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Background <p>ATPR (4-amino-2-trifluoromethyl-phenyl retinate), a derivative of ATRA (all-trans retinoic acid), exhibits potent anti-cancer activity by restoring the differentiation capacity of tumor cells. It has lower cytotoxicity compared to ATRA, making it a clinically valuable therapeutic agent. Endocan, encoded by ESM-1, a glycoprotein secreted by endothelial cells, is involved in multiple cellular proliferation processes. The high invasive capacity of gastric cancer is associated with abnormal differentiation. This study aims to investigate the mechanism by which ATPR modulates the differentiation capacity of gastric cancer cells and to elucidate the critical role of endocan in this process.</p> Methods <p>Gastric cancer cells (SGC-7901) were cultured and treated with a specific concentration of ATPR. We then performed Hoechst dye staining to assess cell viability, measured the activities of alkaline phosphatase (AKP) and lactate dehydrogenase (LDH) and examined endocan mRNA and protein levels. Subsequently, SGC-7901 cells cultured with ATPR were transfected with small interfering RNA (siRNA) targeting endocan. Changes in LDH and AKP activities were compared between the control group and the endocan knockdown group.</p> Results and conclusions <p>In gastric cancer cells treated with ATPR, there was a significant reduction in the activities of LDH and AKP, accompanied by a marked increase in endocan expression at both mRNA and protein levels. In stable endocan-knockdown gastric cancer cells, the activities of LDH and AKP were significantly restored. These results suggest that ATPR promotes gastric cancer cell differentiation via endocan.</p>

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ATPR promotes differentiation in gastric cancer cells by endocan

  • 期刊论文

  • 发表日期：

    2026年7月2日

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  • Jian Zhong,
  • Qingya He,
  • Xiaoli Jiang,
  • Wenjing Zhou,
  • Zihan Wang,
  • Shengquan Zhang,
  • Sumei Zhang

摘要

Background

ATPR (4-amino-2-trifluoromethyl-phenyl retinate), a derivative of ATRA (all-trans retinoic acid), exhibits potent anti-cancer activity by restoring the differentiation capacity of tumor cells. It has lower cytotoxicity compared to ATRA, making it a clinically valuable therapeutic agent. Endocan, encoded by ESM-1, a glycoprotein secreted by endothelial cells, is involved in multiple cellular proliferation processes. The high invasive capacity of gastric cancer is associated with abnormal differentiation. This study aims to investigate the mechanism by which ATPR modulates the differentiation capacity of gastric cancer cells and to elucidate the critical role of endocan in this process.

Methods

Gastric cancer cells (SGC-7901) were cultured and treated with a specific concentration of ATPR. We then performed Hoechst dye staining to assess cell viability, measured the activities of alkaline phosphatase (AKP) and lactate dehydrogenase (LDH) and examined endocan mRNA and protein levels. Subsequently, SGC-7901 cells cultured with ATPR were transfected with small interfering RNA (siRNA) targeting endocan. Changes in LDH and AKP activities were compared between the control group and the endocan knockdown group.

Results and conclusions

In gastric cancer cells treated with ATPR, there was a significant reduction in the activities of LDH and AKP, accompanied by a marked increase in endocan expression at both mRNA and protein levels. In stable endocan-knockdown gastric cancer cells, the activities of LDH and AKP were significantly restored. These results suggest that ATPR promotes gastric cancer cell differentiation via endocan.