Related Experiment Video
Updated: Jun 23, 2026
09:18
Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
Published on: December 27, 2016
REG Ialpha protein may function as a trophic and/or anti-apoptotic factor in the development of gastric cancer
Akira Sekikawa1, Hirokazu Fukui, Shigehiko Fujii
1Department of Gastroenterology and Hepatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Gastroenterology
|March 15, 2005
Summary
Regenerating gene (REG) Ialpha protein promotes early gastric cancer growth and survival. Cytokines like interferon-gamma and interleukin-6 induce REG Ialpha, which may act as a mitogenic and antiapoptotic factor in gastric cancer development.
Area of Science:
- Gastroenterology
- Oncology
- Molecular Biology
Background:
- Regenerating gene (REG) Ialpha protein is found in normal and cancerous gastric tissues, but its role in gastric cancer is unclear.
- Investigating the pathophysiologic role of REG Ialpha in early gastric cancer development is crucial.
Purpose of the Study:
- To investigate REG Ialpha protein expression in early gastric cancers.
- To determine if cytokines regulate REG Ialpha gene expression.
- To assess the trophic and antiapoptotic effects of REG Ialpha protein on gastric cancer cells.
Main Methods:
- Immunohistochemistry used to analyze REG Ialpha protein and PCNA in early gastric cancer specimens.
- Luciferase reporter assay and Northern blot analysis examined cytokine effects on REG Ialpha.
- MTT and TUNEL assays assessed REG Ialpha's impact on cell growth and apoptosis.
Main Results:
- REG Ialpha-positive cancers showed higher PCNA index and inflammation.
- Interferon-gamma and interleukin-6 enhanced REG Ialpha gene expression and promoter activity.
- REG Ialpha protein promoted cell growth, inhibited apoptosis, enhanced Akt phosphorylation, and increased Bcl-xL expression.
Conclusions:
- REG Ialpha gene is inducible by cytokine stimulation.
- REG Ialpha protein acts as a mitogenic and antiapoptotic factor in early gastric cancer development.
Related Concept Videos
02:15Experimental RNAi
RNA interference (RNAi) is a cellular mechanism that inhibits gene expression by suppressing its transcription or activating the RNA degradation process. The mechanism was discovered by Andrew Fire and Craig Mello in 1998 in plants. Today, it is observed in almost all eukaryotes, including protozoa, flies, nematodes, insects, parasites, and mammals. This precise cellular mechanism of gene silencing has been developed into a technique that provides an efficient way to identify and determine the...
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...
01:17The Extrinsic Apoptotic Pathway
The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
01:31The Intrinsic Apoptotic Pathway
Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
01:17Gastritis-II: Pathophysiology
Gastritis is marked by disruption of the mucosal barrier that usually protects the stomach tissue from digestive juices and manifests in acute and chronic forms.
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
01:26Gastritis II: Pathophysiology
The pathophysiology of gastritis begins with the colonization of the stomach lining by Helicobacter pylori (H. pylori). This bacterium spreads mainly via the oral-oral route through saliva or shared utensils, and can also be transmitted in overcrowded or unhygienic environments through contaminated water, despite its brief survival outside the body.ColonizationOnce ingested, H. pylori enters the stomach and begins colonization by navigating through the mucus layer lining the stomach wall. It...