Related Experiment Video
Updated: Jul 11, 2026

Induction of Invasive Transitional Cell Bladder Carcinoma in Immune Intact Human MUC1 Transgenic Mice: A Model for Immunotherapy Development
Published on: October 30, 2013
Cystatin M / E expression in inflammatory and neoplastic skin disorders
P L J M Zeeuwen1, I M J J van Vlijmen-Willems, H Egami
1Department of Dermatology, University Medical Center St Radboud, PO Box 9101, 6500 HB Nijmegen, the Netherlands. p.zeeuwen@derma.azn.nl
Cystatin M/E, a skin-specific protein, is upregulated during inflammation and wound healing, potentially regulating cysteine proteinases. Its expression in neoplastic skin is limited to differentiated cells, not distinguishing between benign and malignant growths.
Area of Science:
- Dermatology and Molecular Biology
- Proteinase Inhibition
- Skin Physiology
Background:
- Cystatins are natural inhibitors of cysteine proteinases, crucial for regulating proteolysis in various diseases.
- Cystatin M/E, a novel cystatin family member, is uniquely expressed in the skin, with unknown physiological functions.
- Imbalances between proteinases and inhibitors contribute to skin damage in inflammation and tumor invasion.
Purpose of the Study:
- To investigate cystatin M/E expression in inflammatory and neoplastic skin conditions.
- To elucidate the potential function of cystatin M/E in skin pathology.
- To determine if cystatin M/E expression can differentiate between various skin neoplasias.
Main Methods:
- Immunohistochemical detection of cystatin M/E using specific antibodies.
- Analysis of biopsy samples from normal skin, atopic dermatitis, psoriasis, wound healing, and various epidermal neoplasms.
- Comparison with squamous neoplasias of non-cutaneous origin.
Main Results:
- Cystatin M/E is constitutively expressed in normal skin appendages and the stratum granulosum.
- Expression extends to the stratum spinosum in inflammatory conditions (atopic dermatitis, psoriasis).
- In epidermal neoplasms, cystatin M/E is restricted to differentiated cells and keratinized nests.
Conclusions:
- Inflammation induces cystatin M/E expression in spinous layers, potentially co-localizing with transglutaminase.
- Increased cystatin M/E expression may play a role in controlling cysteine proteinases during inflammation and infection.
- Cystatin M/E expression in neoplastic epidermis is confined to well-differentiated cells, lacking discriminatory power between benign and (pre)malignant lesions.
Related Concept Videos
Mitogens and the Cell Cycle
Abnormal Proliferation
The Tumor Microenvironment
Metastasis
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
Induced Pluripotent Stem Cells
Somatic cells are...

