Related Experiment Video
Updated: Jul 3, 2026
06:52
Discovery of Driver Genes in Colorectal HT29-derived Cancer Stem-Like Tumorspheres
Published on: July 22, 2020
Increased Rac1b expression sustains colorectal tumor cell survival
1Centre of Human Genetics, National Health Institute Dr. Ricardo Jorge, Lisbon, Portugal.
Molecular Cancer Research : MCR
|July 23, 2008
Summary
Colorectal cancer cells rely on the Rac1b protein for survival. Inhibiting Rac1b triggers apoptosis and slows cell cycle progression, highlighting its role in cancer cell viability.
Area of Science:
- Molecular Biology
- Oncology
- Cell Biology
Background:
- The small GTPase Rac1 influences cell transformation via signaling pathways.
- Rac1 activation of NFkappaB promotes cell survival and proliferation.
- The Rac1b splicing variant is overexpressed in colorectal tumors, potentially driving oncogenesis.
Purpose of the Study:
- To investigate the role of endogenous Rac1b in colorectal cancer cells.
- To determine if Rac1b signaling is essential for the survival of colorectal cancer cells.
Main Methods:
- Depletion of Rac1b using small interfering RNAs (siRNAs).
- Assessment of NFkappaB activation.
- Measurement of cell viability and apoptosis.
- Analysis of cell cycle progression (G1-S phase).
Main Results:
- Rac1b depletion significantly inhibited NFkappaB activation.
- Cell viability was reduced by 50% within 48 hours of Rac1b depletion.
- Increased apoptosis was the primary cause of reduced cell viability.
- A reduced G1-S progression rate was also observed.
Conclusions:
- Colorectal cancer cells expressing Rac1b are dependent on its signaling for survival.
- Rac1b plays a critical role in maintaining colorectal cancer cell viability by promoting anti-apoptotic responses and cell cycle progression.
Related Concept Videos
02:38The 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...
Ras is a superfamily...
02:23Abnormal 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...
03:03mTOR 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...
The mTOR pathway or the...
02:53Adaptive Mechanisms in Cancer Cells
Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
01:20The 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,...
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,...
02:07Tumor 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...
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...