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TGFBI Expression in Cancer Stromal Cells is Associated with Poor Prognosis and Hematogenous Recurrence in Esophageal Squamous Cell Carcinoma

  • Translational Research and Biomarkers
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Abstract

Background

Esophageal squamous cell carcinoma (ESCC) is an important cause of cancer-related death worldwide. To improve prognoses in patients with ESCC, we evaluated the potential of transforming growth factor-beta-induced protein (TGFBI), which is overexpressed in ESCC, as a therapeutic candidate.

Methods

We examined the clinical significance of TBFBI in 102 ESCC samples using real-time RT-PCR. Immunohistochemical studies were conducted to examine the localization of TGFBI. Knockdown of TGFBI in cocultured fibroblasts was performed to determine the roles of TGFBI in migration and invasion.

Results

The level of TGFBI in ESCC tissues was higher than that in normal tissues. The high TGFBI expression group (n = 16) had higher TGFB1 expression and more frequent hematogenous recurrence than the low-expression group (n = 86). High TGFBI expression was an independent prognostic factor in patients with ESCC. TGFBI was mainly localized in stromal cells of ESCC. Moreover, suppression of TGFBI in fibroblasts inhibited the migration and invasion capacity of TE8 ESCC cells.

Conclusions

High TGFBI expression in ESCC tissues could be a powerful biomarker of poor prognosis and hematogenous recurrence. TGFBI in stromal cells might be a promising molecular target for ESCC treatment.

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Acknowledgment

The authors thank Ms. Yukie Saito, Ms. Tomoko Yano, Ms. Yuka Matsui, Ms. Ayaka Ishida, and Ms. Ayaka Ishikubo for their assistance. This work was supported in part by Grants-in-Aid for Scientific Research from the Japan Society for the Promotion of Science (JSPS), Grant Numbers 21591690, 22591450, and 23591857.

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Correspondence to Daigo Ozawa MD.

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Ozawa, D., Yokobori, T., Sohda, M. et al. TGFBI Expression in Cancer Stromal Cells is Associated with Poor Prognosis and Hematogenous Recurrence in Esophageal Squamous Cell Carcinoma. Ann Surg Oncol 23, 282–289 (2016). https://doi.org/10.1245/s10434-014-4259-4

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  • DOI: https://doi.org/10.1245/s10434-014-4259-4

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