Cancer cells exhibit an unregulated cell cycle, leading to uncontrolled growth and division.
A tumor may remain localized but poses a risk for infiltration into surrounding normal tissues.
A cancer cell can detach from the primary tumor and migrate into nearby healthy tissue.
This migration can lead to further division and the creation of new tumor sites.
Migration refers to cancer cells moving a short distance from the original tumor.
Metastasis involves the spread of cancer cells to distant locations in the body.
Requires entry into blood vessels or the lymphatic system.
Following entry, cancer cells travel through the circulatory system to colonize distant organs.
Example: Breast cancer cells commonly migrate to the lungs, resulting in secondary lung tumors.
Once in circulation, cells must exit blood vessels into surrounding tissues to form new tumors.
Angiogenesis is the process through which tumors develop new blood vessels.
Tumors need blood vessels to sustain growth beyond a certain size by accessing nutrients (e.g., glucose) and oxygen.
Cancer cells secrete growth factors that stimulate the formation of blood vessels, enabling access to these essential resources.
The relationship between angiogenesis and tumor growth can inadvertently enhance metastasis due to the presence of blood vessels facilitating the spread of cancer cells.
Actin polymerization contributes to cellular movement by pushing the membrane forward during migration.
Motor proteins, such as myosin, participate in contraction at the rear end of the cell, aiding in movement.
Cancer cells may not actively replicate while in transit; replication occurs once they successfully exit the blood/lymphatic system in a new location.
The lac operon is a key regulatory mechanism in bacteria for lactose utilization.
Comprised of regulator genes (e.g., lacI), structural genes (e.g., lacZ, lacY), a promoter, and an operator.
Negative Regulation: The repressor (lacI protein) binds to the operator to inhibit transcription in the absence of lactose.
Lactose binding to the repressor induces a conformational change, preventing binding to the operator, thereby promoting transcription.
Positive Regulation: The CAP (catabolite activator protein) binds to a specific site to enhance RNA polymerase binding, contingent upon cAMP presence—indicating low glucose levels in the cell.
Negative feedback is observed through the degradation of cyclins, which are proteins that regulate the cell cycle transitions via CDK (cyclin-dependent kinase) activation.
Cyclin levels fluctuate throughout the cell cycle due to their synthesis and degradation, while CDK levels remain constant.
MPF (M-phase promoting factor) is activated through cyclin-CDK complexes, facilitating progression into mitosis.
Degradation of cyclins initiates the exit from mitosis.
Differentiation between cyclins for various phases (S-phase, M-phase), each playing distinct roles in cell cycle regulation, such as chromatin condensation and spindle formation.
Understanding these biological processes, including migration, metastasis, and cell cycle regulation, is crucial for comprehending cancer progression and potential therapeutic targets.