Cell culture involves growing cells in a controlled laboratory environment, separate from their original living organism. This method allows scientists to observe cellular behavior directly, offering insights into biological processes. For cancer research, studying cancer cells in culture has been instrumental in deciphering the characteristics that define malignancy, revealing how these cells differ from healthy ones and providing clues about their behavior within the body.
Exhibit Uncontrolled Proliferation
A key observation of cancer cells in culture is their ability to proliferate without typical restraints, a behavior distinctly different from normal cells. Healthy cells exhibit contact inhibition, growing in a single, organized layer and ceasing division upon contact with neighbors. Cancer cells, however, ignore these signals, continuing to divide and pile up, forming disorganized clumps known as foci. This unchecked growth mirrors tumor formation in the body.
Normal cells require specific external signals, growth factors, to initiate and sustain their division. These factors bind to cell surface receptors, triggering internal pathways that promote cell cycle progression. Cancer cells bypass this dependence, either by producing their own growth factors or by having mutations that permanently activate internal signaling pathways, even without external cues. This enables them to divide continuously, contributing to the rapid expansion characteristic of cancerous growths.
Achieve Cellular Immortality
Another defining characteristic of cancer cells in culture is their capacity for seemingly endless division, termed cellular immortality. Normal human cells, when grown in a laboratory setting, have a finite number of divisions before they stop dividing and eventually die, a phenomenon known as the Hayflick limit. This limit is around 40 to 60 divisions, after which cells enter senescence or programmed cell death. This built-in biological clock acts as a natural barrier against uncontrolled proliferation.
Cancer cells, in contrast, overcome this inherent limitation, dividing indefinitely in culture. The mechanism behind this immortality involves the maintenance of telomeres, protective caps at the ends of chromosomes. With each normal cell division, telomeres naturally shorten, and once critically short, the cell stops dividing. Many cancer cells reactivate an enzyme called telomerase, which rebuilds and maintains telomere length. This continuous restoration bypasses cellular aging, granting cancer cells unlimited replicative potential, a property rarely seen in healthy somatic cells.
Lose Anchorage Dependence
Observations in cell culture reveal that cancer cells lose their requirement for anchorage, a key difference from normal cells. Healthy cells need to be attached to a solid surface, like the extracellular matrix or a culture dish, to grow and divide. This “anchorage dependence” acts as a natural control, ensuring cells remain in their appropriate tissue locations and do not proliferate without structural support. It helps maintain tissue integrity and organization.
Cancer cells, however, grow and divide even when suspended, without surface attachment. This is observed in lab experiments where cancer cells are grown in a soft agar medium, a gel-like substance that prevents cell attachment. While normal cells fail to proliferate in such a medium, cancer cells readily form colonies, indicating their independence from physical anchors. This loss of anchorage dependence directly relates to the metastatic potential of cancer cells, allowing them to detach from a primary tumor, survive in suspension within bodily fluids, and potentially establish new growths in distant sites.
Display Genetic and Phenotypic Instability
When cancer cells are grown in culture, a consistent observation is their genetic and phenotypic instability, meaning they are prone to rapid changes. Unlike normal cells, which maintain a stable genome, cancer cells accumulate mutations and chromosomal abnormalities at a higher rate. This instability can manifest as changes in chromosome number (aneuploidy), structural rearrangements, or point mutations in individual genes. This heightened mutational rate contributes to the diverse nature within a cancer cell population.
This genetic instability leads to phenotypic instability, where observable characteristics of cancer cells can change, even within the same culture. As a result, a cancer cell population is not uniform; instead, it is a heterogeneous mix of cells, each potentially having slightly different properties. This constant state of flux allows for rapid evolution within the cancer cell population, potentially leading to increased aggressiveness, enhanced survival capabilities, or the development of resistance to anti-cancer treatments. The dynamic nature observed in culture helps explain the challenges in treating complex cancers in patients.