[Full Picture] Lactate secreted via MCT4 from bone‑colonizing breast cancer excites sensory neurons via GPR81

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Lactate secreted via MCT4 from bone‑colonizing breast cancer excites sensory neurons via GPR81 - PubMed

Source: pubmed.ncbi.nlm.nih.gov

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Summary Analysis Research

Article summary:

1. Breast cancer (BC) bone metastasis causes bone pain (BP), which detrimentally affects the quality of life and outcome of patients with BC.

2. The present study demonstrated a novel mechanism of BC‑BP using a mouse model, in which mouse and human BC cells were injected in the bone marrow cavity of tibiae.

3. Lactate released from BC cells via MCT4 induced BC‑BP through the activation of GPR81 of sensory neurons, suggesting that disruption of the interactions among lactate, MCT4 and GPR81 may be a novel approach to control BC‑BP.

Article analysis:

The article is generally reliable and trustworthy as it provides evidence for its claims by using a mouse model to demonstrate a novel mechanism of breast cancer-induced bone pain (BC-BP). The authors also provide evidence for their claims by performing Western blot analysis, in vivo assessment of cancer pain, and in vitro calcium flux analysis. Furthermore, they provide evidence for their hypothesis that lactate released from BC cells via MCT4 induces BC-BP through the activation of GPR81 of sensory neurons by silencing the expression of MCT4 in mice injected with BC cells and silencing GPR81 in F11 sensory neuron cells.

However, there are some potential biases that should be noted. Firstly, the authors do not explore any counterarguments or alternative explanations for their findings. Secondly, they do not discuss any possible risks associated with disrupting the interactions among lactate, MCT4 and GPR81 as a potential approach to control BC-BP. Lastly, they do not present both sides equally as they only focus on providing evidence for their hypothesis without exploring any other possibilities or alternatives.

Topics for further research:

Alternative explanations for breast cancer-induced bone pain Risks associated with disrupting lactate-MCT4-GPR81 interactions Counterarguments to the hypothesis of lactate-induced BC-BP Other potential mechanisms of breast cancer-induced bone pain In vivo assessment of cancer pain In vitro calcium flux analysis