10.4 Cancer and the Cell Cycle
3 min read•june 14, 2024
Cancer is a complex disease arising from uncontrolled cell growth. It develops when mutations disrupt normal cell cycle control, leading to the formation of tumors. Understanding the interplay between , , and tumor suppressors is crucial for grasping cancer biology.
Cell cycle regulation is tightly controlled by checkpoints, cyclins, and mechanisms. When these systems fail, cells can divide uncontrollably, leading to cancer. activation in cancer cells allows for unlimited replication, further driving tumor growth and progression.
Cancer and Cell Cycle Regulation
Cell growth and cancer
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- Uncontrolled cell growth leads to the development of cancer
- Accumulation of mutations in genes regulating cell growth and division disrupts normal cell cycle control mechanisms
- Mutations in proto-oncogenes and are the primary drivers of cancer development
- Proto-oncogenes promote cell growth and division when activated (, , )
- Tumor suppressors inhibit cell growth and division (, , )
- Mutations in proto-oncogenes and are the primary drivers of cancer development
- Uncontrolled cell proliferation results in the formation of tumors
- Benign tumors remain localized and do not invade surrounding tissues
- Malignant tumors invade nearby tissues and can metastasize to distant sites in the body (lungs, liver, brain)
- is crucial for tumor growth and , providing blood supply to the growing tumor
- Accumulation of mutations in genes regulating cell growth and division disrupts normal cell cycle control mechanisms
Proto-oncogenes vs oncogenes
- Proto-oncogenes are normal genes that regulate cell growth, differentiation, and survival
- Tightly regulated under normal conditions to maintain proper cell function
- Examples include genes encoding growth factors, growth factor receptors, and signaling molecules (Ras, Myc, Src)
- Oncogenes are mutated or overexpressed versions of proto-oncogenes that promote uncontrolled cell growth
- Mutations occur through various mechanisms (point mutations, gene amplification, chromosomal translocations)
- Constitutive activation or overexpression of the gene product results in aberrant cell signaling and growth
- Drive cancer development by promoting cell proliferation, survival, and invasion
- Examples include (cell signaling), (growth factor receptor), (fusion protein from chromosomal translocation)
Functions of tumor suppressors
- are normal genes that inhibit cell growth, promote cell cycle arrest, and initiate when necessary
- Act as "brakes" on cell proliferation and ensure proper cell cycle progression
- Respond to DNA damage, cellular stress, and abnormal growth signals by halting the cell cycle or triggering apoptosis
- Examples include p53 ("guardian of the genome"), RB (retinoblastoma protein), PTEN (phosphatase regulating cell signaling)
- Mutations in tumor suppressor genes lead to a loss of function, allowing uncontrolled cell growth and division
- Typically recessive, requiring both alleles to be inactivated for cancer development ()
- Cells bypass normal checkpoints and continue to proliferate despite DNA damage or other abnormalities
- Accumulation of additional mutations and genomic instability promotes cancer progression
Oncogenes vs tumor suppressors
- Oncogenes promote cell cycle progression and uncontrolled cell growth
- Stimulate by increasing activity or decreasing activity
- Promote cell survival by inhibiting apoptosis and enhancing cell metabolism
- Mutated tumor suppressors fail to regulate the cell cycle and allow cells to bypass normal checkpoints
- Loss of p53 function prevents cell cycle arrest and apoptosis in response to DNA damage, leading to mutation accumulation
- Inactivation of RB allows cells to enter without proper regulation, leading to uncontrolled cell division
- Both contribute to cancer progression by promoting cell proliferation, survival, and genomic instability
- Combination of activated oncogenes and inactivated tumor suppressors leads to hallmarks of cancer (sustained proliferative signaling, evasion of growth suppressors, resistance to cell death)
- Additional mutations occur as cancer progresses, leading to more aggressive and invasive tumor behavior
- Clonal evolution selects for cancer cells with increased growth and survival advantages
- Contributes to tumor heterogeneity and treatment resistance
Cell Cycle Regulation and Cancer
- are critical control points that ensure proper cell division
- Dysregulation of these checkpoints is a hallmark of cancer
- proteins play a crucial role in regulating cell cycle progression
- Abnormal cyclin expression can lead to uncontrolled cell division
- DNA repair mechanisms are essential for maintaining genomic stability
- Defects in DNA repair pathways contribute to cancer development
- Telomerase activation in cancer cells allows for unlimited replicative potential
- Normal cells have limited telomere length, while cancer cells often reactivate telomerase
Key Terms to Review (30)
Acetylcholinesterase: Acetylcholinesterase is an enzyme that breaks down the neurotransmitter acetylcholine in the synaptic cleft. It plays a crucial role in terminating synaptic transmission and allowing muscle relaxation.
Aliphatic hydrocarbons: Aliphatic hydrocarbons are organic compounds consisting solely of carbon and hydrogen atoms arranged in straight or branched chains, but not containing aromatic rings. They can be saturated (alkanes) or unsaturated (alkenes and alkynes).
Angiogenesis: Angiogenesis is the biological process through which new blood vessels form from existing ones. This process is crucial for growth and development, but it becomes particularly significant in the context of cancer, as tumors require a blood supply to grow and spread. When angiogenesis is activated by certain signals, it can contribute to the progression of cancer by enhancing nutrient and oxygen delivery to tumor cells.
Apoptosis: Apoptosis is a programmed cell death process that occurs in multicellular organisms, characterized by a series of tightly regulated events leading to the elimination of unwanted or damaged cells. This mechanism is crucial for maintaining tissue homeostasis, regulating the cell cycle, and ensuring proper development and functioning of organisms.
BCR-ABL: BCR-ABL is a fusion gene created by the translocation of chromosome 9 and chromosome 22, which results in the combination of the BCR gene from chromosome 22 and the ABL gene from chromosome 9. This abnormal gene encodes for a tyrosine kinase protein that is constitutively active, leading to uncontrolled cell division and is primarily associated with chronic myeloid leukemia (CML). Understanding BCR-ABL is crucial as it links genetic mutations to cancer development and highlights the impact of gene regulation on cellular processes.
Carcinogenesis: Carcinogenesis is the process by which normal cells transform into cancerous cells through a series of genetic mutations and changes in cellular behavior. This transformation often involves disruptions in the cell cycle regulation, leading to uncontrolled cell proliferation and the potential for tumor formation. Understanding carcinogenesis is crucial as it highlights how environmental factors, genetic predispositions, and lifestyle choices can all contribute to cancer development.
CDK: Cyclin-dependent kinases (CDKs) are a family of protein kinases that play crucial roles in regulating the cell cycle by modifying target proteins through phosphorylation. They are activated by binding to cyclins, which are regulatory proteins whose levels fluctuate throughout the cell cycle. This interaction ensures that the cell cycle progresses in a timely manner and that cellular activities are coordinated, linking cell division with growth and developmental signals.
CDK inhibitor: A CDK inhibitor is a type of protein that prevents the activity of cyclin-dependent kinases (CDKs), which are crucial for regulating the cell cycle. By inhibiting CDKs, these proteins help to control cell division and prevent uncontrolled proliferation, making them important players in cancer biology, where cell cycle dysregulation often occurs.
Cell cycle checkpoints: Cell cycle checkpoints are critical regulatory mechanisms that ensure the proper progression of the cell cycle, preventing cells from dividing inappropriately. These checkpoints monitor and assess the integrity of the cell's DNA, its size, and the completion of key processes before allowing the cell to proceed to the next phase. By coordinating cellular events, these checkpoints play a vital role in maintaining genomic stability and preventing the development of diseases such as cancer.
Cyclin: Cyclins are a family of proteins that play a crucial role in regulating the cell cycle by activating cyclin-dependent kinases (CDKs). These proteins are produced and degraded in a cyclical manner, ensuring that the cell cycle progresses smoothly through its various phases, including cell division. Cyclins are essential for controlling key transitions within the cell cycle, such as the transition from G1 to S phase and G2 to M phase, and their dysregulation can lead to cancer development.
DNA repair: DNA repair refers to the collection of processes by which a cell identifies and corrects damage to its DNA molecules that encode its genome. This is crucial for maintaining genomic stability and preventing mutations that can lead to cancer and other diseases. Effective DNA repair mechanisms are essential for the proper functioning of the cell cycle, as they ensure that damaged DNA does not lead to errors during cell division.
G1 phase: The G1 phase, or Gap 1 phase, is the first stage of interphase in the cell cycle, where the cell grows, carries out normal functions, and prepares for DNA replication. During this phase, the cell increases in size and synthesizes various proteins and organelles essential for DNA synthesis and subsequent cell division.
G1/S transition: The G1/S transition is a crucial checkpoint in the cell cycle where a cell decides whether to proceed with division or enter a resting phase. This transition is significant because it assesses the cell's size, DNA integrity, and environmental conditions, ensuring that only healthy cells continue to replicate. This decision-making process directly impacts growth and development, and its disruption is often linked to cancer progression.
HER2: HER2, or Human Epidermal Growth Factor Receptor 2, is a protein that promotes cell growth and division. In the context of cancer, HER2 is often overexpressed in certain types of breast cancer, leading to aggressive tumor growth. This overexpression is linked to disruptions in normal cell signaling pathways and has significant implications for targeted therapies.
Knudson's two-hit hypothesis: Knudson's two-hit hypothesis suggests that two genetic 'hits' or mutations are required for the development of certain types of cancer, particularly those that are inherited. This model highlights how a combination of inherited mutations and additional somatic mutations contribute to tumorigenesis, emphasizing the role of both hereditary factors and environmental influences in cancer development.
KRAS: KRAS is an essential gene that encodes a protein involved in transmitting signals within cells that regulate cell growth, division, and survival. Mutations in the KRAS gene are commonly associated with various types of cancer, making it a critical player in cancer biology and the cell cycle by driving uncontrolled cell proliferation and tumorigenesis.
Metastasis: Metastasis is the process by which cancer cells spread from the original (primary) tumor to distant sites in the body, forming secondary tumors. This process is a key feature of cancer progression, as it enables cancer to invade tissues and organs beyond the initial site, making treatment more complex and challenging. Metastasis involves several steps, including local invasion, entry into the bloodstream or lymphatic system, survival in circulation, and colonization at new sites.
Mitosis: Mitosis is the process of cell division that results in two genetically identical daughter cells, each containing the same number of chromosomes as the original cell. This process is essential for growth, development, and tissue repair in multicellular organisms, linking it to various biological concepts including cellular organization and reproduction.
Myc: Myc is a family of regulator genes and proteins that play a critical role in cell cycle progression, apoptosis, and cellular transformation. These genes encode transcription factors that help control the expression of various genes involved in cell growth and proliferation, making Myc a significant player in cancer development when dysregulated.
Oncogenes: Oncogenes are mutated forms of normal genes, known as proto-oncogenes, that drive the growth and proliferation of cancer cells. They play a critical role in the development of cancer by promoting uncontrolled cell division, often by encoding proteins that stimulate cell cycle progression or inhibit apoptosis. The activation of oncogenes can be caused by various factors, including genetic mutations, chromosomal rearrangements, and viral infections.
P53: p53 is a crucial tumor suppressor protein that regulates the cell cycle and helps maintain genomic stability by preventing the proliferation of cells with damaged DNA. It plays a significant role in the control of cell growth, ensuring that cells do not divide uncontrollably, which is particularly important in the context of cancer development and gene regulation.
Proto-oncogenes: Proto-oncogenes are normal genes that play essential roles in cell growth, differentiation, and division. When mutated or abnormally expressed, these genes can become oncogenes, which contribute to the development of cancer by promoting uncontrolled cell proliferation. Understanding proto-oncogenes is crucial as they are key players in the regulation of the cell cycle and can influence cancer progression and gene regulation.
PTEN: PTEN (Phosphatase and Tensin Homolog) is a crucial tumor suppressor gene that plays a vital role in regulating cell growth and division. It functions primarily by dephosphorylating the phosphatidylinositol-3,4,5-trisphosphate (PIP3), thus inhibiting the PI3K/Akt signaling pathway, which is often overactive in various cancers. By keeping this pathway in check, PTEN helps prevent uncontrolled cellular proliferation and promotes apoptosis, making it an essential player in cancer biology.
Ras: Ras is a family of small GTPase proteins that play a crucial role in transmitting signals within cells, particularly in the regulation of cell growth and differentiation. These proteins act as molecular switches that toggle between an active GTP-bound state and an inactive GDP-bound state, influencing key pathways involved in the cell cycle and cell signaling, making them integral to understanding processes like cell division and cancer development.
RB: RB, or retinoblastoma protein, is a crucial tumor suppressor that plays a significant role in regulating the cell cycle. It controls the transition from the G1 phase to the S phase, preventing excessive cell growth and division. When functional, RB binds to and inhibits transcription factors that promote cell cycle progression, ensuring that cells do not proliferate uncontrollably, which is a key aspect of cancer development.
S phase: The S phase, or synthesis phase, is a key part of the cell cycle where DNA replication occurs, allowing a cell to double its genetic material before division. This phase is critical for ensuring that each daughter cell receives an identical set of chromosomes, maintaining genetic consistency and integrity across generations of cells.
Src: Src is a non-receptor tyrosine kinase that plays a crucial role in cell signaling and is often associated with the processes of cell proliferation, survival, and migration. This protein kinase is involved in the regulation of various signaling pathways that can lead to cancerous transformations, making it a key player in understanding the relationship between cancer and the cell cycle. Src's activity can be influenced by growth factors, leading to changes in cellular behavior that are characteristic of malignant cells.
Telomerase: Telomerase is an enzyme that adds repetitive nucleotide sequences to the ends of chromosomes, known as telomeres, thus preventing chromosome deterioration during DNA replication. This enzyme plays a crucial role in maintaining genomic stability, particularly in stem cells and cancer cells, where it allows for continuous cell division without losing important genetic information.
Tumor suppressor genes: Tumor suppressor genes are segments of DNA that regulate cell growth by inhibiting cell division and promoting apoptosis. They play a crucial role in preventing cancer development by maintaining genomic stability.
Tumor suppressor genes: Tumor suppressor genes are crucial segments of DNA that help regulate cell growth and division, preventing cells from growing uncontrollably. They produce proteins that function as checkpoints in the cell cycle, ensuring that damaged or abnormal cells do not proliferate, which is essential in maintaining normal cellular function and preventing cancer.