Related Experiment Video

Updated: Sep 30, 2026

Modeling Oral-Esophageal Squamous Cell Carcinoma in 3D Organoids
10:43

Modeling Oral-Esophageal Squamous Cell Carcinoma in 3D Organoids

Published on: December 23, 2022

Overexpression of extracellular-signal regulated kinases on oral squamous cell carcinoma

Kenji Mishima1, Kazuya Inoue, Yoshio Hayashi

  • 1Department of Pathology, Tokushima University of Dentistry, 3-18-15, Kuramoto-cho, Japan. kmishima@dent.tokushima-u.ac.jp

Oral Oncology
|July 12, 2002
PubMed

Insights

Mitogen-activated protein kinases (MAPKs) are crucial in cell proliferation and death. Investigating MAPK subfamilies like ERK, JNK, and p38 is vital for developing targeted oral squamous cell carcinoma (OSCC) therapies.

Area of Science:

  • Cellular signaling and molecular biology
  • Cancer research
  • Oncology

Background:

  • Mitogen-activated protein kinases (MAPKs) comprise three main subfamilies: ERK, JNK, and p38.
  • The extracellular-signal regulated kinases (ERK MAPKs) pathway is central to cell proliferation and often overexpressed in cancers like oral squamous cell carcinoma (OSCC).
  • Other MAPK subfamilies, c-Jun N-terminal kinases (JNK MAPKs) and p38 MAPKs, are implicated in cell death and cancer growth suppression, respectively.

Purpose of the Study:

  • To explore the role of different Mitogen-activated protein kinase (MAPK) subfamilies in oral squamous cell carcinoma (OSCC).
  • To investigate the potential of MAPK pathways as therapeutic targets for OSCC treatment.

Main Methods:

  • Literature review and analysis of existing data on MAPK pathways in cancer.
  • Examination of the roles of ERK, JNK, and p38 MAPKs in cell proliferation, death, and inflammation relevant to OSCC.

Main Results:

  • Overexpression and activation of ERK MAPKs are frequently observed in OSCC, suggesting a role in cancer progression.
  • JNK MAPKs may regulate chemotherapy-induced cell death.
  • p38 MAPKs, activated by inflammatory stimuli, show potential for suppressing cancer growth.

Conclusions:

  • Each MAPK subfamily (ERK, JNK, p38) presents distinct roles in OSCC.
  • Targeting specific MAPK pathways holds promise for novel therapeutic strategies in oral squamous cell carcinoma (OSCC).
  • Further investigation into MAPK signaling is essential for advancing OSCC treatment.

Related Concept Videos

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...
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
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...
Induced Pluripotent Stem Cells01:06

Induced Pluripotent Stem Cells

Stem cells are undifferentiated cells that divide and produce different cell types. Ordinarily, cells that have differentiated into a specific cell type are terminally differentiated; however, scientists have found a way to reprogram these mature cells so that they dedifferentiate and return to an unspecialized, proliferative state. These cells are pluripotent like embryonic stem cells—able to produce all cell types—and are called induced pluripotent stem cells (iPSCs).
Somatic cells are...
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...
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...