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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...
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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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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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Dipeptidyl peptidase 4 (DPP-4) is a serine protease widely distributed in the body. It's involved in the inactivation of GLP-1 and GIP hormones, which are crucial for insulin regulation. DPP-4 inhibitors, such as sitagliptin (Januvia), saxagliptin (Onglyza), linagliptin (Tradjenta), alogliptin (Nesina), and vildagliptin (Galvus), help increase the proportion of active GLP-1, enhancing insulin secretion. These inhibitors work by competitively binding to DPP-4. This binding causes a significant...
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Phenformin-Induced Apoptosis: A Potential Mechanism for Cervical Cancer Cell Inhibition.

Gehad M Subaiea1,2, Yernar Amangelsin3, Kamila Sagatbekova3

  • 1Department of Pharmacology and Toxicology, College of Pharmacy, University of Ha'il, Hail 55473, Saudi Arabia.

International Journal of Molecular Sciences
|June 12, 2026
PubMed
Summary

Phenformin, a biguanide diabetes drug, shows anticancer potential by reducing cancer cell proliferation. It may work by triggering apoptosis, a key cell death pathway, and potentially influencing autophagy.

Keywords:
apoptosiscervical cancerdrug repurposingphenformin

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Published on: August 26, 2021

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Phenformin, a biguanide, was withdrawn for diabetes due to lactic acidosis risk.
  • Cancer proliferation is often linked to disrupted apoptotic and autophagic pathways.
  • Phenformin exhibits promising anticancer activity in preliminary studies.

Purpose of the Study:

  • To investigate phenformin's anticancer effects on various cancer cell lines.
  • To elucidate phenformin's impact on apoptosis and autophagy.
  • To assess phenformin's potential to enhance resveratrol and vistusertib efficacy.

Main Methods:

  • Phenformin's antiproliferative effects were tested on breast, pancreatic, cervical cancer, hepatocellular carcinoma, and melanoma cell lines.
  • Apoptosis and autophagy protein expression was analyzed in susceptible cervical cancer cells.
  • Combinatorial effects of phenformin with resveratrol and vistusertib were evaluated.

Main Results:

  • Phenformin demonstrated dose-dependent antiproliferative effects across tested cancer cell lines.
  • Phenformin increased the pro-apoptotic Bax protein and decreased the anti-apoptotic Bcl-2 protein.
  • Phenformin showed potential to increase autophagic flux in cervical cancer cells.

Conclusions:

  • Phenformin effectively reduces cancer cell proliferation, potentially through apoptosis induction.
  • Phenformin warrants further investigation as a repurposed anticancer agent.
  • Phenformin may modulate both apoptotic and autophagic pathways in cancer treatment.