Background: The regulation of p21 in the pyroptosis of cartilage cells still needs to be further clarified. We aimed to explore the regulation of p21 on the pyroptosis of cartilage cells and to reveal the improvement of osteoarthritis. Methods: Chondrocytes were collected and isolated from patients with osteoarthritis (average age 58.64 ± 4.32) in Xuzhou Third People's Hospital, China in 2019, and healthy volunteers (average age 58.23 ± 3.91) were enrolled as the control group. mRNA expression levels of p21 and pyroptosis-related proteins (NLRP3, ASC, total caspase1 and cleaved-Caspase1) were detected by Western blot and real-time PCR. Cell activity, total number of cells and number of dead cells were calculated with CCK-8, MTT. And the regulation of p21 on the pyroptosis of cartilage cells was verified with overexpression and knockdown of p21 in cartilage cells. Results: In cartilage cells of patients with osteoarthritis, the transcription and translation levels of pyrolysis-related genes (NLRP3, cleaved-caspase 1, and ASC) significantly increased (P<0.01). p21 expression was up-regulated and positively correlated with the changing trend of pyrolysis-related proteins (P<0.01). Overexpressing p21 genes in normal cartilage cells significantly increased the expression of pyrolysis-related proteins (P<0.01). Conclusion: The pyroptosis of cartilage cells is causally related to the process of osteoarthritis, and can be regulated by transcription factor p21, which is a potential therapeutic target for osteoarthritis.Osteoarthritis

Objective: p21 is a transcriptional target of p53 and is down-regulated in pancreatic cancer. This study aimed to investigate the functional significance of p21 in pancreatic cancer progression through its epigenetic restoration with demethylating agent 5-Aza-29-deoxycytidine (5-Aza-dC).Materials and Methods: Human pancreatic cancer stem cells (CSCs) (CD44+/CD24+/ESA+) have been characterized. CSCs were cultured in DMEM. Cell cycle distribution and of pancreatic cancer cells after treatment with Aza-5-dC and untreated controls were determined by flow cytometry DNA analysis Evaluation of mRNA expression levels was down by quantitative real time-PCR.Results: Re-expression of p21 in CSCs and in human pancreatic cancer cell lines upon treatment with 5-AzadC strongly inhibited the cell proliferation, cell cycle progression, self-renewal.Conclusion: The present study thus demonstrates the role of p21 as a critical regulator of pancreatic cancer progression by the regulating CSC characteristics. The restoration of its expression by 5-Aza-dC will provide mechanistic insight and therapeutic targets for pancreatic cancer.