In addition, the protein expression levels of MMP13 were significantly increased in OA tissues and IL‑1β‑treated CHON‑001 cells compared with the controls. SNHG16 knockdown significantly increased the expression levels of aggrecan, and decreased the expression levels of MMP13, cleaved caspase‑3 and p21 in IL‑1β‑treated CHON‑001 cells. In addition, IL‑1β induced CHON‑001 cell apoptosis, while SNHG16 knockdown decreased IL‑1β‑induced apoptosis. Furthermore, the luciferase activity assay suggested that SNHG16 negatively regulated miR‑373‑3p in OA. Finally, the results suggested that the proinflammatory effect of IL‑1β on CHON‑001 cells was significantly reduced by SNHG16 knockdown. In conclusion, lncRNA SNHG16 knockdown significantly limited the progression of OA by sponging miR‑373‑3p in vitro, which suggested that SNHG16 may serve as a potential therapeutic target for OA.Accumulating evidence indicates that long non‑coding RNAs (lncRNAs) may serve essential roles during tumorigenesis of colorectal cancer (CRC). The lncRNA ZFPM2‑AS1 was observed to be involved in the progression of numerous types of cancer, such as lung adenocarcinoma and cervical cancer. The aim of the present study was to investigate the expression levels and function of ZFPM2‑AS1 in CRC. Expression levels of ZFPM2‑AS1 in tissue and CRC cells were measured by reverse transcription‑quantitative PCR. Furthermore, cell proliferation and Transwell assays were conducted to investigate the functional role of ZFPM2‑AS1 in vitro. In addition, bioinformatics analysis, luciferase reporter assay, RNA immunoprecipitation assay and western blotting were performed to explore the possible underlying mechanism. The expression levels of ZFPM2‑AS1 were significantly upregulated in tissue samples from patients with CRC and CRC cell lines compared with normal tissue and normal human colorectal mucosa cell line. Notably, the upregulation of ZFPM2‑AS1 was significantly associated with tumor size, histological differentiation, lymph node metastasis and TNM stage. In addition, ZFPM2‑AS1 knockdown significantly inhibited cell proliferation, migration and invasion compared with the control group in vitro. Sardomozide mw Moreover, it was found that ZFPM2‑AS1 positively regulated tripartite motif containing 24 (TRIM24) expression by sponging miR‑137. In conclusion, the present study indicated that ZFPM2‑AS1 may serve as an oncogene in CRC by regulating the miR‑137/TRIM24 axis.The present study explored the association of long non‑coding RNA (lncRNA) antisense non‑coding RNA in the INK4 locus (ANRIL) with the development of acute myeloid leukemia (AML) clinical features and prognosis of patients with AML. Bone marrow mononuclear cells (BMMCs) were obtained from 178 patients with de novo AML prior to initial therapy and from 30 healthy donors. The expression of lncRNA ANRIL in BMMCs was detected by reverse transcription‑quantitative PCR. Complete remission (CR) was assessed after induction therapy. Event‑free survival (EFS) and overall survival (OS) were evaluated during the follow‑up. The levels of lncRNA ANRIL were increased in patients with AML compared with those in healthy donors and were capable of distinguishing patients with AML from healthy donors (area under the curve, 0.886; 95% CI, 0.820‑0.952). Furthermore, lncRNA ANRIL was associated with an increased occurrence internal tandem duplications in the FMS‑like tyrosine kinase 3, decreased occurrence inv(16) or t(16;6), intet for AML.Acute progressive hypoxic respiratory failure caused by various predisposing factors is known as acute respiratory distress syndrome (ARDS). Although penehyclidine hydrochloride (PHC), an anticholinergic drug, is widely applied in clinical practice, the specific mechanisms underlying PHC in the treatment of ARDS are not completely understood. In the present study, BEAS‑2B cells were treated with 10 ng/ml lipopolysaccharide (LPS) to establish an ARDS cell model and a rat model of acute lung injury (ALI). The influences of PHC and/or autophagy inhibitor (3‑methyladenine (3‑MA)) on the morphology, autophagy, proliferation and apoptosis of cells and tissues were evaluated using hematoxylin and eosin staining, Cell Counting Kit‑8 assays, Hoechst staining, TUNEL staining, flow cytometry, immunofluorescence assays, ELISAs and scanning electron microscopy. The expression levels of apoptosis‑ and autophagy‑related proteins were measured via western blotting. The results indicated that PHC enhanced proliferation and autophagy, and decreased apoptosis and the inflammatory response in LPS‑induced BEAS‑2B cells and ALI model rats. In addition, 3‑MA reversed the effects of PHC on proliferation, inflammation, apoptosis and autophagy in LPS‑induced BEAS‑2B cells. Therefore, the present study suggested that PHC demonstrated a protective effect in LPS‑induced ARDS by regulating an autophagy‑related pathway.Anthracyclines, such as doxorubicin (DOX), have been widely used in the treatment of a number of different solid and hematological malignancies. However, these drugs can inflict cumulative dose‑dependent and irreversible damage to the heart, and can occasionally lead to heart failure. The cardiotoxic susceptibility varies among patients treated with anthracycline, and delays in the recognition of cardiotoxicity can result in poor prognoses. Accordingly, if the risk of cardiotoxicity could be predicted prior to drug administration, it would aid in safer and more effective chemotherapy treatment. The present study was carried out to identify genes that can predict DOX‑induced cardiotoxicity (DICT). In an in vivo study, mice cumulatively treated with DOX demonstrated increases in serum levels of cardiac enzymes (aspartate aminotransferase, lactate dehydrogenase, creatine kinase MB isoenzyme and troponin T), in addition to decreases in body and heart weights. These changes were indicative of DICT, but the severity of these effects varied among individual mice. In the current study, the correlation in these mice between the extent of DICT and circulating blood concentrations of relevant transcripts before DOX administration was analyzed. Among various candidate genes, the plasma mRNA levels of the genes encoding interleukin 6 (Il6) and programmed cell death 1 (Pdcd1) in blood exhibited significant and positive correlations with the severity of DICT. In an in vitro study using cardiomyocyte H9c2 cells, knockdown of Il6 or Pdcd1 by small interfering RNA was revealed to enhance DOX‑induced apoptosis, as determined by luminescent assays. These results suggested that the levels of transcription of Il6 and Pdcd1 in cardiomyocytes serve a protective role against DICT, and that the accumulation of these gene transcripts in blood is a predictive marker for DICT. To the best of our knowledge, this is the first report to demonstrate a role for Il6 and Pdcd1 mRNA expression in DICT.