erent p53 statuses in cancer progression.Circulating tumor cells (CTCs) that are shed from the primary tumor invade the blood stream or surrounding parenchyma to form new tumors. The present study aimed to explore the underlying mechanism of cisplatin resistance in lung adenocarcinoma CTCs and provide clinical treatment guidance for lung cancer treatment. CTCs from the blood samples of 6 lung adenocarcinoma patients were treated with different concentrations of cisplatin along with A549 and H1299 cells. The sensitivity of CTCs to cisplatin was explored by detecting the inhibitory rate via CCK‑8 assay. The related molecular mechanism was investigated by western blot analysis. miR‑10a expression was detected using quantitative real‑time PCR (RT‑qPCR). The relationship between miR‑10a and phosphatidylinositol‑4,5‑bisphosphate 3‑kinase catalytic subunit α (PIK3CA) was verified and further confirmed by luciferase reporter assay, western blotting and RT‑qPCR assay. The results revealed that CTCs exhibited lower cisplatin sensitivity than A549 and H1299 cells. Moreover, CTCs treated with cisplatin demonstrated higher miR‑10a expression and lower PIK3CA expression than that in A549 and H1299 cells (P less then 0.01). Expression of phosphoinositide 3‑kinase (PI3K) and protein kinase B (Akt) phosphorylation were also decreased in A549 and H1299 cells compared with CTCs after cisplatin treatment. PIK3CA is a target of miR‑10a, and both miR‑10a overexpression and PIK3CA knockdown obviously decreased the sensitivity of A549 and H1299 cells to cisplatin as well as the expression of PI3K and phosphorylation of Akt. PIK3CA overexpression attenuated the cisplatin resistance of A549 and H1299 cells induced by miR‑10a. In conclusion, miR‑10a suppressed the PI3K/Akt pathway to strengthen the resistance of CTCs to cisplatin via targeting PIK3CA, providing a new therapeutic target for lung cancer treatment.Mutations of p53 occur in approximately 50% of advanced non‑small cell lung cancer (NSCLC) cases, leading to loss of tumor suppressive function and/or gain of p53 oncogenic activity. Reactivation of mutant p53 and consequently induction of apoptosis in cancer cells is the goal of p53‑targeted therapy. Recently, several p53 mutant reactivating compounds were discovered including SCH 529074. However, the role of SCH 529074 in NSCLC has not been fully explored. In the present study, the effects of this compound on cell survival, cell cycle progression, induction of apoptosis and modulation of cell signaling in p53 mutant NSCLC cells (H1975, H322 and H157) and p53 wild‑type NSCLC cells (A549), was investigated. Cell‑based functional assays, real‑time RT‑qPCR and western blot assays were used. HCT116 [p53 wild‑type (WT)] and HCT116 p53‑/‑ (p53 null) were used as control cells. The results demonstrated that SCH 529074 treatment caused significant reduction in cell viability and colony formation activity in p53 mutant, p53 WT and p53‑deficient cells. The treatment of NSCLC cells with SCH 529074 resulted in a dose‑dependent induction of apoptosis and G0/G1 cell cycle arrest, which was associated with the activation of caspases (3 and 7), p53‑independent upregulation of p21 and PUMA as well as increased LC3II, a biomarker of autophagy. The combination treatment with the autophagy inhibitor chloroquine (CQ) and SCH 529074 led to decreased cell viability, colony formation and increased induction of apoptosis. The data indicated that SCH 529074 may exert its growth inhibitory function in a p53‑independent manner in NSCLC cells.Articular cartilage tissue has a poor healing potential, and when subjected to traumatic damage this tissue undergoes cartilage degeneration and osteoarthritis.  https://www.selleckchem.com/  The association between the regulation of cell cycle checkpoints and tissue regeneration has been previously investigated, and p21 was initially identified as a potent inhibitor of cell cycle progression. However, the effects of p21 defects on damaged tissue remain controversial. Therefore, the aim of the present study was to evaluate the effects of p21 deficiency on cartilage repair. A mouse model of articular cartilage repair was generated by inducing a patellar groove scratch in 8‑week‑old p21‑knockout (KO) mice and C57Bl/6 wild‑type (WT) mice. Mice were sacrificed at 4 and 8 weeks post‑surgery. The present study also investigated the effect of p21 deficiency on cartilage differentiation in ATDC5 cells in vitro. Safranin O staining results indicated that cartilage repair initially occurred in p21 KO mice. In addition, immunohistochemical analysis demonstrated that p21 KO upregulated proliferating cell nuclear antigen and increased cell proliferation. However, type II collagen and Sox9 expression levels remained unchanged in p21 KO and WT mice. Moreover, it was identified that p21 downregulation did not affect Sox9 and type II collagen expression levels in vitro. Furthermore, p21 deficiency promoted healing of articular cartilage damage, which was associated with cell proliferation in vivo, and increased chondrocyte proliferation but not differentiation in vitro. Therefore, the present results suggested that p21 does not affect Sox9 or type II collagen expression levels during cartilage differentiation in the repair of cartilage defects.Bone marrow mesenchymal stem cells (BM‑MSCs) regulate the balance between regulatory T cells (Tregs) and T helper 17 (Th17) cells. However, the role of different factors on BM‑MSCs‑mediated regulation of the Treg/Th17 balance is unknown. BM‑MSCs and CD4+ T lymphocytes were co‑cultured with various treatments. The ratio of Treg/Th17 cells was calculated and the expression of different cytokines was measured. BM‑MSCs were found to have a proliferative effect on Th17 cells at a basal concentration and at a 2‑fold increase in the number of BM‑MSCs. However, when the number of BM‑MSCs used was increased 4‑fold, they had an inhibitory effect on the Th17 cells. The effect of BM‑MSCs on Tregs was inhibited by the addition of tacrolimus but not rapamycin. The effect of BM‑MSCs on Th17 cells was inhibited by rapamycin. Additionally, the effect of BM‑MSCs on Tregs were inhibited by the addition of a transforming growth factor‑β (TGF‑β) blocker, whereas these TGF‑β‑blockers had no effect on Th17 cells. Addition of an interleukin (IL)‑2 blocker reduced the proportion of Th17 cells when co‑cultured with a high number of MSCs compared with the low concentration group and the proportion of Treg cells was significantly decreased when cells were treated with an IL‑2 blocker compared with the control group.