Related Experiment Video
Updated: Jan 21, 2026
10:42
Generation and Culturing of Primary Human Keratinocytes from Adult Skin
Published on: December 22, 2017
17.3K
Do DLX3 and CD271 Protect Human Keratinocytes from Squamous Tumor Development?
Elisabetta Palazzo1, Alessandra Marconi2, Carlo Pincelli2
1Laboratory of Cutaneous Biology, Department of Surgical, Medical, Dental and Morphological Sciences, University of Modena and Reggio Emilia, 41100 Modena, Italy. elisabetta.palazzo1@gmail.com.
International Journal of Molecular Sciences
|July 24, 2019
Summary
This study explores the connection between CD271 and DLX3 in skin cells, suggesting it may prevent squamous skin cancer by regulating epidermal homeostasis.
Area of Science:
- Dermatology
- Molecular Biology
- Cancer Research
Background:
- Epidermal homeostasis is vital for skin health, and its disruption can lead to skin cancer.
- Transcription factors like DLX3 and neurotrophin receptors (Trk, CD271) play roles in skin regulation.
- The function of CD271 in cutaneous squamous cell carcinoma (cSCC) is not fully understood.
Purpose of the Study:
- To investigate the role of CD271 and its connection with DLX3 in keratinocytes.
- To explore the potential of the CD271-DLX3 pathway in preventing squamous skin cancer.
Main Methods:
- Analysis of CD271 expression in primary cSCC cells and SCC spheroids.
- Examination of CD271 and DLX3 expression in normal epidermis.
- Investigating the effect of neurotrophins (BDNF, NT3) on DLX3 expression in keratinocytes.
Main Results:
- CD271 is expressed at low levels in primary cSCC cells, with higher expression correlating with cell cohesion.
- In normal epidermis, CD271 is found in progenitor cells, while DLX3 is in differentiated keratinocytes.
- Brain-derived neurotrophic factor (BDNF) and neurotrophin 3 (NT3) enhance DLX3 expression.
Conclusions:
- A potential link between CD271 and DLX3 in keratinocytes is identified.
- This CD271-DLX3 interaction may be crucial for maintaining epidermal homeostasis and preventing skin cancer.
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