Related Concept Videos
The Tumor Microenvironment
6.6K
Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
6.6K
Tumor Immunotherapy
491
Immunotherapy is a treatment that boosts or manipulates the immune system to fight diseases, including cancer. For instance, by stimulating an immune response through vaccinations against viruses that cause cancers, like hepatitis B virus and human papillomavirus, these diseases can be prevented. Nonetheless, some cancer cells can avoid the immune system due to their rapid mutation and division. The immune response to many cancers involves three phases: elimination, equilibrium, and escape.
491
mTOR Signaling and Cancer Progression
3.8K
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...
3.8K
T Cell Types and Functions
961
When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
961
TICRR Overexpression Enhances Disease Aggressiveness and Immune Infiltration of Cutaneous Melanoma.
Cheng Chen1, Yong Zou1, Xiangbing Zheng1
1Department of Burn and Plastic Surgery, The Second People's Hospital of Yibin (West China Yibin Hospital, Sichuan University), Yibin, Sichuan, People's Republic of China.
Pharmacogenomics and Personalized Medicine
|September 9, 2024
View abstract on PubMed
Summary
TopBP1 interacting checkpoint and replication regulator (TICRR) is overexpressed in cutaneous melanoma (CM), worsening prognosis. Suppressing TICRR inhibits CM cell growth and migration, suggesting it as a potential therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
Background:
- Cutaneous melanoma (CM) is a significant public health concern.
- Identifying novel prognostic biomarkers and therapeutic targets for CM is crucial.
Purpose of the Study:
- To investigate the role of TopBP1 interacting checkpoint and replication regulator (TICRR) in CM.
- To evaluate TICRR as a prognostic biomarker and therapeutic target for CM.
Main Methods:
- TICRR expression analysis using TCGA and GTEx databases.
- Kaplan-Meier survival analysis, nomogram, and risk score modeling.
- In vitro experiments to assess TICRR's effect on CM cell aggressiveness and underlying mechanisms.
- Immune cell infiltration analysis.
Main Results:
- TICRR is overexpressed in CM and correlates with poor prognosis.
- TICRR knockdown reduces CM cell proliferation, migration, and invasion.
- TICRR suppression attenuates PI3K/AKT/mTOR signaling.
- TICRR is associated with increased immune cell infiltration.
Conclusions:
- TICRR overexpression enhances CM aggressiveness by activating PI3K/AKT/mTOR signaling and promoting immune infiltration.
- TICRR serves as a potential prognostic biomarker and therapeutic target for CM.


