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Editor’s note iNature is China’s largest academic official account.
It is jointly created by the doctoral team of Tsinghua University, Harvard University, Chinese Academy of Sciences and other units.
The iNature Talent Official Account is now launched, focusing on talent recruitment, academic progress, scientific research information, and interested parties Long press or scan the QR code below to follow us.
iNature is known to be beneficial to bone homeostasis by mechanical load on bones, and helps to inhibit osteolysis caused by tumors in loaded bones.
However, it is not clear whether the loaded hind limbs can inhibit tumor growth in the distant brain.
On May 24, 2021, Harbin Medical University Hiroki Yokota and Li Baiyan jointly published a research paper entitled "Mechanical tibial loading remotely suppresses brain tumors by dopamine-mediated downregulation of CCN4" in Bone Research (IF=11.
51) online.
This research It shows that loading high levels of tyrosine hydroxylase (a rate-limiting enzyme in dopamine synthesis) in the tibia can significantly reduce the progression of brain tumors.
Simultaneous application of antipsychotic drug dopamine modulator fluphenazine (FP) can enhance tumor suppression ability.
Dopamine and FP exert anti-tumor effects through the dopamine receptors DRD1 and DRD2, respectively.
It is worth noting that dopamine down-regulates Lrp5 in tumor cells through DRD1.
Cytokine array analysis showed that the reduction of CCN4 is essential for load-driven dopamine-mediated tumor suppression.
Silencing of Lrp5 reduced CCN4, and administration of CCN4 enhanced oncogenes such as MMP9, Runx2 and Snail.
All in all, this study shows that mechanical load inhibits the Lrp5-CCN4 axis through DRD1, thereby regulating dopaminergic signaling and remotely inhibiting brain tumors, indicating the possibility of developing auxiliary bone-mediated load therapy.
Mechanical loading is very important in treatment, especially in bone homeostasis.
For example, loading on the tibia will activate the classic Wnt signal and enhance the weight-bearing capacity of the tibia.
The process of transforming this external environmental force into intracellular signals in osteoblasts is carefully planned by the force-sensitive bone cells in the bone matrix.
It is worth noting that mechanically sensitive bone cells also show the ability to inhibit tumors in breast cancer.
It was previously shown in a mouse model that the correct mechanical load on the tibia can inhibit osteolysis caused by tibial tumors.
About one in eight women in the United States will develop breast cancer during their lifetime, and invasive cancers preferentially metastasize to bone, liver, lung, and brain tissues.
Brain metastasis is one of the worst prognosis, and its overall survival rate is extremely low.
Although neurosurgery, radiotherapy, and stereotactic radiosurgery are common treatments, these treatments can severely impair neurocognitive ability and quality of life, but have limited survival benefits.
Dopamine modulators (such as A77636, trifluoperazine and fluphenazine) can reduce breast cancer progression through two types of dopamine receptors (DRD1 and DRD2).
It is important that dopamine cannot cross the blood-brain barrier.
Therefore, intravenous administration will not deliver dopamine to the brain.
In the synthesis of dopamine, tyrosine hydroxylase (TH) is the rate-limiting enzyme.
Although electrical stimulation has been shown to increase dopamine levels in the midbrain, the tibia up-regulates TH through Erk signaling and promotes dopamine synthesis in the ventral tegmental area (VTA).
The study showed that loading high levels of tyrosine hydroxylase (a rate-limiting enzyme in dopamine synthesis) in the tibia can significantly reduce the progression of brain tumors.
Simultaneous application of the antipsychotic dopamine modulator fluphenazine (FP) can enhance tumor suppression.
Dopamine and FP exert anti-tumor effects through the dopamine receptors DRD1 and DRD2, respectively.
It is worth noting that dopamine down-regulates Lrp5 in tumor cells through DRD1.
Cytokine array analysis showed that the reduction of CCN4 is essential for load-driven dopamine-mediated tumor suppression.
Silencing of Lrp5 reduced CCN4, and administration of CCN4 enhanced oncogenes such as MMP9, Runx2 and Snail.
All in all, this study shows that mechanical load inhibits the Lrp5-CCN4 axis through DRD1, thereby regulating dopaminergic signaling and remotely inhibiting brain tumors, indicating the possibility of developing auxiliary bone-mediated load therapy.
Reference message:
It is jointly created by the doctoral team of Tsinghua University, Harvard University, Chinese Academy of Sciences and other units.
The iNature Talent Official Account is now launched, focusing on talent recruitment, academic progress, scientific research information, and interested parties Long press or scan the QR code below to follow us.
iNature is known to be beneficial to bone homeostasis by mechanical load on bones, and helps to inhibit osteolysis caused by tumors in loaded bones.
However, it is not clear whether the loaded hind limbs can inhibit tumor growth in the distant brain.
On May 24, 2021, Harbin Medical University Hiroki Yokota and Li Baiyan jointly published a research paper entitled "Mechanical tibial loading remotely suppresses brain tumors by dopamine-mediated downregulation of CCN4" in Bone Research (IF=11.
51) online.
This research It shows that loading high levels of tyrosine hydroxylase (a rate-limiting enzyme in dopamine synthesis) in the tibia can significantly reduce the progression of brain tumors.
Simultaneous application of antipsychotic drug dopamine modulator fluphenazine (FP) can enhance tumor suppression ability.
Dopamine and FP exert anti-tumor effects through the dopamine receptors DRD1 and DRD2, respectively.
It is worth noting that dopamine down-regulates Lrp5 in tumor cells through DRD1.
Cytokine array analysis showed that the reduction of CCN4 is essential for load-driven dopamine-mediated tumor suppression.
Silencing of Lrp5 reduced CCN4, and administration of CCN4 enhanced oncogenes such as MMP9, Runx2 and Snail.
All in all, this study shows that mechanical load inhibits the Lrp5-CCN4 axis through DRD1, thereby regulating dopaminergic signaling and remotely inhibiting brain tumors, indicating the possibility of developing auxiliary bone-mediated load therapy.
Mechanical loading is very important in treatment, especially in bone homeostasis.
For example, loading on the tibia will activate the classic Wnt signal and enhance the weight-bearing capacity of the tibia.
The process of transforming this external environmental force into intracellular signals in osteoblasts is carefully planned by the force-sensitive bone cells in the bone matrix.
It is worth noting that mechanically sensitive bone cells also show the ability to inhibit tumors in breast cancer.
It was previously shown in a mouse model that the correct mechanical load on the tibia can inhibit osteolysis caused by tibial tumors.
About one in eight women in the United States will develop breast cancer during their lifetime, and invasive cancers preferentially metastasize to bone, liver, lung, and brain tissues.
Brain metastasis is one of the worst prognosis, and its overall survival rate is extremely low.
Although neurosurgery, radiotherapy, and stereotactic radiosurgery are common treatments, these treatments can severely impair neurocognitive ability and quality of life, but have limited survival benefits.
Dopamine modulators (such as A77636, trifluoperazine and fluphenazine) can reduce breast cancer progression through two types of dopamine receptors (DRD1 and DRD2).
It is important that dopamine cannot cross the blood-brain barrier.
Therefore, intravenous administration will not deliver dopamine to the brain.
In the synthesis of dopamine, tyrosine hydroxylase (TH) is the rate-limiting enzyme.
Although electrical stimulation has been shown to increase dopamine levels in the midbrain, the tibia up-regulates TH through Erk signaling and promotes dopamine synthesis in the ventral tegmental area (VTA).
The study showed that loading high levels of tyrosine hydroxylase (a rate-limiting enzyme in dopamine synthesis) in the tibia can significantly reduce the progression of brain tumors.
Simultaneous application of the antipsychotic dopamine modulator fluphenazine (FP) can enhance tumor suppression.
Dopamine and FP exert anti-tumor effects through the dopamine receptors DRD1 and DRD2, respectively.
It is worth noting that dopamine down-regulates Lrp5 in tumor cells through DRD1.
Cytokine array analysis showed that the reduction of CCN4 is essential for load-driven dopamine-mediated tumor suppression.
Silencing of Lrp5 reduced CCN4, and administration of CCN4 enhanced oncogenes such as MMP9, Runx2 and Snail.
All in all, this study shows that mechanical load inhibits the Lrp5-CCN4 axis through DRD1, thereby regulating dopaminergic signaling and remotely inhibiting brain tumors, indicating the possibility of developing auxiliary bone-mediated load therapy.
Reference message:
