New study shows how mitochondria help cancer cells survive and spread

Why does breast cancer spread? Researchers trace the answer to mitochondria, where glutathione import activates survival signals that drive deadly metastasis

Most cancer-related deaths occur not because of the primary tumour, but due to the disease’s spread to other organs.

 

A new study, Mitochondrial glutathione import enables breast cancer metastasis via integrated stress response signaling, published recently in Cancer Discovery, reveals how a critical mitochondrial process fuels this deadly progression.

 

The research, led by scientists at Rockefeller University, New York, found that glutathione—an antioxidant imported into mitochondria—enables breast cancer cells to survive stressful conditions and metastasise (spread to other parts of the body) such as the lungs. The study offers new insights into cancer biology and potential therapeutic targets.

 

 

Why is cancer metastasis so dangerous?

 

Cancer metastasis is the process by which tumour cells break free from their original site and spread to distant organs. It is the leading cause of cancer-related deaths worldwide.

 

According to the study, while doctors have long known that cancer spread is deadly, the precise reasons why some tumour cells survive the journey while others do not have remained unclear. 

How are mitochondria linked to cancer spread?

 

Mitochondria are known as the “powerhouse of the cell” because they generate energy. But scientists are increasingly discovering that they do much more, including producing metabolites—small molecules that influence cell behaviour. Researchers have found that mitochondrial activity contributes to the spread of breast, pancreatic and kidney cancers.

 

What role does glutathione play in breast cancer metastasis?

 

Glutathione is a well-known antioxidant that reduces oxidative stress and supports detoxification. But in this study, scientists found it also plays a surprising role in helping breast cancer cells spread.

 

By comparing breast tumour cells that stayed at the original site with those that travelled to the lung, the team discovered that metastatic cells had strikingly high levels of glutathione inside their mitochondria.

 

According to the researchers, glutathione did not promote metastasis by acting as an antioxidant. Instead, it functioned as a signal. Mitochondrial glutathione activated ATF4, a transcription factor that allows cancer cells to cope with low-oxygen, high-stress environments—precisely the kind of conditions they face when invading a new organ.

 

Could this lead to new cancer therapies?

 

Now that scientists know how glutathione enters the mitochondria, they say the transporter protein responsible could become a potential drug target.

 

Unlike conventional therapies that affect many cellular processes, a drug designed to block this transporter could specifically hinder metastasis with fewer side effects.

 

The study emphasised the need to examine not just overall metabolism, but how metabolites function within specific cellular compartments like mitochondria. By zeroing in on these precise mechanisms, researchers hope to develop more targeted cancer treatments in the future. 

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