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Intervertebral disc degeneration (IVDD) is a disease with high morbidity and high disability in middle-aged and elderly people. The pathophysiological mechanism has not been fully studied. This study investigated the differential expression of linc01776 in IVDD and explored the molecular mechanism of IVDD through bioinformatics. This may provid a target for the treatment of IVDD. According to Pffirrmann score, degenerative disc tissues were divided into control group and IVDD group and qRT-PCR was used to verify the differential expression of linc01776 in degenerated intervertebral discs. The Linc01776 knocking-out plasmid expression vector was constructed to study the biofunctionality of Linc01776 in IVDD. The competitinge endogenous RNA (CeRNA) regulatory mechanism involved in Linc01776 was predicted. The expression of linc01776 was significantly increased in the degenerated intervertebral disc. Knocking out linc01776 could promote the expression of Aggrecan and inhabit the expression of the MMP3 and MMP13. What's more, it could further promote the decomposition of extracellular matrix. The regulatory pathway of the CeRNA mechanism of Linc01776/miR-196b-5p/Akt1 was predicted by bioinformatics. Linc01776 promotes the degradation of nucleus pulposus extracellular matrix and regulates the occurrence and development of IVDD. The Linc01776/miR-196b-5p/Akt1 signal axis may be a regulatory pathway for the CeRNA mechanism that regulates IVDD progression. [ABSTRACT FROM AUTHOR]