Related Experiment Video

Updated: Jun 19, 2026

Isolation, Culture, and Characterization of Primary Dermal Fibroblasts from Human Keloid Tissue
04:41

Isolation, Culture, and Characterization of Primary Dermal Fibroblasts from Human Keloid Tissue

Published on: July 28, 2023

X-ray irradiation suppresses keloid growth by inducing G2/M arrest through the phytosphingosine-KIF20A axis

Changyue Wu1, Dan Wu1, Jianlan Liu1

  • 1Department of Dermatology, Huashan Hospital, Fudan University, Shanghai, China.

The Journal of Investigative Dermatology
|June 17, 2026
PubMed

Insights

X-ray exposure reveals phytosphingosine (PHS) and KIF20A mediate keloid radiotherapy effects. Topical PHS or KIF20A agents offer alternatives for patients ineligible for radiation therapy.

Area of Science:

  • Dermatology
  • Molecular Biology
  • Oncology

Background:

  • Keloid radiotherapy is effective but its molecular mechanisms are not fully understood.
  • Limited accessibility of radiotherapy necessitates alternative treatment strategies.

Purpose of the Study:

  • To elucidate the molecular mechanisms of keloid radiotherapy using X-ray exposure.
  • To identify novel therapeutic targets for keloid treatment.

Main Methods:

  • Collected patient keloid samples and primary human keloid and normal skin fibroblasts.
  • Performed non-targeted metabolomics and RNA-sequencing (RNA-seq).
  • Investigated the roles of phytosphingosine (PHS) and KIF20A in keloid pathogenesis.

Main Results:

  • Identified PHS and KIF20A as key mediators in keloid radiotherapy.
  • X-ray irradiation increased PHS release, which, along with exogenous PHS, induced cell death and reduced fibrosis.
  • Combined PHS and irradiation enhanced radiosensitization, boosted G2/M arrest and apoptosis, and reduced fibrosis progression by downregulating KIF20A.

Conclusions:

  • X-ray irradiation enhances PHS secretion, downregulating KIF20A to achieve therapeutic effects in keloids.
  • Topical PHS or KIF20A-targeting agents are potential alternatives for patients unable to undergo radiotherapy.
Keywords:
Cell cycle arrestKIF20AKeloidPhytosphingosineX-ray irradiation

Related Concept Videos

Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
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 daughter...
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
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...
Negative Regulator Molecules01:23

Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
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 rapamycin-insensitive companion...