Related Experiment Video

Updated: Oct 21, 2025

Yeast As a Chassis for Developing Functional Assays to Study Human P53
14:57

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

9.7K

p53-GSDME Elevation: A Path for CDK7 Inhibition to Suppress Breast Cancer Cell Survival

Yueyuan Wang1, Jingyu Peng1, Xuguang Mi2

  • 1Department of Breast Surgery, The First Hospital of Jilin University, Changchun, China.

Frontiers in Molecular Biosciences
|September 7, 2021
PubMed

Insights

Inhibiting cyclin-dependent kinase 7 (CDK7) suppresses breast cancer cell growth by increasing p53 and GSDME protein levels. This CDK7-p53-GSDME pathway offers a potential new strategy for breast cancer treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Elevated cyclin-dependent kinase 7 (CDK7) expression is linked to poor prognosis in breast cancer.
  • CDK7 inhibition demonstrates potential for anti-cancer therapy by suppressing cancer cell growth.

Purpose of the Study:

  • To investigate the novel mechanism by which CDK7 inhibition affects breast cancer cell survival.
  • To elucidate the role of the p53-GSDME axis in CDK7-mediated suppression of breast cancer cells.

Main Methods:

  • Breast cancer cell lines (MCF-7) were treated with CDK7 inhibitors.
  • Protein levels of p53 and Gasdermin E (GSDME) were analyzed.
  • Cell proliferation, colony formation, and apoptosis rates were assessed.
  • The effect of p53 suppression on CDK7 inhibition outcomes was evaluated.

Main Results:

  • CDK7 inhibition repressed breast cancer cell proliferation and colony formation.
  • Inhibition of CDK7 led to increased apoptotic cell rates.
  • CDK7 inhibition elevated p53 and GSDME protein levels.
  • Suppression of p53 counteracted the effects of CDK7 inhibition, reducing GSDME levels and promoting cell proliferation.

Conclusions:

  • CDK7 inhibition suppresses breast cancer cell proliferation and colony formation in a p53-GSDME dependent manner.
  • The CDK7-p53-GSDME signaling axis represents a critical pathway influencing breast cancer cell survival.
  • Targeting CDK7 offers a promising therapeutic strategy for breast cancer treatment.
Keywords:
CDK7CDK7 inhibitorGSDMEbreast cancerp53

More Related Videos

Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment11:13

Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment

Published on: June 9, 2023

1.8K
Comparison of Three Different Methods for Determining Cell Proliferation in Breast Cancer Cell Lines12:35

Comparison of Three Different Methods for Determining Cell Proliferation in Breast Cancer Cell Lines

Published on: September 3, 2016

19.7K

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...
4.7K
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

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...
5.1K
DNA Damage can Stall the Cell Cycle02:37

DNA Damage can Stall the Cell Cycle

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...
9.6K
Negative Regulator Molecules01:23

Negative Regulator Molecules

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.
36.7K
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...
6.7K
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...
4.0K