Department of Orthopedics, General Hospital of Western Theater Command, Rongdu Avenue No. 270, Chengdu, 610000, People's Republic of China.
Chengdu Medical College, Rongdu Avenue No. 601, Chengdu, 610000, People's Republic of China.
J Orthop Surg Res. 2023 Jan 2;18(1):3. doi: 10.1186/s13018-022-03473-y.
The expression of GPR84 in bone marrow-derived monocytes/macrophages (BMMs) can inhibit osteoclast formation; however, its role in bone metastasis of colorectal cancer (CRC) is still unknown. To investigate the effects of GPR84 on bone metastasis of CRC, the murine CRC cell line MC-38 was injected into tibial bone marrow. We found that the expression of GPR84 in BMMs was gradually downregulated during bone metastasis of CRC, and the activation of GPR84 significantly prevented osteoclastogenesis in the tumor microenvironment. Mechanistically, the MAPK pathway mediated the effects of GPR84 on osteoclast formation. Moreover, we found that IL-11 at least partly inhibited the expression of GPR84 in the tumor microenvironment through the inactivation of STAT1. Additionally, activation of GPR84 could prevent osteolysis during bone metastasis of CRC. Our results suggest that CRC cells downregulate the expression of GPR84 in BMMs to promote osteoclastogenesis in an IL-11-dependent manner. Thus, GPR84 could be a potential therapeutic target to attenuate bone destruction induced by CRC metastasis.
GPR84 在骨髓来源的单核细胞/巨噬细胞(BMM)中的表达可以抑制破骨细胞的形成;然而,其在结直肠癌(CRC)骨转移中的作用尚不清楚。为了研究 GPR84 对 CRC 骨转移的影响,将鼠 CRC 细胞系 MC-38 注射到胫骨骨髓中。我们发现,GPR84 在 CRC 骨转移过程中 BMM 中的表达逐渐下调,GPR84 的激活显著防止了肿瘤微环境中的破骨细胞生成。在机制上,MAPK 途径介导了 GPR84 对破骨细胞形成的影响。此外,我们发现至少部分通过 STAT1 的失活,IL-11 抑制了肿瘤微环境中 GPR84 的表达。此外,GPR84 的激活可以预防 CRC 骨转移过程中的骨溶解。我们的结果表明,CRC 细胞下调 BMM 中 GPR84 的表达,以依赖于 IL-11 的方式促进破骨细胞生成。因此,GPR84 可能是减轻 CRC 转移引起的骨破坏的潜在治疗靶点。