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Related Concept Videos

The Ras Gene02:38

The Ras Gene

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 superfamily...
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...
The Retinoblastoma Gene01:20

The Retinoblastoma Gene

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,...
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

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...
Rous Sarcoma Virus (RSV) and Cancer01:03

Rous Sarcoma Virus (RSV) and Cancer

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...
Small GTPases - Ras and Rho01:24

Small GTPases - Ras and Rho

Ras and Rho are small monomeric GTPases that act downstream of receptor tyrosine kinase (RTK) and regulate various cellular processes. These GTPases switch between active and inactive states by binding to guanine nucleotides.
Three regulatory proteins control their activity:

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Related Experiment Video

Updated: Jul 7, 2026

Murine Prostate Micro-dissection and Surgical Castration
08:49

Murine Prostate Micro-dissection and Surgical Castration

Published on: May 11, 2016

Rad9 has a functional role in human prostate carcinogenesis.

Aiping Zhu1, Charles Xia Zhang, Howard B Lieberman

  • 1Center for Radiological Research, Columbia University, College of Physicians and Surgeons, New York, NY 10032, USA.

Cancer Research
|March 5, 2008
PubMed
Summary

Elevated Rad9 protein levels are common in prostate cancer, linked to aberrant methylation and gene amplification. Lowering Rad9 reduces tumor growth, suggesting its role as a biomarker and therapeutic target.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Prostate cancer is a leading cause of cancer death in men.
  • Cell cycle checkpoint proteins, like Rad9, are crucial for genome stability.
  • The role of Rad9 in prostate cancer pathogenesis requires investigation.

Purpose of the Study:

  • To investigate the relationship between Rad9 protein levels and prostate cancer.
  • To determine the mechanisms underlying elevated Rad9 expression in prostate cancer cells.
  • To evaluate Rad9 as a potential biomarker and therapeutic target for prostate cancer.

Main Methods:

  • Analysis of Rad9 protein levels in prostate cancer cell lines and human tumor samples.
  • Investigation of DNA methylation patterns in Rad9 intron 2 using 5'-aza-2'-deoxycytidine treatment.
  • Assessment of Rad9 gene copy number using Southern blot analysis.
  • Evaluation of Rad9's functional role by small interfering RNA-mediated knockdown and tumorigenicity assays in nude mice.

Main Results:

  • Four prostate cancer cell lines exhibited significantly higher Rad9 protein levels compared to normal prostate cells.
  • Hypermethylation of Rad9 intron 2 in DU145 cells and gene amplification in PC-3 cells were identified as mechanisms for elevated Rad9.
  • Rad9 knockdown reduced the tumorigenicity of prostate cancer cells in vivo.
  • High Rad9 protein levels were detected in a majority of human prostate tumor samples, correlating with advanced cancer stage.

Conclusions:

  • Aberrant DNA methylation and gene amplification contribute to elevated Rad9 protein levels in prostate cancer.
  • Rad9 plays an active role in prostate cancer development and progression.
  • Rad9 protein abundance serves as a promising biomarker for advanced prostate cancer and a potential target for novel diagnostic, prognostic, and therapeutic strategies.