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P2 expression, suggesting a potential mechanism. Thus, lncRNA‑XLOC_I2_006631 may be used as a biomarker of HT.The long non‑coding RNA KCNQ1OT1 is generally recognized as an oncogenic molecule in several human malignant tumors. Tamoxifen cell line However, to the best of our knowledge, the role of KCNQ1OT1 in glioma has not been fully investigated. The current study aimed to probe the biological function of KCNQ1OT1 in human glioma cell lines and its mechanisms. The glioma cell lines U251 and U87‑MG were used as cell models. Cell proliferation and apoptosis assays were used to measure the effects of different treatments on survival, and reverse transcription‑quantitative PCR and western blotting were used to investigate the expression profiles of key molecules. Migration and invasion assays were conducted to reveal the biological features of glioma cells. The results indicated that KCNQ1OT1 was upregulated in glioma tissues compared with adjacent tissues, which was associated with poor prognosis. Additionally, knockdown of KCNQ1OT1 in U251 and U87‑MG cells inhibited cell proliferation, migration and invasion, but had no effect on apoptosis. The effects of KCNQ1OT1 on migration and invasion were partially attributed to enhanced Yes‑associated protein (YAP) expression levels and epithelial‑mesenchymal transition (EMT) signaling. Furthermore, microRNA (miR)‑375 functioned as a link between KCNQ1OT1 and YAP in regulating cell proliferation. Finally, the KCNQ1OT1/miR‑375/YAP axis modulated cell proliferation and cell fate by affecting the modulated YAP‑mediated EMT signaling. In conclusion, the KCNQ1OT1/miR‑375/YAP axis modulated migration and invasion of glioma cells by affecting EMT signaling; thus, targeting KCNQ1OT1 may represent a promising strategy in glioma therapeutics.Circular (circ)RNAs are an important group of non‑coding RNAs involved in different pathological and physiological functions, such as longitudinal bone growth. However, the effects of an increase or decrease in circRNA expression on idiopathic short stature (ISS) remain largely unknown. The present study compared the circRNA expression patterns of patients with ISS and healthy individuals to identify differentially expressed circRNAs involved in the regulation of ISS pathogenesis and their target microRNAs (miR). Microarray analysis revealed that 145 circRNAs were differentially expressed in patients with ISS, including 83 up‑ and 62 downregulated circRNAs. Reverse transcription‑quantitative PCR confirmed that hsa_circRNA_0079201 was increased in patients with ISS compared with that in the normal individuals, whilst hsa_circRNA_0079201 overexpression in human chondrocytes was shown to significantly suppress their proliferation, hypertrophy and endochondral ossification abilities. Luciferase reporter assays identified that circRNA_0079201 acted as an miR‑140‑3p sponge. In situ hybridization confirmed the co‑localization of circRNA_0079201 and miR‑140‑3p in the human chondrocyte and neonatal femur growth plate of C57 mice, while rescue experiments demonstrated that miR‑140‑3p overexpression reversed the inhibition of human chondrocyte proliferation, hypertrophy and endochondral ossification, caused by circRNA_0079201 overexpression. Bioinformatics analysis and luciferase reporter assays revealed that SMAD2 was a potential target gene of miR‑140‑3p. Furthermore, overexpressing circRNA_0079201 in human chondrocytes suppressed miR‑140‑3p and increased SMAD2 protein expression level. Taken together, chondrocyte proliferation, hypertrophy and endochondral ossification in ISS was suppressed by a novel regulatory axis consisting of the hsa_circRNA_0079201/miR‑140‑3p/SMAD2 pathway. The present study provided evidence that hsa_circRNA_0079201 may be a potential target for ISS therapy.Long intergenic non‑coding RNA 01232 (LINC01232) was identified as a critical regulator of the development of pancreatic adenocarcinoma. The present study investigated the expression and regulatory roles of LINC01232 in esophageal squamous cell carcinoma (ESCC). The main aim of the present study was to elucidate the underlying mechanisms through which LINC01232 affects the malignancy of ESCC. Initially, LINC01232 expression in ESCC was analyzed using the TCGA and GTEx databases and was confirmed using reverse transcription‑quantitative polymerase chain reaction. ESCC cell proliferation, apoptosis and migration and invasion were assessed using the Cell Counting kit‑8 assay, flow cytometric analysis, and migration and invasion assays, respectively. ESCC tumor growth in vivo was examined using a xenograft mouse model. As shown by the results, a high LINC01232 expression was detected in ESCC tissues and cell lines. LINC01232 downregulation suppressed the proliferation, migration and invasion of ESCC cells, and promoted cell apoptosis in vitro. In addition, LINC01232 depletion restricted tumor growth in vivo. Mechanistically, LINC01232 was shown to function as an microRNA‑654‑3p (miR‑654‑3p) sponge in ESCC cells, and hepatoma‑derived growth factor (HDGF) was identified as a direct target of miR‑654‑3p. LINC01232 could bind competitively to miR‑654‑3p and decrease its expression in ESCC cells, thereby promoting HDGF expression. Rescue experiments reconfirmed that the effects of LINC01232 deficiency in ESCC cells were restored by increasing the output of the miR‑654‑3p/HDGF axis. On the whole, the present study demonstrates that LINC01232 plays a tumor‑promoting role during the progression of ESCC by regulating the miR‑654‑3p/HDGF axis. The LINC01232/miR‑654‑3p/HDGF pathway may thus provide a novel theoretical basis for the management of ESCC.Circadian rhythm plays an important role in diverse physiological processes. Abnormal expression of circadian rhythm genes is associated with increased risk of disease, including different types of cancer. The cancer stem cell (CSC) hypothesis suggests that there is a small subset of stem‑like cells within tumors that are responsible for tumor initiation. However, the biological effect of circadian rhythm on CSCs remains largely unknown. Studies have highlighted that the circadian rhythm protein CLOCK controls key aspects of various diseases. In the present study, lung cancer stem‑like cells were successfully enriched using a sphere formation assay. Next, it was observed that CLOCK mRNA and protein expression levels in the A549 and H1299 sphere cells were notably increased compared with those in the corresponding parental cells. In addition, flow cytometry was performed to isolate CD133+ cells and, consistently, CLOCK expression was also found to be markedly upregulated in CD133+ lung cancer cells. Subsequently, to determine the effect of CLOCK on lung cancer stem cells in detail, CLOCK was knocked down using targeted short inhibiting RNA and the results demonstrated that the sphere‑forming ability of the A549 and H1299 cell lines was reduced.