Related Experiment Video

Updated: May 25, 2026

Flow Cytometric Detection of Newly-formed Breast Cancer Stem Cell-like Cells After Apoptosis Reversal
11:21

Flow Cytometric Detection of Newly-formed Breast Cancer Stem Cell-like Cells After Apoptosis Reversal

Published on: January 26, 2019

JNK-induced apoptosis, compensatory growth, and cancer stem cells

Fei Chen1

  • 1Department of Pharmaceutical Sciences, Eugene Applebaum College of Pharmacy and Health Sciences, Wayne State University, Detroit, Michigan 48201, USA.

Cancer Research
|January 19, 2012
PubMed

Insights

Stress-responsive kinases, known as JNKs (c-Jun N-terminal kinases), play a dual role in cancer. This review explores their contradictory functions in tumor suppression and promotion, focusing on cancer stem cell regulation.

Area of Science:

  • Cellular biology
  • Molecular oncology
  • Cancer research

Background:

  • Stress-responsive kinases, including JNKs (c-Jun N-terminal kinases), are crucial in regulating apoptosis and tumor suppression.
  • Paradoxically, JNK signaling pathways have also been linked to malignant transformation and cancer development.
  • Understanding the dual role of JNKs is critical for cancer pathogenesis research.

Purpose of the Study:

  • To reconcile the contradictory roles of JNKs in cancer.
  • To explore the involvement of JNKs in compensatory cell growth and stem cell regulation.
  • To provide new mechanistic insights into cancer stem cell biology and cancer pathogenesis.

Main Methods:

  • Literature review of recent discoveries on JNK signaling in cancer.
  • Analysis of JNK's role in compensatory growth of neighboring and stem cells.
  • Synthesis of existing data to elucidate JNK's function in cancer stem cells.

Main Results:

  • JNKs mediate apoptosis, a tumor-suppressive process.
  • JNK signaling is implicated in promoting cell malignancy and tumorigenesis.
  • Recent findings highlight JNK's role in compensatory growth, affecting stem cell populations.

Conclusions:

  • JNKs exhibit dual functions in cancer, acting as both tumor suppressors and promoters.
  • JNK-mediated compensatory growth in stem cells offers a new perspective on their role in cancer.
  • Further research into JNK signaling in cancer stem cells may reveal novel therapeutic targets.

More Related Videos

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen19:44

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen

Published on: May 30, 2012

Related Concept Videos

Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
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...
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...
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.
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...