin in contact inhibition and cancer［J］.Oncogene，2018，37（35）：4769-4780.
［9］ Manjula CP， Meghana B. A study of E-cadherin expression in esophageal carcinoma［J］.Arch Med Health Sci，2023，11（2）：229-233.
［10］ Muhammad AS， Sidrah， Suresh K. Analysis of E-cadherin expression in patients with esophageal squamous cell carcinoma［J］.Pak J Med Health Sci，2023，17（4）：412.
［11］ Hu K， Zheng QM， Wang YP， et al. Clinical and prognostic features of E-cadherin in adenocarcinoma of the esophagogastric junction patients［J］.Eur J Cancer Prev，2023，32（2）：119-125.
［12］ Song WP， Wang SY， Zhou SC， et al. Prognostic and clinicopathological value of twist expression in esophageal cancer： a meta-analysis［J］.World J Gastrointest Oncol，2022，14（9）：1874-1886.
［13］ Nascimento RB， Machado IAR， Silva JC， et al. Differential expression of cadherins switch and caveolin-2 during stages of oral carcinogenesis［J］.J Oral Maxillofac Pathol，2023，27（3）：507-514.
［14］ Shu C， Liu L， Xue J， et al. The downregulation of LINC00273 inhibits the proliferation， invasion， and migration of ovarian cancer cells in vivo and in vitro［J］.Ann Transl Med，2022，10（20）：1139.
［15］ Santana DAD， Braga RP， Coutinho CMC， et al. E-CADERIN， N-CADERIN， SLUG， SNAIL， and TWIST contribute to epithelial-mesenchymal transition in salivary gland tumors［J］.J Oral Pathol Med，2024，53（3）：193-200.
［16］ Sun Y， Du R， Shang Y， et al. Rho GTPase-activating protein 35 suppresses gastric cancer metastasis by regulating cytoskeleton reorganization and epithelial-to-mesenchymal transition［J］.Bioengineered，2022，13（6）：14605-14615.
［17］ Li C， Ma YQ. Prognostic significance of sex determining region Y-box 2， E-cadherin， and vimentin in esophageal squamous cell carcinoma［J］.World J Clin Cases，2022，10（27）：9657-9669.
［18］ Liu B， Li X， Li C， et al. miR-25 mediates metastasis and epithelial-mesenchymal-transition in human esophageal squamous cell carcinoma via regulation of E-cadherin signaling［J］.Bioengineered，2019，10（1）：679-688.
［19］ Li H， Wang S， Li X， et al. CDCA7 promotes TGF-β-induced epithelial-mesenchymal transition via transcriptionally regulating Smad4/Smad7 in ESCC［J］.Cancer Sci，2023，114（1）：91-104.
［20］ Pal M， Bhattacharya S， Kalyan G， et al. Cadherin profiling for therapeutic interventions in Epithelial Mesenchymal Transition （EMT） and tumorigenesis［J］.Exp Cell Res，2018，368（2）：137-146.
［21］ Rostami Abookheili A， Asadi J， Khosravi A， et al. Fucosyltransferase 3 and 8 promote the metastatic capacity of cancer stem-like cells via CD15s and E-cadherin in esophageal cancer［J］.Iran J Basic Med Sci，2024，27（8）：985-995.
［22］ Shirai R， Biebighauser T， Walker D， et al. Cadherin-11 contributes to the heterogenous and dynamic Wnt-Wnt-β-catenin pathway activation in Ewing sarcoma［J］.PLoS One，2024，19（6）：e0305490.
［23］ Wang H， Peng D， Gan M， et al. CPEB3 overexpression caused by miR-106b-5p inhibition inhibits esophageal carcinoma in-vitro progression and metastasis［J］.Anticancer Drugs，2022，33（4）：335-351.
［24］ Xie B， Maker A， Priest AV， et al. Molecular mechanism for strengthening E-cadherin adhesion using a monoclonal antibody［J］.Proc Natl Acad Sci U S A，2022，119（32）：e2204473119.
［25］ 朱凤昌，叶潇，崇小萌，等.国际细胞治疗临床研究发展现状及监管政策研究［J］.中国药物评价，2024，41（4）：257-264.
［26］ Subramani A， Cui W， Zhang Y， et al. Modulation of E-cadherin function through the AmotL2 Isoforms promotes ameboid cell invasion［J］.Cells，2023，12（13）：1682.
［27］ Shen Y， Yang L， Li L. Cancer stem-like cells contribute to paclitaxel resistance in esophageal squamous cell carcinoma［J］.Int J Clin Exp Pathol，2022，15（4）：183-190.
［28］ Zou G， Huang Y， Zhang S， et al. E-cadherin loss drives diffuse-type gastric tumorigenesis via EZH2-mediated reprogramming［J］.J Exp Med，2024，221（4）：e20230561.
［29］ Balamurugan K， Poria DK， Sehareen SW， et al. Stabilization of E-cadherin adhesions by COX-2/GSK3β signaling is a targetable pathway in metastatic breast cancer［J］.JCI Insight，2023，8（6）：e156057.
/
| 〈 |
|
〉 |