Jove
Visualize
お問い合わせ
JoVE
x logofacebook logolinkedin logoyoutube logo
JoVEについて
概要リーダーシップブログJoVEヘルプセンター
著者向け
出版プロセス編集委員会範囲と方針査読よくある質問投稿
図書館員向け
推薦の声購読アクセスリソース図書館諮問委員会よくある質問
研究
JoVE JournalMethods CollectionsJoVE Encyclopedia of Experimentsアーカイブ
教育
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab Manual教員リソースセンター教員サイト
利用規約
プライバシーポリシー
ポリシー

関連する概念動画

The Retinoblastoma Gene01:20

The Retinoblastoma Gene

4.2K
Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
4.2K
Tumor Progression02:07

Tumor Progression

6.5K
Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
6.5K
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

5.1K
Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
5.1K
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

8.0K
Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
8.0K
Replicative Cell Senescence02:15

Replicative Cell Senescence

3.7K
Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds...
3.7K
Rous Sarcoma Virus (RSV) and Cancer01:03

Rous Sarcoma Virus (RSV) and Cancer

5.4K
Rous Sarcoma virus or RSV was discovered by F. Peyton Rous in the year 1911 as a filterable transmissible agent that could cause tumors in chickens. He won a Nobel Prize for this discovery in 1966. His experiments clearly demonstrated that some cancers could be caused by infectious agents and led to the discovery of many more cancer-causing viruses in animals as well as humans.
RSV is a retrovirus that contains two copies of a plus-strand  RNA genome. Its genome consists of four main open...
5.4K

こちらも読む

関連記事

共著者、ジャーナル、引用グラフによってこの研究に関連する記事。

並び替え
Same author

Skin Epidermal Progenitor Maintenance by the SRCAP-H2A.Z Axis Downstream to Extracellular Signal-Regulated Kinase and mTOR Signaling.

The Journal of investigative dermatology·2025
Same author

CASZ1 Is Essential for Skin Epidermal Terminal Differentiation.

The Journal of investigative dermatology·2024
Same author

Nucleoporin downregulation modulates progenitor differentiation independent of nuclear pore numbers.

Communications biology·2023
Same author

NUP98 and RAE1 sustain progenitor function through HDAC-dependent chromatin targeting to escape from nucleolar localization.

Communications biology·2023
Same author

CDK9 activity switch associated with AFF1 and HEXIM1 controls differentiation initiation from epidermal progenitors.

Nature communications·2022
Same author

GPSmatch: an R package for comparing Genomic-binding Profile Similarity among transcriptional regulators using customizable databases.

Bioinformatics (Oxford, England)·2021

関連する実験動画

Updated: Sep 10, 2025

In Vivo CRISPR/Cas9 Screening to Simultaneously Evaluate Gene Function in Mouse Skin and Oral Cavity
07:52

In Vivo CRISPR/Cas9 Screening to Simultaneously Evaluate Gene Function in Mouse Skin and Oral Cavity

Published on: November 2, 2020

6.6K

支配的なSRCAP断片化変異は,状細胞がんの進行を促進する.

Stephenie H Droll1, Elena I O Dewar1, Celia Xue1

  • 1Northwestern University, Department of Molecular Biosciences, Evanston, IL, 60208, USA.

Oncogenesis
|August 26, 2025
PubMed
まとめ

新種のSRCAP変異 (SRCAP-1879) は上皮がんの進行を促し,増殖と侵入を増加させます. これは浮遊港症候群に関連したSRCAP変異とは異なり,皮膚がんの発症における新たな役割を強調しています.

さらに関連する動画

Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer
28:15

Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer

Published on: July 28, 2010

12.5K
An Immunofluorescent Method for Characterization of Barrett’s Esophagus Cells
08:54

An Immunofluorescent Method for Characterization of Barrett’s Esophagus Cells

Published on: July 20, 2014

14.1K

関連する実験動画

Last Updated: Sep 10, 2025

In Vivo CRISPR/Cas9 Screening to Simultaneously Evaluate Gene Function in Mouse Skin and Oral Cavity
07:52

In Vivo CRISPR/Cas9 Screening to Simultaneously Evaluate Gene Function in Mouse Skin and Oral Cavity

Published on: November 2, 2020

6.6K
Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer
28:15

Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer

Published on: July 28, 2010

12.5K
An Immunofluorescent Method for Characterization of Barrett’s Esophagus Cells
08:54

An Immunofluorescent Method for Characterization of Barrett’s Esophagus Cells

Published on: July 20, 2014

14.1K

科学分野:

  • 腫瘍学
  • 分子生物学
  • 遺伝学

背景:

  • 皮膚状細胞癌 (cSCC) を含む上皮がんは,がんによる死亡の主な原因である.
  • 染色体リモデレータであるSRCAP遺伝子は,cSCCで頻繁に変異します.
  • SRCAP変異は浮遊港症候群 (FHS) を引き起こすことが知られているが,cSCCにおけるその役割は理解されていない.

研究 の 目的:

  • cSCCの病原性における特定のSRCAP切断変異 (SRCAP-1879) の役割を調査する.
  • FHSに関連するSRCAP変異とSRCAP変異の影響を区別する.

主な方法:

  • cSCC変異の分析により,ホットスポットSRCAP切断 (SRCAP-1879) を特定する.
  • cSCCモデルと原始ヒトケラチノサイトにおけるSRCAP-1879およびSRCAP-FHS断片化の表現
  • 増殖,分化,侵入,遺伝子発現 (MMP9) と細胞運動性の評価

主要な成果:

  • SRCAP-1879変異は,cSCCモデルにおける増殖を大幅に増加させ,差別化を阻害し,侵入を加速した.
  • SRCAP-1879は,H2A. Zの占有率を変えることなく,ケラチノシートの主要な癌に関連する遺伝子を乱用しました.
  • SRCAP- FHS変異とは異なり,MMP9発現とケラチノシートの運動性を強く誘導した.

結論:

  • SRCAP-1879の断片化変異は,上皮がんの進行,特に侵入を促進する際には,独特で重要な役割を果たします.
  • この発見は,SRCAPがFHSにおける既知の役割を超えて,癌における機能の理解を広げています.
  • MMP9をターゲットにすることで,SRCAP-1879変異によって引き起こされるcSCCの治療戦略を提案することができる.