Related Experiment Video

Updated: Sep 20, 2026

Applying an Inducible Expression System to Study Interference of Bacterial Virulence Factors with Intracellular Signaling
08:51

Applying an Inducible Expression System to Study Interference of Bacterial Virulence Factors with Intracellular Signaling

Published on: June 25, 2015

Overexpression of BAD preferentially augments anoikis

Masashi Idogawa1, Masaaki Adachi, Takae Minami

  • 1First Department of Internal Medicine, Sapporo Medical University, Sapporo, Japan.

International Journal of Cancer
|September 2, 2003
PubMed

Insights

Overexpression of BAD protein enhances anoikis, a form of apoptosis triggered by anchorage loss. This suggests BAD

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • BAD is a BH3-only protein that regulates apoptosis.
  • Its activity is negatively controlled by serine phosphorylation.

Purpose of the Study:

  • To investigate the role of BAD in anchorage loss-induced apoptosis (anoikis).
  • To explore the potential of BAD as a gene therapeutic agent for cancer.

Main Methods:

  • Gene transfer-mediated overexpression of BAD in MDCK and COS-7 cells.
  • Cell culture under attached and suspended conditions.
  • Analysis of BAD phosphorylation and subcellular localization.
  • Cotransfection with Akt cDNA and dominant-negative calcineurin.

Main Results:

  • BAD overexpression preferentially augmented anoikis in suspended cells.
  • Unphosphorylated BAD increased and localized to mitochondria during suspension culture.
  • Akt activity inhibited the increase in unphosphorylated BAD, while phosphatases did not.
  • BAD overexpression increased cancer cell sensitivity to anoikis.

Conclusions:

  • BAD plays a preferential role in anoikis.
  • Akt-mediated phosphorylation regulates BAD's contribution to anoikis.
  • BAD holds potential as a gene therapy target to inhibit carcinoma progression.

Related Concept Videos

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...
Autophagic Cell Death01:18

Autophagic Cell Death

Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and pro-apoptotic...
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...
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...
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...