As previously reported, long intergenic non‑protein‑coding RNA 1006 (LINC01006) plays crucial roles in prostate, pancreatic and gastric cancers. However, whether it plays important roles in cervical cancer remains unclear. The present study thus aimed to determine the precise role of LINC01006 in cervical cancer and elucidate its regulatory mechanisms. The expression of LINC01006 in cervical cancer was examined by reverse transcription‑quantitative polymerase chain reaction. Cell proliferation assay, flow cytometric analysis, Transwell migration and invasion assays, and tumor xenograft model experiments were performed to elucidate the roles of LINC01006 in cervical cancer. Bioinformatics analysis, luciferase reporter assay, RNA immunoprecipitation and rescue experiments were performed for mechanistic analyses. The expression of LINC01006 was found to be upregulated in cervical cancer and to be associated with a poor prognosis. The absence of LINC01006 inhibited the proliferation, migration and invasion of cervical cancer cells, whereas it promoted cell apoptosis in vitro. The downregulation of LINC01006 impeded tumor growth in vivo. LINC01006 was verified as an endogenous 'sponge' that competed for microRNA‑28‑5p (miR‑28‑5p), which resulted in the upregulation of the miR‑28‑5p target P21‑activated kinase 2 (PAK2). Rescue experiments revealed that the suppression of miR‑28‑5p expression or the overexpression of PAK2 abrogated the effects of LINC01006 downregulation on malignant cellular functions in cervical cancer. On the whole, the present study demonstrates that LINC01006 exhibits tumor‑promoting functions in cervical cancer via the regulation of the miR‑28‑5p/PAK2 axis. These findings may provide the basis for the identification of LINC01006‑targeted clinical therapy.Acute kidney injury (AKI) is the most common complication of sepsis. The current incidence of sepsis is high (0.3% of total population) worldwide, and septic AKI may cause death in patients. Long non‑coding (lnc)RNAs serve important roles in the pathogenesis of AKI. Therefore, the present study investigated the mechanism underlying lncRNA plasmacytoma variant translocation 1 (PVT1)‑mediated regulation of pyroptosis in septic AKI. Septic kidney injury was induced in mice using the caecal ligation and puncture method, and lipopolysaccharide (LPS)‑induced HK‑2 cell models were also established. Haematoxylin‑eosin staining was performed to assess pathological alterations of kidney tissues in the mice. The levels of IL‑1β, IL‑18 and lactate dehydrogenase were determined by conducting ELISAs. Reverse transcription‑quantitative PCR was used to detect the expression levels of PVT1 and microRNA (miR)‑20a‑5p. To assess pyroptosis, the protein expression levels of nucleotide‑binding oligomerization domain‑like receptor uggested that PVT1 modulated NLRP3‑mediated pyroptosis in septic AKI by targeting miR‑20a‑5p, which might suggest significant potential therapeutic targets for septic AKI.Rheumatoid arthritis (RA) is one of the most critical articular diseases, which is characterized by synovial hyperplasia and impaired quality of life. The clinical features of RA include chronic inflammation of the joints associated with synovial cell overgrowth. However, the mechanism regulating the outgrowth of fibroblast‑like synoviocytes (FLS) is not fully understood. The present study reported that grap2 cyclin D interacting protein (GCIP), an inhibitor of DNA binding/differentiation (ID)‑like helix‑loop‑helix protein, interacted with cAMP‑response element‑binding protein (CREB)‑binding protein (CBP). Furthermore, GCIP repressed CREB‑ and NF‑κB‑dependent gene expression by inhibiting CBP binding to RNA polymerase II complexes. GCIP depletion via small interfering RNA enhanced FLS growth, whereas stable GCIP expression suppressed the growth of 293 cells.  https://www.selleckchem.com/products/VX-770.html  In addition, GCIP depletion in FLS induced the expression of cyclin D1, a CREB target gene. The present study identified a novel inhibitory mechanism in which an ID protein may functionally target the transcriptional coactivator CBP. These results suggested that GCIP downregulation may be pivotal in FLS outgrowth.Long non‑coding RNAs (lncRNAs) are a class of non‑protein coding transcripts that are involved in the regulation of gene expression in mammalian cells. Transcriptional co‑activator Yes associated protein 1 (YAP1) plays a key role in the progression of ovarian cancer. However, the regulation of Hippo/YAP signaling in ovarian cancer remains elusive. In the present study, the expression levels of lncRNA ASAP1‑IT1 were investigated. The analysis indicated that lncRNA ASAP1‑IT1 expression was downregulated in ovarian tumor samples and ovarian cancer cells. The overexpression of ASAP1‑IT1 inhibited ovarian cancer cell proliferation and induced cell apoptosis. Bioinformatics analysis predicted that miR‑2278, a previously reported upregulated miRNA in ovarian tumors, may bind to ASAP1‑IT1. Dual luciferase assay confirmed the direct regulatory association between ASAP1‑IT1 and miR‑2278. In addition, the data demonstrated that large tumor suppressor 2 (LATS2) was a target gene of miR‑2278, whose expression was upregulated by ASAP1‑IT1 in ovarian cancer cells. By regulating the expression of LATS2, ASAP1‑IT1 induced the downregulation of YAP1 expression in ovarian cancer cells. Moreover, the silencing of LATS2 attenuated the inhibition of cell proliferation and the apoptosis induced by ASAP1‑IT1 overexpression in ovarian cancer cells. The association among the expression levels of ASAP1‑IT1, miR‑2278 and LATS2 was observed in specimens obtained from patients with ovarian cancer. Taken together, the data presented herein demonstrate that ASAP1‑IT1 functions as a potential tumor suppressor lncRNA by upregulating LATS2 expression in ovarian cancer.Human periodontal ligament stem cells (hPDLSCs) associated with bone regeneration serve an important role in the treatment of periodontal disease. Long non‑coding RNAs are involved in the osteogenesis of multiple stem cells and can act as a sponge of microRNAs (miRs). The present study aimed to investigate the interaction between Prader Willi/Angelman region RNA 6 (PWAR6) and miR‑106a‑5p, as well as their influences on the osteogenic differentiation of hPDLSCs. hPDLSCs were isolated and cultured in osteogenic medium (OM) or growth medium (GM) for 7 days prior to transfection with PWAR6 overexpression vector, short hairpin RNA PWAR6 or miR‑106a‑5p mimic. The expression levels of runt‑related transcription factor 2, osteocalcin and bone morphogenetic protein 2 (BMP2) were detected by western blotting and reverse transcription‑quantitative PCR (RT‑qPCR), and the expression levels of PWAR6, miR‑106a‑5p and alkaline phosphatase (ALP) were determined by RT‑qPCR. ALP activity assays and Alizarin red staining were performed to detect osteogenesis and mineralization, respectively.