<p>Spinal tuberculosis is the most common extrapulmonary tuberculosis, characterized by intervertebral disc destruction, which seriously affects people’s quality of life. Recent studies have suggested that the TGF-β1/SMADs signaling pathway plays an important regulatory role in the process of intervertebral disc destruction caused by spinal tuberculosis. However, the abnormal TGF-β1/SMADs signaling pathway in spinal tuberculosis is not fully understood. Herein, we found for the first time that HCG18 was significantly upregulated in spinal tuberculosis nucleus pulposus clinical samples and confirmed that HCG18 negatively regulates the proliferation and migration ability of nucleus pulposus cells (NPCs). In vitro experiments further suggest that overexpression of HCG18 can significantly promote TGF-β1/SMADs pathway activity and inhibit proliferation, migration, and apoptosis of NPCs, an effect which can be reversed by overexpressing hsa-miR-146a-5p. On the contrary, knocking down HCG18 yields the opposite result. In vivo experiments suggest that knocking down HCG18 can significantly alleviate the destruction of the nucleus pulposus in rats with spinal tuberculosis by inhibiting the activity of the TGF-β1/SMADs pathway. In summary, our research suggests that HCG18 can promote the progression of spinal tuberculosis by alleviating the inhibitory effect of hsa-miR-146a-5p on the TGF-β1/SMADs pathway. This study provides new insights into the occurrence and development of spinal tuberculosis, as well as new strategies for the prevention and treatment of spinal tuberculosis.</p>