Downregulation of PTEN expression in psoriatic lesions

Yadi Li1, Xiaohong Man, Liping You

  • 1Department of Dermatology, Xuanwu Hospital, Capital Medical University, Beijing, China; Department of Dermatology, Beijing Tongren Hospital, Capital Medical University, Beijing, China.

Abstract

Insights

Reduced phosphatase and tensin homolog (PTEN) expression in psoriasis lesions may drive keratinocyte hyperproliferation by overactivating the PI3K/Akt pathway. This study investigated PTEN levels in psoriatic skin.

Area of Science:

  • Dermatology
  • Molecular Biology
  • Oncology

Background:

  • Tumor suppressor phosphatase and tensin homolog (PTEN) inhibits cell proliferation via the PI3K/Akt pathway.
  • PTEN loss-of-function is common in human tumors.
  • Akt activity is elevated in psoriatic lesions, but PTEN's role is unknown.

Purpose of the Study:

  • Investigate PTEN expression in psoriasis.
  • Determine the correlation between PTEN and the PI3K/Akt pathway in psoriasis.

Main Methods:

  • Quantitative RT-PCR to measure PTEN mRNA levels.
  • Western blotting and immunohistochemistry to assess PTEN protein expression.
  • Analysis of skin samples from 18 psoriasis patients and 19 healthy controls.

Main Results:

  • PTEN mRNA levels were significantly decreased in psoriatic lesions compared to normal skin.
  • PTEN protein expression was also lower in psoriatic lesions.
  • Reduced PTEN mRNA correlated with decreased PTEN protein levels.

Conclusions:

  • Downregulation of PTEN expression in psoriasis may contribute to PI3K/Akt pathway overactivation.
  • Reduced PTEN correlates with psoriatic keratinocyte hyperproliferation.

Related Concept Videos

Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
4.0K
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
10.3K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
5.2K
Receptor Downregulation in MVBs01:15

Receptor Downregulation in MVBs

Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
The EGFR can initiate signaling pathways that  lead to cell proliferation, migration, and differentiation. Overexpression of EGFR  stimulates cells to proliferate. Excessive  EGFR...
2.0K
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
7.2K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
3.6K