Related Experiment Video
Updated: Jun 10, 2026
08:19
Transfer of Manipulated Tumor-associated Neutrophils into Tumor-Bearing Mice to Study their Angiogenic Potential In Vivo
Published on: July 20, 2019
NFYA Activates REG1A Expression to Promote Malignant Progression and Chemosensitivity in Rectal Cancer
Xiaolu Zhai1, Mei Hua1, Ying Chen1
1Department of Oncology, Nantong First People's Hospital and Affiliated Hospital 2 of Nantong University, Nantong, China.
Annals of Clinical and Laboratory Science
|June 8, 2026
Summary
The Nuclear Transcription Factor Y subunit alpha (NFYA) promotes Regenerating Islet-1 Alpha (REG1A) expression, enhancing rectal cancer progression and resistance to therapy. Targeting the NFYA-REG1A axis may offer new rectal cancer treatment strategies.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Genomics
Background:
- Rectal cancer (RC) progression involves complex molecular mechanisms.
- Understanding these mechanisms is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the molecular drivers of rectal cancer progression.
- To identify potential therapeutic targets for rectal cancer treatment.
Main Methods:
- Utilized TCGA, GEPIA, TIMER, and UALCAN databases for gene expression analysis.
- Performed qPCR, Western Blot, CCK-8, ChIP, and DLR assays for validation.
- Conducted in vivo experiments to confirm gene-target interactions.
Main Results:
- Identified Regenerating Islet-1 Alpha (REG1A) as significantly upregulated in rectal cancer.
- Demonstrated that Nuclear Transcription Factor Y subunit alpha (NFYA) drives REG1A expression.
- Showed the NFYA-REG1A axis enhances rectal cancer cell survival and resistance to radiation therapy (RT) and chemotherapy (CT).
Conclusions:
- The NFYA-REG1A axis is a key player in rectal cancer malignant progression and therapeutic resistance.
- Targeting the NFYA-REG1A interaction presents a potential therapeutic strategy for rectal cancer.
Related Concept Videos
02:26NF-κB-dependent Signaling Pathway
The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
02:38Mitogens and the Cell Cycle
Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
01:28Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists
Neurokinin 1 (NK1) receptors are distributed across the GI tract, vagal afferents, and key CNS regions including the central vomiting center and chemoreceptor trigger zone (CTZ) Chemotherapy agents stimulate enterochromaffin cells in the gastrointestinal (GI) tract to release large amounts of substance P (SP). SP is a neuropeptide released by specific sensory nerves in response to many different stressors, including those in the GI mucosa affected by chemotherapy. SP binds and activates these...
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...
01:11Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase
Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
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...