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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...
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,...
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...
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:
Tumor Progression02:07

Tumor Progression

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...
Tumor Progression02:07

Tumor Progression

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...

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Related Experiment Video

Updated: May 31, 2026

RhoC GTPase Activation Assay
09:58

RhoC GTPase Activation Assay

Published on: August 22, 2010

GPRC6A regulates prostate cancer progression.

Min Pi1, L Darryl Quarles

  • 1Department of Medicine, University of Tennessee Health Science Center, Memphis, Tennessee 38163, USA. mpi@uthsc.edu

The Prostate
|June 18, 2011
PubMed
Summary

G-protein coupled receptor 6A (GPRC6A) promotes prostate cancer growth and progression. Inhibiting GPRC6A in mice significantly slowed cancer development and improved survival, identifying it as a potential therapeutic target.

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Sequencing Small Non-coding RNA from Formalin-fixed Tissues and Serum-derived Exosomes from Castration-resistant Prostate Cancer Patients
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Sequencing Small Non-coding RNA from Formalin-fixed Tissues and Serum-derived Exosomes from Castration-resistant Prostate Cancer Patients

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RhoC GTPase Activation Assay
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Sequencing Small Non-coding RNA from Formalin-fixed Tissues and Serum-derived Exosomes from Castration-resistant Prostate Cancer Patients
12:13

Sequencing Small Non-coding RNA from Formalin-fixed Tissues and Serum-derived Exosomes from Castration-resistant Prostate Cancer Patients

Published on: November 19, 2019

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Oncology

Background:

  • GPRC6A is a nutrient-sensing receptor activated by amino acids, calcium, zinc, osteocalcin (OC), and testosterone.
  • Increased OC in prostate cancer cells and GPRC6A's association with prostate cancer risk suggest its role in the disease.

Purpose of the Study:

  • To investigate the expression and function of GPRC6A in prostate cancer.
  • To assess the role of GPRC6A in prostate cancer progression in vivo.

Main Methods:

  • Examined GPRC6A expression in human prostate cancer cell lines.
  • Utilized siRNA to knock down GPRC6A expression in vitro.
  • Intercrossed Gprc6a(-/-) mice with the TRAMP prostate cancer model for in vivo studies.

Main Results:

  • GPRC6A transcripts were significantly elevated in prostate cancer cell lines compared to normal cells.
  • GPRC6A ligands stimulated ERK activity, proliferation, and gene expression in prostate cancer cells, effects blocked by GPRC6A knockdown.
  • Gprc6a deficiency in TRAMP mice retarded prostate cancer progression and improved survival.

Conclusions:

  • GPRC6A is a novel target for regulating prostate growth and cancer progression.
  • Elevated GPRC6A may enhance prostate cancer cell proliferation in response to dietary and bone-derived ligands.