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Aberrant expression of p-Smad3 in oral carcinogenesis

Sopee Poomsawat1, Jirapa Punyasingh, Paisarn Vejchapipat

  • 1Department of Oral and Maxillofacial Pathology, Faculty of Dentistry, Mahidol University, Yothi Street, Bangkok, 10400, Thailand, spoomsawat@yahoo.com.

Clinical Oral Investigations
|July 19, 2014
PubMed
Abstract

Insights

Phosphorylated Smad3 (p-Smad3) accumulates in the cytoplasm of oral premalignant lesions and oral squamous cell carcinoma (OSCC). This cytoplasmic p-Smad3 suggests a diminished growth inhibitory effect, with aberrant nuclear localization indicating OSCC.

Area of Science:

  • Oncology
  • Cell Biology
  • Molecular Signaling

Background:

  • Smads are crucial mediators of transforming growth factor β (TGFβ) signaling.
  • TGFβ/Smad pathway dysregulation is implicated in various cancers, including oral squamous cell carcinoma (OSCC).
  • The role of phosphorylated Smad3 (p-Smad3) subcellular localization in oral carcinogenesis remains uncharacterized.

Purpose of the Study:

  • To investigate the subcellular distribution of p-Smad3 in oral leukoplakia (OL) with and without dysplasia and in OSCC.
  • To correlate p-Smad3 localization with oral carcinogenesis progression.

Main Methods:

  • Immunohistochemical analysis of p-Smad3 expression in 150 oral tissue samples (OSCC, OL with/without dysplasia, normal mucosa).
  • Quantification of cytoplasmic and nuclear p-Smad3-positive cells.
  • Statistical comparison of p-Smad3 expression frequencies across different tissue types.

Main Results:

  • Cytoplasmic p-Smad3 expression was significantly elevated in OL with dysplasia compared to normal mucosa.
  • Both cytoplasmic and cytoplasmic plus nuclear p-Smad3 expression were significantly higher in OSCC than in normal mucosa and OL.
  • Aberrant cytoplasmic and/or nuclear p-Smad3 staining was observed.

Conclusions:

  • Increased cytoplasmic p-Smad3 in OL with dysplasia and OSCC suggests a nonfunctional state, diminishing its growth-inhibitory role.
  • Cytoplasmic p-Smad3 may serve as a biomarker for oral premalignant lesions.
  • Cytoplasmic plus nuclear p-Smad3 staining could be a potential biomarker for OSCC.

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