Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

3.7K
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...
3.7K
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

4.6K
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...
4.6K
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

7.4K
The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...
7.4K
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

6.4K
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...
6.4K
Oral Hypoglycemic Agents: Biguanides and Glitazones01:26

Oral Hypoglycemic Agents: Biguanides and Glitazones

160
Biguanides, particularly metformin (Glucophage), are insulin sensitizers that enhance glucose uptake, thereby reducing insulin resistance. Unlike sulfonylureas, metformin doesn't prompt insulin secretion, which helps to curb hypoglycemia risk. Metformin is beneficial in treating conditions like polycystic ovary syndrome due to its insulin-resistance reduction capability. The drug's primary action involves curtailing hepatic gluconeogenesis, a significant contributor to high blood...
160
Abnormal Proliferation02:23

Abnormal Proliferation

4.4K
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...
4.4K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Oncogenic PIK3CA reprograms glutamine metabolism to drive bladder cancer progression.

Cell communication and signaling : CCS·2026
Same author

Complex I drives glutamine-dependent TCA cycle to support viability of MYC<sup>high</sup> breast cancer cells.

Cell reports·2026
Same author

Tumor Heterogeneity Induces Pro- and Anti-metastatic Myeloid Cell Phenotypes in Breast Cancer Lung Metastasis.

bioRxiv : the preprint server for biology·2026
Same author

Alanine catabolism as a targetable vulnerability for MYC-driven liver cancer.

Cell reports·2026
Same author

Nutrition support practices in cardiothoracic surgery patients with gastrointestinal complications: An observational study.

Australian critical care : official journal of the Confederation of Australian Critical Care Nurses·2026
Same author

Fine tuning of TCR signaling via CD8αβ and PD-1 and the fate of autoreactive thymocytes during negative selection.

ImmunoHorizons·2026

Related Experiment Video

Updated: May 28, 2025

Studying Pancreatic Cancer Stem Cell Characteristics for Developing New Treatment Strategies
07:29

Studying Pancreatic Cancer Stem Cell Characteristics for Developing New Treatment Strategies

Published on: June 20, 2015

19.5K

Biguanides antithetically regulate tumor properties by the dose-dependent mitochondrial reprogramming-driven c-Src

Jun Hyoung Park1, Kwang Hwa Jung1, Dongya Jia2

  • 1Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030, USA.

Cell Reports. Medicine
|February 11, 2025
PubMed
Summary

Metformin, an anti-cancer drug, may unexpectedly boost breast cancer growth by activating fatty acid oxidation (FAO) and Src signaling in some patients. Inhibiting FAO or using Src inhibitors with metformin shows promise for treating aggressive triple-negative breast cancer.

Keywords:
Src kinasefatty acid β-oxidationmetforminmitochondriatriple-negative breast cancer

More Related Videos

Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment
11:13

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

Published on: June 9, 2023

1.5K
Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen
19:44

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen

Published on: May 30, 2012

18.7K

Related Experiment Videos

Last Updated: May 28, 2025

Studying Pancreatic Cancer Stem Cell Characteristics for Developing New Treatment Strategies
07:29

Studying Pancreatic Cancer Stem Cell Characteristics for Developing New Treatment Strategies

Published on: June 20, 2015

19.5K
Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment
11:13

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

Published on: June 9, 2023

1.5K
Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen
19:44

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen

Published on: May 30, 2012

18.7K

Area of Science:

  • Oncology
  • Metabolic pathways
  • Cancer signaling

Background:

  • Metformin, a biguanide, is investigated for anti-cancer properties by attenuating mitochondrial oxidation.
  • Clinical studies indicate metformin may increase proliferation and fatty acid β-oxidation (FAO) in a subset of breast cancer (BC) patients.
  • FAO activation of Src kinase is implicated in aggressive triple-negative breast cancer (TNBC).

Purpose of the Study:

  • To investigate the hypothesis that low-dose biguanide-driven signaling (AMPK-ACC-FAO) activates the Src pathway in TNBC.
  • To explore the synergistic effects of biguanides, FAO inhibition, and Src inhibitors in TNBC models.

Main Methods:

  • Utilized TNBC xenograft models to mimic low-dose metformin effects due to its low bioavailability.
  • Assessed the impact of pharmacological and genetic inhibition of FAO on biguanide efficacy.
  • Evaluated the combined effects of metformin and dasatinib (a Src inhibitor) on TNBC growth and metastasis.
  • Investigated the influence of high-fat diet on the efficacy of the combination therapy.

Main Results:

  • Pharmacological or genetic inhibition of FAO significantly enhanced the anti-tumor effects of biguanides.
  • Lower doses of biguanides were found to induce Src signaling, while higher doses suppressed it.
  • Metformin and dasatinib demonstrated synergistic inhibition of TNBC patient-derived xenograft growth, an effect not observed in high-fat diet-fed mice.
  • The combination therapy also suppressed TNBC metastatic progression.

Conclusions:

  • Low-dose biguanide-driven FAO signaling can activate the Src pathway in TNBC, potentially counteracting anti-tumor effects.
  • Inhibiting FAO or combining biguanides with Src inhibitors offers a synergistic strategy to target metastatic TNBC.
  • This combination therapy presents a promising approach for treating TNBC, particularly in patients with limited options.