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Updated: Jan 28, 2026

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WISP2 exhibits its potential antitumor activity via targeting ERK and E-cadherin pathways in esophageal cancer cells

Da-Min Chai1, Yan-Zi Qin1, Shi-Wu Wu1

  • 1Department of Pathology, the First Affiliated Hospital of Bengbu Medical University, Bengbu Medical College, Changhuai road 287#, Bengbu, Anhui, 233000, People's Republic of China.

Journal of Experimental & Clinical Cancer Research : CR
|February 28, 2019
PubMed
Abstract

Insights

WISP2 acts as a tumor suppressor in esophageal squamous cell carcinoma (ESCC). Activating WISP2 inhibits ESCC cell growth, migration, and invasion, offering a potential therapeutic strategy.

Area of Science:

  • Oncology
  • Molecular Biology

Background:

  • WISP2 (Wnt-1 inducible signaling pathway protein 2) is implicated in cancer cell proliferation, migration, invasion, and metastasis.
  • The specific role of WISP2 in esophageal squamous cell carcinoma (ESCC) remains largely uncharacterized.

Purpose of the Study:

  • To investigate the functional role of WISP2 in ESCC.
  • To elucidate the underlying molecular mechanisms by which WISP2 influences ESCC cell behavior.

Main Methods:

  • Assessed cell proliferation (MTT assay) and apoptosis (FACS) following WISP2 modulation in ESCC cells.
  • Analyzed cell migration (wound healing assay) and invasion (Transwell assay).
  • Quantified expression of ERK1/2, Slug, and E-cadherin via Western blot; WISP2 expression in ESCC tissues determined by IHC.

Main Results:

  • WISP2 overexpression correlated with improved survival in ESCC patients.
  • Overexpression of WISP2 suppressed ESCC cell growth, induced apoptosis, and inhibited migration and invasion, also retarding tumor growth in vivo.
  • Downregulation of WISP2 promoted cell growth, inhibited apoptosis, and enhanced migration and invasion.
  • WISP2 exerts tumor-suppressive effects through regulating ERK1/2, Slug, and E-cadherin pathways.

Conclusions:

  • WISP2 functions as a tumor suppressor in ESCC.
  • WISP2's regulation of ERK1/2, Slug, and E-cadherin mediates its anti-cancer effects.
  • Activating WISP2 presents a promising therapeutic avenue for ESCC treatment.
Keywords:
Esophageal cancerInvasionMigrationProliferationWISP2

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