Related Experiment Video
Updated: Aug 7, 2026
Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols
Published on: June 6, 2017
Cell cycle dysregulation in oral cancer
1Department of Oral & Maxillofacial Surgery, Massachusetts General Hospital/Harvard School of Dental Medicine, Boston, MA 02115, USA. randy_todd@hms.harvard.edu
Abstract:
The dysregulation of the molecular events governing cell cycle control is emerging as a central theme of oral carcinogenesis. Regulatory pathways responding to extracellular signaling or intracellular stress and DNA damage converge on the cell cycle apparatus. Abrogation of mitogenic and anti-mitogenic response regulatory proteins, such as the retinoblastoma tumor suppressor protein (pRB), cyclin D1, cyclin-dependent kinase (CDK) 6, and CDK inhibitors (p21(WAF1/CIP1), p27(KIP1), and p16(INK4a)), occur frequently in human oral cancers. Cellular responses to metabolic stress or genomic damage through p53 and related pathways that block cell cycle progression are also altered during oral carcinogenesis. In addition, new pathways and cell cycle regulatory proteins, such as p12(DOC-1), are being discovered. The multistep process of oral carcinogenesis likely involves functional alteration of cell cycle regulatory members combined with escape from cellular senescence and apoptotic signaling pathways. Detailing the molecular alterations and understanding the functional consequences of the dysregulation of the cell cycle apparatus in the malignant oral keratinocyte will uncover novel diagnostic and therapeutic approaches.
Insights
Cell cycle control dysregulation is key in oral cancer development, affecting proteins like pRB and p53. Understanding these molecular changes in oral keratinocytes can lead to new diagnostics and therapies.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Cell cycle control is crucial for preventing cancer.
- Dysregulation of cell cycle proteins is common in oral cancers.
- Pathways involving p53, pRB, and cyclins are frequently altered.
Purpose of the Study:
- To explore the role of cell cycle dysregulation in oral carcinogenesis.
- To identify molecular alterations in oral cancer.
- To uncover novel diagnostic and therapeutic targets.
Main Methods:
- Analysis of molecular events governing cell cycle control.
- Investigation of regulatory pathways responding to signaling, stress, and DNA damage.
- Examination of alterations in key cell cycle proteins (pRB, cyclins, CDKs, CDK inhibitors, p53).
Main Results:
- Frequent abrogation of regulatory proteins like pRB, cyclin D1, CDK6, p21, p27, and p16 in oral cancers.
- Altered cellular responses to stress and DNA damage via p53 pathways.
- Discovery of new pathways and proteins, such as p12(DOC-1).
Conclusions:
- Oral carcinogenesis involves functional alterations in cell cycle regulators.
- Escape from senescence and apoptosis contributes to cancer development.
- Detailed molecular understanding can yield new diagnostic and therapeutic strategies for oral cancer.
Related Concept Videos
01:04What is the Cell Cycle?
02:11The Cell Cycle Control System
00:56What is the Cell Cycle?
02:11The Cell Cycle Control System
01:28The Cell Cycle Control System
Cyclins and cyclin-dependent kinases (Cdks) are the primary cell cycle regulators and function at the cell...
01:27Molecular Factors Affecting Cell Division
Several proteins function as internal regulators to ensure each cell cycle stage is completed faithfully before proceeding to the next. Regulator molecules may act directly or influence the activity or production of other...