4.7 Article

CD36 Expression Is Associated with Cancer Aggressiveness and Energy Source in Esophageal Squamous Cell Carcinoma

Journal

ANNALS OF SURGICAL ONCOLOGY
Volume 28, Issue 2, Pages 1217-1227

Publisher

SPRINGER
DOI: 10.1245/s10434-020-08711-3

Keywords

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Funding

  1. Japan Society for the Promotion of Science [17K19893, 18K07665, 18H02877]
  2. Princess Takamatsu Cancer Research Fund
  3. Suzuken Memorial Foundation
  4. Pancreas Research Foundation of Japan
  5. Grants-in-Aid for Scientific Research [17K19893, 18H02877, 18K07665] Funding Source: KAKEN

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High CD36 expression is significantly associated with ESCC progression, and CD36 suppression can reduce proliferation and invasiveness in ESCC cells. ESCC cells under CD36 suppression use specific EAAs as energy sources, while cell viability under CD36 expression depends on FAs.CD36 may serve as a potential biomarker and therapeutic target in ESCC.
Background Esophageal squamous cell carcinoma (ESCC) is an important cause of cancer-related death worldwide. CD36, a long-chain fatty acid (FA) receptor, can initiate metastasis in human oral squamous cell carcinoma (SCC), and its expression is associated with poor prognosis in several cancers. The clinical significance of CD36 expression and its function in ESCC remain unknown. Methods We examined the clinical significance of CD36 expression in 160 ESCC samples using immunohistochemical staining. Functional analysis was performed to determine the association between CD36 and ESCC characteristics (proliferative ability, invasive ability, and energy source dependency). Results Thirty (18.8%) ESCC cases showed high CD36 expression, indicating a significant association with progression. CD36 suppression inhibited proliferation and invasiveness in ESCC cells. ESCC cells with CD36 suppression used specific essential amino acids (EAAs) as energy sources. Cell viability depended on FAs under CD36 expression. The viability of ESCC cells with CD36 suppression depended on EAAs but not FAs. Conclusions CD36 may be a good biomarker and therapeutic target in ESCC. Our data provide new insights into the basic mechanism of CD36-dependent energy utilization for ESCC survival. CD36 might be a key regulator of the dependency of FAs as energy source in ESCC cells.

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