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Related Concept Videos

DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

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In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
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DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

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In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
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Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

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The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
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Abnormal Proliferation02:23

Abnormal Proliferation

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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...
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Negative Regulator Molecules01:23

Negative Regulator Molecules

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Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
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mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

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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.
The mTOR pathway or the...
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Related Experiment Video

Updated: Dec 29, 2025

Combining Mitotic Cell Synchronization and High Resolution Confocal Microscopy to Study the Role of Multifunctional Cell Cycle Proteins During Mitosis
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The function of p27 KIP1 during tumor development.

Jinhwa Lee1, Sung Soo Kim

  • 1Department of Clinical Lab Science, Dongseo University, Busan 617-716, Korea.

Experimental & Molecular Medicine
|November 6, 2009
PubMed
Summary

The cell cycle regulator p27(KIP1) acts as both a tumor suppressor and oncogene, depending on its location and regulation. Its dual role, independent of gene mutation, offers insights into cancer development.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Oncology

Background:

  • Cell cycle progression relies on cyclin-dependent kinases (CDKs) tightly regulated by cyclin-dependent kinase inhibitors (CKIs).
  • p27(KIP1) is a crucial CKI whose cellular localization and regulation impact its function.
  • Dysregulation of p27(KIP1) is linked to various human cancers.

Purpose of the Study:

  • To review the fundamental characteristics and novel aspects of p27(KIP1).
  • To explore the distinct tumor-suppressing and oncogenic functions of p27(KIP1).
  • To understand the implications of p27(KIP1) dysregulation in cancer biology.

Main Methods:

  • Review of existing literature on p27(KIP1) regulation, localization, and function.
  • Analysis of studies investigating the dual roles of p27(KIP1) in normal and tumor cells.

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Analysis of Cell Cycle Position in Mammalian Cells
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  • Examination of the mechanisms underlying p27(KIP1) inactivation and its correlation with cancer prognosis.

    • Main Results:

    • p27(KIP1) exhibits context-dependent roles, functioning as a tumor suppressor in the nucleus and potentially as an oncogene in the cytoplasm.
    • Its tumor suppressor activity involves inhibition of cyclin/CDK complexes, while its oncogenic function is independent of these interactions.
    • Downregulation and cytoplasmic mislocalization of p27(KIP1) are associated with poor prognosis in several cancers.

    Conclusions:

    • p27(KIP1) is an unconventional tumor suppressor, with its oncogenic potential arising from altered regulation and localization rather than gene mutation.
    • Understanding the separable tumor-suppressing and oncogenic functions of p27(KIP1) is critical for cancer research and therapeutic strategies.
    • Further investigation into p27(KIP1) regulation and localization may reveal new targets for cancer treatment.