Expression of SLC7A11 in esophageal squamous cell carcinoma tissues and its preliminary study on mediating tumor cell metabolism
10.19405/j.cnki.issn1000–1492.2026.02.012
- VernacularTitle:SLC7A11在食管鳞癌组织中的表达及其介导肿瘤细胞代谢的初步探究
- Author:
Huakun ZHANG
1
;
Mengfei SUN
2
;
Qi SUN
2
;
Ziru ZHOU
1
;
Jie YU
3
;
Yunzhao CHEN
3
;
Xiaobin CUI
1
Author Information
1. Department of Pathology， School of Medicial Sciences， Shihezi University， Shihezi 832002
2. Department of Pathology，Nanjing Drum Tower Hospital， The Affiliated Hospital of Nanjing University Medical School， Nanjing 210008
3. Department of Pathology， Zhejiang Provincial People’s Hospital & Affiliated People’s Hospital to Hangzhou Medical College， Hangzhou 310014
- Publication Type:Journal Article
- Keywords:
SLC7A11;
ESCC;
proliferation;
ferroptosis;
tumor microenvironment;
glucose metabolism;
lactate metabolism;
ATP metabolism
- From:
Acta Universitatis Medicinalis Anhui
2026;61(2):270-276
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo investigate the relationship between solute carrier family 7 member 11 （SLC7A11） expression in esophageal squamous cell carcinoma （ESCC） and clinical prognosis， and to determine its effects on ESCC cell growth， migration， and other biological activities. MethodsSLC7A11 protein expression was measured in 310 ESCC tissues and 259 adjacent normal tissues using immunohistochemistry to statistically assess the association of SLC7A11 with clinicopathologic characteristics and prognosis in ESCC patients. The expression of SLC7A11 in ESCC cell lines was suppressed through siRNA-mediated knockdown. The specific effects of SLC7A11 knockdown on proliferation and migration were evaluated using CCK-8， clonogenic assay， and Transwell assays. Adenosine triphosphate （ATP）， lactic acid and pyruvate assays were used to measure ESCC metabolism. ResultsSLC7A11 protein expression was localized predominantly in the cytoplasm of ESCC tissues. Significantly higher SLC7A11 expression levels were observed in ESCC tissues compared to adjacent normal tissues （P<0.001）. High SLC7A11 expression was associated with poorer differentiation in patients （P<0.01）. Kaplan-Meier survival analysis demonstrated significantly shorter overall survival in patients with high SLC7A11 expression compared to those with low expression （P<0.05）. CCK-8 and colony formation assays demonstrated that the knockdown of SLC7A11 expression significantly suppressed the proliferative capacity of tumor cells （P<0.001）. Furthermore， Transwell assays revealed a marked decline in tumor cell migration capacity following SLC7A11 suppression （P<0.001）. Critically， SLC7A11 knockdown also reduced intracellular levels of ATP， lactate， and pyruvate， demonstrating that SLC7A11 modulated metabolic activity in ESCC cells（P<0.001）. ConclusionThe expression level of SLC7A11 is relatively high in ESCC and is strongly associated with poor prognosis. Silencing SLC7A11 significantly inhibits esophageal cancer cell growth and migration. SLC7A11 has the ability to regulate glucose， lactic acid and ATP metabolism levels in ESCC， thereby affecting the metabolic microenvironment of ESCC.
