Background/Aims: Nucleus pulposus cell (NPC) apoptosis is the main factor in intervertebral disc degeneration (IDD); thus, inhibiting the excessive apoptosis of nucleus pulposus cells may be a potential way to alleviate IDD. The effect of Hemeoxygenase-1 (HO-1) on human NPC apoptosis has never been reported. Our study aimed to investigate the effect and mechanism of HO-1 on apoptosis in human degenerative NPCs. Methods: Nucleus pulposus tissues were collected from patients with lumbar vertebral fracture (LVF) and IDD. The expression of HO-1 and P65 in intervertebral discs was determined using immunohistochemistry and western blot analysis. Apoptosis of human nucleus pulposus cells was quantified by flow cytometric analysis. A recombinant lentiviral vector overexpressing HO-1 and HO-1-siRNA was used to promote or silence the expression of HO-1 in nucleus pulposus cells. The NF-κB inhibitor PDTC was used to inhibit the NF-κB pathway. Results: Our study demonstrated that compared with normal samples, IDD samples showed down-regulation of HO-1 expression and up-regulation of P65 expression. Overexpression of HO-1 inhibited the increase in nucleus pulposus cell apoptosis after IL-1β treatment and simultaneously inhibited the expression of p-P65. Furthermore, after treatment with PDTC, the number of apoptotic cells was significantly decreased with or without overexpression of HO-1. Conclusion: HO-1 might play a significant role in IDD, and HO-1 protected degenerative human NPCs against apoptosis induced by IL-1β through the NF-κB pathway. These findings would aid in the development of novel therapeutic approaches for IDD treatment.

Background: Disabled homolog 2-interacting protein (DAB2IP), a Ras GTPase-activating protein, is downregulated in several cancers. Its depletion is involved in tumor cell proliferation, apoptosis, and metastasis, as well as epithelial-mesenchymal transition. The present study aimed to explore the potential role of DAB2IP in cutaneous squamous cell carcinoma (cSCC) and provide a theoretical basis for the diagnosis and targeted therapy of cSCC. Methods:The clinicopathological features of DAB2IP expression in cSCC were analyzed by immunohistochemistry, and the effects of DAB2IP on SCL-1 cell behavior were determined via genetic interference in vitro. SCL-1 cell lines that exhibited reduced expression of DAB2IP and a scrambled shRNA control were constructed using a lentivirus vector-based shRNA technique. RNA extraction, reverse transcription-quantitative PCR (RT-qPCR), MTT assay, colony formation test, cell cycle analysis, apoptosis test, transwell assay, wound-healing assay, in vitro invasive assay were used in this study. Results:The immunohistochemical results demonstrated that the expression of DAB2IP was higher in cSCC tissues than in soft fibroma. The level of DAB2IP expression was associated with the degree of malignancy and the depth of tumor infiltration; however, it had no association with patients' sex, tumor size, location, or phenotype. The results of the MTT, cell cycle, apoptosis, and invasion experiments demonstrated that knockdown of DAB2IP inhibited the viability and invasion of SCL-1 cells in vitro.Conclusions: High expression of DAB2IP may contribute to the development and proliferation of cSCC.