Cancer Cell Characteristics and Energetics

Cancer cells can produce their own growth factors, making them independent of external signals.

A decrease in E-cadherin expression allows cancer cells to lose their connection with neighboring cells, leading to uncontrolled growth.

Cancer cells evade programmed cell death (apoptosis) by overexpressing proteins like Bcl-2, which block the apoptotic process.

A mutation in the p53 gene, known as the 'guardian of the genome,' allows cancer cells to escape apoptosis.

Cancer cells maintain their telomeres (protective caps on chromosomes) by overactivating telomerase, granting them limitless replication potential.

VEGF, a key growth factor, promotes the formation of new blood vessels (angiogenesis) in tumors, providing them with nutrients and oxygen.

Cancer cells are often considered 'immortal' because they overactivate telomerase, preventing the shortening of their telomeres during replication.

Cancer cells secrete enzymes called MMPs, which break down the surrounding extracellular matrix (ECM), allowing invasion of nearby tissues.

Loss of TGF-β signaling in cancer cells causes them to become unresponsive to signals that normally suppress growth.

The MAPK pathway is often altered in cancer, leading to uncontrolled growth signal transduction.

Cancer cells rely primarily on glycolysis for energy production, even in the presence of oxygen, a phenomenon known as the Warburg effect.

Cancer cells primarily use glycolysis, even in oxygen-rich conditions, for ATP production, unlike normal cells.

Cancer cells prioritize protein synthesis to support rapid growth and division.

The Warburg effect, although less energy-efficient, supports rapid growth and energy generation in cancer cells.

Lactate is the main byproduct of cancer cell metabolism under aerobic conditions.

GLUT1, a glucose transporter, is upregulated in cancer cells to enhance glucose uptake, fueling their high energy needs.

Cancer cells have increased anabolic activity, including nucleotide synthesis, to support rapid growth.

Cancer cells have adapted to tolerate high reactive oxygen species (ROS) levels by enhancing their antioxidant systems.

HIF-1, a transcription factor, is activated under hypoxic conditions in cancer cells, promoting angiogenesis and survival.

Chronic inflammation in the tumor microenvironment promotes angiogenesis, supporting tumor growth.

MMPs, produced by both cancer cells and inflammatory cells, degrade the ECM, allowing tumor invasion and metastasis.

HIF-1, a transcription factor, is constitutively activated in hypoxic tumor environments, promoting survival and angiogenesis.

M1 macrophages, a type of immune cell, play a pro-inflammatory role in tumors, fighting tumor progression.

ROS plays a role in DNA mutation and damage, contributing to tumor growth and progression.

Innate immunity involves macrophages and neutrophils, which provide a first line of defense against pathogens.

Dendritic cells present antigens to T cells, initiating an adaptive immune response.

Cytotoxic CD8+ T cells directly kill tumor cells, playing a crucial role in anti-tumor immunity.

Hypoxia in tumors leads to T cell exhaustion, reducing their effectiveness in fighting cancer.

M1 macrophages are pro-inflammatory, fighting tumor progression, while M2 macrophages are immunosuppressive and can promote tumor growth.

B cells produce antibodies, which target specific antigens in the adaptive immune response.

TGF-β, a signaling molecule, contributes to immune suppression in the tumor microenvironment, favoring tumor growth.

Regulatory T cells (Tregs) suppress the immune system, preventing it from attacking the tumor.

Myeloid cells initially play an anti-tumor role, but can switch to a pro-tumor phenotype in later stages.

Collagen is the primary structural protein in the extracellular matrix (ECM), providing strength and support.

MMPs degrade ECM components, allowing cancer cells to invade surrounding tissues.

Fibronectin and laminin are adhesive proteins that provide support and attachment for cells in the ECM.

The ECM provides structural support and regulates cell behavior and function in tumors, contributing to growth and invasion.

Cancer-associated fibroblasts (CAFs) remodel the ECM by secreting TGF-β and FGF, promoting tumor growth.

The ECM becomes denser and stiffer in tumors, impeding immune cell infiltration and promoting angiogenesis.

TGF-β polarizes fibroblasts into CAFs, leading to the alteration of the ECM.

Increased collagen deposition in the ECM increases its stiffness, promoting tumor growth and invasion.

Integrins act as receptors for ECM components, regulating cell communication and function.

ECM remodeling by MMPs provides haptokinetic cues that guide tumor cells during invasion and metastasis.

Epithelial-to-mesenchymal transition (EMT) involves a loss of cell-cell adhesion and an increase in cell motility, allowing cancer cells to invade and spread.

TGF-β signaling is a key driver of EMT in cancer, causing cells to lose their epithelial properties.

Intravasation is the first step after EMT, where tumor cells penetrate blood vessels to enter the bloodstream.

Mesenchymal migration, a type of movement, involves the extension of cellular projections and is the primary mode of migration for most solid tumors.

MMPs degrade the ECM components, creating pathways for tumor cells to invade surrounding tissues and spread.