Apoptosis and lung cancer: a review

Narayan Shivapurkar1, Jyotsna Reddy, Preet M Chaudhary

  • 1Hamon Center for Therapeutic Oncology Research, University of Texas Southwestern Medical Center, Dallas, Texas 75390-8593, USA. adi.gazdar@UTSouthwestern.edu

Insights

Understanding how cancer cells die (apoptosis) and evade death is key to improving chemotherapy. This review focuses on lung cancer subtypes, small cell lung carcinoma (SCLC) and non-small cell lung carcinoma (NSCLC), and their differing apoptosis sensitivities.

Area of Science:

  • Molecular biology
  • Cancer research
  • Cell death pathways

Background:

  • Defects in apoptosis contribute to cancer development and drug resistance.
  • Chemotherapy failure is often linked to tumor cells evading programmed cell death.
  • Understanding these mechanisms is crucial for developing effective cancer therapies.

Purpose of the Study:

  • To review the molecular mechanisms of drug-induced apoptosis in cancer.
  • To explore how tumors evade apoptotic death.
  • To focus on the differential apoptosis sensitivity in lung cancer subtypes.

Main Methods:

  • Literature review of studies on apoptosis regulation in cancer.
  • Analysis of molecular events in drug-induced apoptosis.
  • Comparison of apoptosis evasion strategies in tumor cells.
  • Focus on small cell lung carcinoma (SCLC) and non-small cell lung carcinoma (NSCLC).

Main Results:

  • Apoptosis defects are implicated in tumorigenesis and drug resistance.
  • Tumor evasion of apoptosis is a significant cause of chemotherapy failure.
  • Lung cancer subtypes, SCLC and NSCLC, exhibit distinct sensitivities to apoptosis induction.

Conclusions:

  • Elucidating apoptosis regulation in lung cancer is critical for treatment.
  • Differential apoptosis sensitivity between SCLC and NSCLC impacts therapeutic strategies.
  • Rational anticancer drug design requires understanding cancer genetics and treatment sensitivity.

Related Concept Videos

Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
Overview of Cell Death01:30

Overview of Cell Death

Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the 20th century...
Apoptosis01:30

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size reduction of the tissue.
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...