Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Abnormal Proliferation02:23

Abnormal Proliferation

5.4K
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...
5.4K
Abnormal Proliferation02:23

Abnormal Proliferation

3.8K
3.8K
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

11.8K
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...
11.8K
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

6.0K
6.0K
The Ras Gene02:38

The Ras Gene

7.5K
The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a...
7.5K
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

10.0K
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...
10.0K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Association Between Stress Hyperglycemia Ratio and Death in Patients With Moderate to Severe Tricuspid Regurgitation.

Journal of the American Heart Association·2026
Same author

A pilot study assessing the feasibility of contrast-enhanced ultrasound for triaging fine-needle aspiration in lateral cervical lymph nodes of papillary thyroid carcinoma.

BMC cancer·2026
Same author

Hypoactivity, abnormal development of dendrites relevant to impaired synaptic transmission of calretinin-expressing interneurons in the medial prefrontal cortex underlies social deficits of mouse model in autism.

Translational psychiatry·2026
Same author

[Trends, predictions, and etiological characteristics of the incidence and mortality of lower respiratory infections among children under 14 years in China from 1990 to 2021].

Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics·2026
Same author

Exosome-derived mtDNA disrupts endothelial barrier integrity and accelerates sepsis progression by inducing mitochondrial dysfunction through the PKCδ gene.

Biochimica et biophysica acta. General subjects·2026
Same author

A TMAD-based rapid assessment model for left ventricular systolic function in patients with coronary artery disease: a multicenter prospective development and validation study.

The international journal of cardiovascular imaging·2026

Related Experiment Video

Updated: Mar 24, 2026

Targeted in Situ Mutagenesis of Histone Genes in Budding Yeast
08:48

Targeted in Situ Mutagenesis of Histone Genes in Budding Yeast

Published on: January 26, 2017

16.5K

H2A/K pseudogene mutation may promote cell proliferation.

Jisheng Guo1, Ruirui Jing1, Xin Lv1

  • 1Cancer Research Center, Shandong University School of Medicine, Jinan 250012, China.

Mutation Research
|March 9, 2016
PubMed
Summary
This summary is machine-generated.

Mutant histone H2A/K long non-coding RNAs (lncRNAs) were found to promote kidney cancer progression. These mutant H2A/K lncRNAs upregulate oncogenes, including proliferating cell nuclear antigen (PCNA), driving cell proliferation.

Keywords:
Cell proliferationH2A/KLncRNAQuantitative proteomics

More Related Videos

Engineering Oncogenic Heterozygous Gain-of-Function Mutations in Human Hematopoietic Stem and Progenitor Cells
12:04

Engineering Oncogenic Heterozygous Gain-of-Function Mutations in Human Hematopoietic Stem and Progenitor Cells

Published on: March 10, 2023

5.1K
Discovery of Driver Genes in Colorectal HT29-derived Cancer Stem-Like Tumorspheres
06:52

Discovery of Driver Genes in Colorectal HT29-derived Cancer Stem-Like Tumorspheres

Published on: July 22, 2020

7.1K

Related Experiment Videos

Last Updated: Mar 24, 2026

Targeted in Situ Mutagenesis of Histone Genes in Budding Yeast
08:48

Targeted in Situ Mutagenesis of Histone Genes in Budding Yeast

Published on: January 26, 2017

16.5K
Engineering Oncogenic Heterozygous Gain-of-Function Mutations in Human Hematopoietic Stem and Progenitor Cells
12:04

Engineering Oncogenic Heterozygous Gain-of-Function Mutations in Human Hematopoietic Stem and Progenitor Cells

Published on: March 10, 2023

5.1K
Discovery of Driver Genes in Colorectal HT29-derived Cancer Stem-Like Tumorspheres
06:52

Discovery of Driver Genes in Colorectal HT29-derived Cancer Stem-Like Tumorspheres

Published on: July 22, 2020

7.1K

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • The role of histone H2A/K pseudogenes in disease remains understudied.
  • Previous findings indicated a high prevalence of mutant H2A/K pseudogenes in kidney cancer patients.

Purpose of the Study:

  • To investigate the relationship between mutant H2A/K long non-coding RNAs (lncRNAs) and cell proliferation in kidney cancer.
  • To elucidate the molecular mechanisms by which mutant H2A/K lncRNAs influence cancer cell growth.

Main Methods:

  • Shotgun and label-free quantitative proteomics were employed to analyze protein expression changes.
  • Protein-protein interaction network analysis was performed to identify key molecular players.
  • Western blotting and cell proliferation assays were utilized for validation.

Main Results:

  • Mutant H2A/K lncRNAs significantly upregulated the expression of multiple oncogenes, thereby promoting cell proliferation.
  • A proliferating cell nuclear antigen (PCNA)-centered protein interaction network was identified as crucial for cell proliferation.
  • Western blotting confirmed the upregulation of PCNA by mutant H2A/K lncRNAs.
  • Specific mutations (C290T, C228A, A45G) in H2A/K lncRNAs were shown to enhance cell proliferation.

Conclusions:

  • Mutant H2A/K lncRNAs promote cell proliferation in kidney cancer, at least partly through the upregulation of PCNA and other oncogenes.
  • Mutant H2A/K lncRNAs represent a potential novel factor in the development of renal carcinogenesis.