Related Experiment Video

Updated: Jun 24, 2026

Murine Prostate Micro-dissection and Surgical Castration
08:49

Murine Prostate Micro-dissection and Surgical Castration

Published on: May 11, 2016

The role of SRC-1 in murine prostate cancinogenesis is nonessential due to a possible compensation of SRC-3/AIB1

Jean Ching-Yi Tien1, Suoling Zhou, Jianming Xu

  • 11. Department of Molecular and Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX, USA.

International Journal of Biological Sciences
|March 24, 2009
PubMed

Insights

Steroid receptor coactivator-1 (SRC-1) is not essential for prostate cancer development in mice, unlike SRC-3. SRC-1 loss did not affect tumor progression, suggesting SRC-3 may compensate for SRC-1 deficiency.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Androgen receptor (AR) signaling is crucial for prostate cancer.
  • Steroid receptor coactivators (SRCs), including SRC-1 and SRC-3, modulate AR activity.
  • SRC-1 and SRC-3 are implicated in endocrine cancers, with SRC-3 deficiency suppressing prostate carcinogenesis in mice.

Purpose of the Study:

  • To investigate the role of SRC-1 in prostate cancer development and progression in vivo.
  • To compare the function of SRC-1 with the known essential role of SRC-3 in prostate carcinogenesis.

Main Methods:

  • Deletion of the SRC-1 gene in TRAMP mice (prostate cancer model).
  • Assessment of tumor mass, histology, and metastasis at various ages.
  • Analysis of SRC-1 and SRC-3 expression during prostate tumorigenesis.

Main Results:

  • SRC-1 deficiency did not alter prostate cancer initiation or progression in TRAMP mice.
  • Tumor histology and distant lymph node metastasis were similar between SRC-1 knockout and wild-type mice.
  • SRC-1 expression remained constant, while SRC-3 expression increased during prostate tumorigenesis.

Conclusions:

  • SRC-1 is nonessential for mouse prostate carcinogenesis, contrasting with SRC-3's critical role.
  • SRC-3 overexpression may compensate for the loss of SRC-1 function during prostate tumorigenesis.
  • These findings highlight differential roles of SRC family members in prostate cancer.
Keywords:
AIB1SRC-1SRC-3prostate cancer

More Related Videos

A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer07:25

A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer

Published on: March 6, 2018

Related Concept Videos

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...
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...
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...
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...
Induced Pluripotent Stem Cells01:06

Induced Pluripotent Stem Cells

Stem cells are undifferentiated cells that divide and produce different cell types. Ordinarily, cells that have differentiated into a specific cell type are terminally differentiated; however, scientists have found a way to reprogram these mature cells so that they dedifferentiate and return to an unspecialized, proliferative state. These cells are pluripotent like embryonic stem cells—able to produce all cell types—and are called induced pluripotent stem cells (iPSCs).
Somatic cells are...