Objective:To investigate the relationship between spinal Mas-related gene receptor C (MrgC) and pathophysiological mechanism of bone cancer pain in mice.Methods:Forty male C3H/HeNCrlVr mice, aged 5-7 weeks, weighing 20-25 g, were selected and divided into 4 groups ( n=10 each) using a random number table method: sham operation group (group S), bone cancer pain group (group P), bone cancer pain + MrgC agonist group (group P-agonist) and bone cancer pain + Mrg C antagonist group (group P-Ab). Preparation of the bone cancer pain model: mouse fibrosarcoma cells (NCTC2472) were injected into the upper tibia of mice in P, P-agonist and P-Ab groups, and the equal volume of D-Hanks balanced salt solution was given instead in S group. Fourteen days later cerebrospinal fluid was intrathecally injected in S and P groups, and MrgC agonist and MrgC antibody were intrathecally injected in P-agonist and P-Ab groups. The mechanical paw withdrawal threshold (MWT) to von Frey stimuli was measured before developing the model (T 0), at 7 days after developing the model (T 1), at 14 days after developing the model (before intrathecal injection, T 2), and at 4, 8 and 12 h after intrathecal injection (T 3-5). Results:Compared with group S, no significant change was found in the MWT at T 0 ( P>0.05), and the MWT was significantly decreased at T 1-T 5 in the other groups ( P<0.05). Compared with group P, the MWT was significantly increased at T 3-T 5 in group P-agonist, and the MWT was significantly decreased at T 3-T 5 in group P-Ab ( P<0.05). Conclusions:Spinal MrgC plays an endogenous protective role in the pathophysiological mechanism of bone cancer pain to a certain extent in mice.