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This article is original by Translational Medicine Network.
Please indicate the source for reprinting.
Author: Catalina Introduction: Recently, researchers from the University of Salford confirmed that the FDA-approved Bedaquiline drug targets the γ subunit of ATP synthase (ATP5F1C) to inhibit The production and transfer of mitochondrial ATP in the body
.
As we all know, cancer cells are extremely cunning.
They can enter the tiny blood vessels, follow the blood flow to various parts of the body, and continue to grow in other tissues to form metastatic cancer
.
According to reports, about 90% of cancer patients die from cancer metastasis
.
One of the big reasons is that metastatic cancer cells are resistant to cancer chemotherapy and radiotherapy, which also urgently generates medical needs to prevent the spread of cancer cells
.
Recently, researchers from the University of Salford published a titled "Bedaquiline, an FDA-approved drug, inhibits mitochondrial ATP production and metastasis in vivo, by targeting the gamma subunit (ATP5F1C) of the ATP synthase" in Nature.
Papers
.
Researchers isolated subgroups of aggressive cancer cells with high ATP levels and confirmed that the FDA-approved Bedaquiline drug targets the γ subunit of ATP synthase (ATP5F1C) to inhibit the production and metastasis of mitochondrial ATP in the body
.
ATP is the universal biological energy "currency" of all living cells and tissues.
In eukaryotes, mitochondria are the "power source" of cells
.
Mitochondria produce large amounts of ATP through the TCA cycle and oxidative phosphorylation (OXPHOS), and glycolysis produces small amounts of ATP
.
Mitochondrial dysfunction can lead to ATP depletion, which subsequently leads to autophagy, apoptosis (programmed cell death) and/or necrosis
.
ATP synthase is the most important molecular machine in the mitochondria of the human body.
It is responsible for converting the energy in the food ingested from the outside world into the energy storage module ATP molecules that can be used by the body's cells
.
As the saying goes, one of the best ways to "empty the fuel tank" is to target the engine that produces ATP
.
In this study, the researchers conducted bioinformatics analysis on 3951 breast cancer patients.
They defined a mitochondrial gene signature associated with metastasis, which was characterized by the gamma subunit of mitochondrial ATP synthase (ATP5F1C)
.
Immunohistochemistry confirmed the relationship between ATP5F1C protein expression and metastasis
.
Next, the researchers used MDA-MB-231 cells as a model system to functionally verify these findings
.
The transfer ability of MDA-MB-231 cells with high ATP increased nearly five times in vivo, knocking down the expression of ATP5F1C can significantly reduce ATP production, independent of anchored growth and cell migration
.
Subsequently, the research team used an FDA-approved drug Bedaquiline, and they found that therapeutic administration of Bedaquiline can down-regulate the expression of ATP5F1C and prevent the spontaneous metastasis of cancer cells
.
In contrast, Bedaquiline has no effect on the growth of non-tumorigenic breast epithelial cells (MCF10A) or primary tumors
.
Even if treatment with Bedaquiline can cause cancer cells to "black out", these findings paved the way for new cancer clinical trials
.
In conclusion, the study revealed that mitochondrial ATP5F1C is a promising new biomarker and molecular target that can be used for future drug development and prevention of metastatic disease progression
.
More specifically, the researchers confirmed the cell proliferation, stem cell characteristics, anchoring independence, cell migration, invasion, multidrug resistance, and high antioxidant capacity by isolating subpopulations of aggressive cancer cells with high ATP levels.
The improvement
.
Professor Lisanti, the author of this article, said: "This simple idea has always been under our noses.
ATP is a new sign of aggressive cancer cells and treatment failure
.
" Therefore, ATP depletion therapy may be a feasible strategy to target And eradicate the most suitable cancer cells
.
Reference materials: https:// Note: This article aims to introduce the progress of medical research and cannot be used as a reference for treatment options
.
If you need health guidance, please go to a regular hospital
.
Please indicate the source for reprinting.
Author: Catalina Introduction: Recently, researchers from the University of Salford confirmed that the FDA-approved Bedaquiline drug targets the γ subunit of ATP synthase (ATP5F1C) to inhibit The production and transfer of mitochondrial ATP in the body
.
As we all know, cancer cells are extremely cunning.
They can enter the tiny blood vessels, follow the blood flow to various parts of the body, and continue to grow in other tissues to form metastatic cancer
.
According to reports, about 90% of cancer patients die from cancer metastasis
.
One of the big reasons is that metastatic cancer cells are resistant to cancer chemotherapy and radiotherapy, which also urgently generates medical needs to prevent the spread of cancer cells
.
Recently, researchers from the University of Salford published a titled "Bedaquiline, an FDA-approved drug, inhibits mitochondrial ATP production and metastasis in vivo, by targeting the gamma subunit (ATP5F1C) of the ATP synthase" in Nature.
Papers
.
Researchers isolated subgroups of aggressive cancer cells with high ATP levels and confirmed that the FDA-approved Bedaquiline drug targets the γ subunit of ATP synthase (ATP5F1C) to inhibit the production and metastasis of mitochondrial ATP in the body
.
ATP is the universal biological energy "currency" of all living cells and tissues.
In eukaryotes, mitochondria are the "power source" of cells
.
Mitochondria produce large amounts of ATP through the TCA cycle and oxidative phosphorylation (OXPHOS), and glycolysis produces small amounts of ATP
.
Mitochondrial dysfunction can lead to ATP depletion, which subsequently leads to autophagy, apoptosis (programmed cell death) and/or necrosis
.
ATP synthase is the most important molecular machine in the mitochondria of the human body.
It is responsible for converting the energy in the food ingested from the outside world into the energy storage module ATP molecules that can be used by the body's cells
.
As the saying goes, one of the best ways to "empty the fuel tank" is to target the engine that produces ATP
.
In this study, the researchers conducted bioinformatics analysis on 3951 breast cancer patients.
They defined a mitochondrial gene signature associated with metastasis, which was characterized by the gamma subunit of mitochondrial ATP synthase (ATP5F1C)
.
Immunohistochemistry confirmed the relationship between ATP5F1C protein expression and metastasis
.
Next, the researchers used MDA-MB-231 cells as a model system to functionally verify these findings
.
The transfer ability of MDA-MB-231 cells with high ATP increased nearly five times in vivo, knocking down the expression of ATP5F1C can significantly reduce ATP production, independent of anchored growth and cell migration
.
Subsequently, the research team used an FDA-approved drug Bedaquiline, and they found that therapeutic administration of Bedaquiline can down-regulate the expression of ATP5F1C and prevent the spontaneous metastasis of cancer cells
.
In contrast, Bedaquiline has no effect on the growth of non-tumorigenic breast epithelial cells (MCF10A) or primary tumors
.
Even if treatment with Bedaquiline can cause cancer cells to "black out", these findings paved the way for new cancer clinical trials
.
In conclusion, the study revealed that mitochondrial ATP5F1C is a promising new biomarker and molecular target that can be used for future drug development and prevention of metastatic disease progression
.
More specifically, the researchers confirmed the cell proliferation, stem cell characteristics, anchoring independence, cell migration, invasion, multidrug resistance, and high antioxidant capacity by isolating subpopulations of aggressive cancer cells with high ATP levels.
The improvement
.
Professor Lisanti, the author of this article, said: "This simple idea has always been under our noses.
ATP is a new sign of aggressive cancer cells and treatment failure
.
" Therefore, ATP depletion therapy may be a feasible strategy to target And eradicate the most suitable cancer cells
.
Reference materials: https:// Note: This article aims to introduce the progress of medical research and cannot be used as a reference for treatment options
.
If you need health guidance, please go to a regular hospital
.
