LncRNA PART1 modulates chondrocyte proliferation, apoptosis, and extracellular matrix degradation in osteoarthritis via regulating miR-373-3p/SOX4 axis

Y.-J. Zhu, D.-M. Jiang

Department of Orthopedics, The First Affiliated Hospital of Chongqing Medical University, No. 1 Friendship Road, Yuanjiagang, Chongqing, China.fuhuyueoruzc@163.com

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• Orthopedics

OBJECTIVE: Osteoarthritis (OA) is a common disease in articular cartilages. It has been reported that long non-coding RNAs (lncRNAs) play an important role in various pathological processes of OA. However, the role of PART1 in OA development is unclear.

PATIENTS AND METHODS: The expression levels of PART1 and miR-373-3p were detected in cartilage tissues and chondrocytes using quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Cell proliferation was assessed by Cell Counting Kit-8 (CCK-8) assay. Cell apoptosis was determined by flow cytometry and Western blot assay. The expression of extracellular matrix (ECM)-related proteins was examined by Western blot assay. Expression of SRY-related high-mobility group box 4 (SOX4) was measured by qRT-PCR or Western blot assay. The interactions among PART1, miR-373-3p, and SOX4 were predicted using starBase v2.0 database and confirmed by Dual-Luciferase reporter assay and RNA immunoprecipitation (RIP) assay.

RESULTS: PART1 and SOX4 were up-regulated while miR-373-3p was down-regulated in OA cartilage tissues and chondrocytes. PART1 silencing hindered cell proliferation and ECM degradation, and triggered cell apoptosis in OA chondrocytes. PART1 modulated SOX4 expression by targeting miR-373-3p. Inhibition of miR-373-3p restored the regulation of cell proliferation, ECM degradation, and apoptosis induced by interfering PART1. Upregulation of SOX4 restored the effects on OA progression induced by inhibiting PART1.

CONCLUSIONS: PART1 promoted OA progression by regulating miR-373-3p/SOX4 axis, providing an effective therapeutic target for osteoarthritis.

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