Your privacy, your choice

We use essential cookies to make sure the site can function. We also use optional cookies for advertising, personalisation of content, usage analysis, and social media.

By accepting optional cookies, you consent to the processing of your personal data - including transfers to third parties. Some third parties are outside of the European Economic Area, with varying standards of data protection.

See our privacy policy for more information on the use of your personal data.

for further information and to change your choices.

Skip to main content
Fig. 2 | Journal of Experimental & Clinical Cancer Research

Fig. 2

From: Mitochondrial transfer in tunneling nanotubes—a new target for cancer therapy

Fig. 2

Mitochondrial transfer from stromal cells to tumor cells. In AML cells, NOX2 in mitochondria can produce ROS to further promote tumor cell proliferation. The possible mechanism is that mitochondrial Reactive Oxygen Species (mtROS) stimulates ERK to further activate the AKT-mTOR signaling pathway. The mtROS generated by mitochondria can also activate the transforming growth factor- β (TGF-β) signaling pathway, thereby promoting tumor metastasis. In prostate cancer, tumor cells change the metabolic pattern of cancer-associated fibroblasts (CAFs), causing them to produce lactate. Then, through their own lactate receptor monocarboxylate transporter 1(MCT1), the lactate is received, further activating PKM2 into the nucleus, and enhancing the demand for CAF mitochondria through the downstream SIRT1-PGC-1α signaling pathway

Back to article page