IFIT3 promotes lymph node metastasis by interacting with LASP1 to activate FAK-ERK signaling in esophageal squamous cell carcinoma

Lymph node metastasis (LNM) is an important cause of poor prognosis in patients with esophageal squamous cell carcinoma (ESCC). However, the mechanism of LNM in ESCC has not been elucidated. Here, we identified interferon-induced proteins with tetratricopeptide repeats 3 (IFIT3) highly expressed in ESCC, especially in LNM tissues. IFIT3 overexpression promoted ESCC cell metastasis in vitro and in vivo. Mechanistically, IFIT3 interacted with LIM and SH3 protein 1 (LASP1) and facilitated the localization of LASP1 to the cell edge, promoting the interaction between LASP1 and Talin1 and the binding of Talin1 to integrin, ultimately activating the FAK-ERK signaling pathway. Clinically, IFIT3 and LASP1 were upregulated in ESCC and LNM tissues and associated with poor prognosis. Moreover, patients with high expression of both IFIT3 and LASP1 have a poorer prognosis. In conclusion, IFIT3 promotes LNM in ESCC through the LASP1/FAK/ERK axis, and IFIT3 is a potential therapeutic target for LNM in ESCC.

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Publication Details

Journal
Cell Death and Disease
Published
2025-12-18
DOI
https://doi.org/10.1038/s41419-025-08327-z
Primary Topic
Cell Adhesion Molecules Research
Type
article
Field-Weighted Citation Impact
0.00

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article

IFIT3 promotes lymph node metastasis by interacting with LASP1 to activate FAK-ERK signaling in esophageal squamous cell carcinoma

Yanbing Shi, Jiajia Chen, Pan Hong, Xiaolin Zhou et al.
Cell Death and Disease
Cell Adhesion Molecules Research
article

IFIT3 promotes lymph node metastasis by interacting with LASP1 to activate FAK-ERK signaling in esophageal squamous cell carcinoma

Yanbing Shi, Jiajia Chen, Pan Hong, Xiaolin Zhou, Wenting Li, J. Wang, Qixiao Cui, Defang Li, Minjing Li, Rui Zhang, Bohan Li, Guoli Wang, Xiaojie Chen, Xiaoli Li, Xiaochuan Zhao, Xihang Gao
article en

Abstract

Lymph node metastasis (LNM) is an important cause of poor prognosis in patients with esophageal squamous cell carcinoma (ESCC). However, the mechanism of LNM in ESCC has not been elucidated. Here, we identified interferon-induced proteins with tetratricopeptide repeats 3 (IFIT3) highly expressed in ESCC, especially in LNM tissues. IFIT3 overexpression promoted ESCC cell metastasis in vitro and in vivo. Mechanistically, IFIT3 interacted with LIM and SH3 protein 1 (LASP1) and facilitated the localization of LASP1 to the cell edge, promoting the interaction between LASP1 and Talin1 and the binding of Talin1 to integrin, ultimately activating the FAK-ERK signaling pathway. Clinically, IFIT3 and LASP1 were upregulated in ESCC and LNM tissues and associated with poor prognosis. Moreover, patients with high expression of both IFIT3 and LASP1 have a poorer prognosis. In conclusion, IFIT3 promotes LNM in ESCC through the LASP1/FAK/ERK axis, and IFIT3 is a potential therapeutic target for LNM in ESCC.

Cell Death and DiseaseVol. 17(1)
Shandong University of Aeronautics (CN), State Administration of Traditional Chinese Medicine of the People's Republic of China (CN), Southwest Medical University (CN)
National Natural Science Foundation of China
Openalex Percentile: Top 47%
Cell Adhesion Molecules Research
DOIOpen Access PDFOpenAlex
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