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Related Concept Videos

MAPK Signaling Cascades01:07

MAPK Signaling Cascades

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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...
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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
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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.
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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...
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The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
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When a ligand binds to a cell-surface receptor, the receptor's intracellular domain changes shape, which may either activate its enzyme function or allow its binding to other molecules. The initial signal is amplified by most signal transduction pathways. This means that a single ligand molecule can activate multiple molecules of a downstream target. Proteins that relay a signal are most commonly phosphorylated at one or more sites, activating or inactivating the protein. Kinases catalyze...
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Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants
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Metastasis and MAPK Pathways.

Mateusz Kciuk1,2, Adrianna Gielecińska2, Adrianna Budzinska3

  • 1Doctoral School of Exact and Natural Sciences, University of Lodz, Banacha Street 12/16, 90-237 Lodz, Poland.

International Journal of Molecular Sciences
|April 12, 2022
PubMed
Summary
This summary is machine-generated.

This review explores cancer metastasis, a major cause of cancer death. It highlights the mitogen-activated protein kinase (MAPK) pathway as a key regulator of cancer cell spread, offering new therapeutic targets.

Keywords:
c-JUN N-terminal kinase (JNK)cancerextracellular signal-regulated kinase (ERK)metastasismitogen-activated kinases (MAPKs)

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Area of Science:

  • Oncology and Molecular Biology

Background:

  • Cancer metastasis is a significant challenge in cancer treatment, limiting therapeutic efficacy.
  • Current treatments primarily target tumor growth or cell death, often neglecting metastasis.
  • Metastasis involves cancer cell spread via blood and lymphatic systems.

Purpose of the Study:

  • To provide a comprehensive review of cancer metastasis.
  • To focus on the role of the mitogen-activated protein kinase (MAPK) pathway in metastasis.
  • To discuss MAPK (ERK/JNK/P38 signaling) as a critical modulator of cancer cell dissemination.

Main Methods:

  • Literature review of cancer metastasis.
  • Analysis of the mitogen-activated protein kinase (MAPK) pathway.
  • Focus on ERK/JNK/P38 signaling in cancer progression.

Main Results:

  • The MAPK pathway plays a crucial role in regulating cancer metastasis.
  • Specific MAPK signaling cascades (ERK, JNK, P38) are implicated in key metastatic processes.
  • Understanding MAPK signaling offers insights into metastasis mechanisms.

Conclusions:

  • The MAPK pathway is a vital target for understanding and potentially treating cancer metastasis.
  • Targeting MAPK signaling could offer novel therapeutic strategies beyond inhibiting tumor growth.
  • Further research into MAPK's role in metastasis is warranted.