Background Long non-coding RNAs (lncRNAs) are involved in various biological processes in non-small cell lung cancer (NSCLC). This study aimed to investigate the key lncRNA OXCT1-AS1/miR-195/CCNE1 axis in the development of NSCLC and its potential molecular mechanism. Methods LncRNA OXCT1-AS1 is considered to be a competitive endogenous RNA (ceRNA) and its potential targeting microRNAs (miRNAs) were predicted through LncBase predicted v.2. The expression of OXCT1-AS1 and miR-195 in NSCLC tissues and cells was detected by reverse transcription polymerase chain reaction (RT-PCR). The Cell Counting Kit-8 (CCK-8) and cell colony-forming test were used to detect the effect of cell proliferation. RT-PCR was used to detect the expression changes of CCND1 and CCNE1 . Western Blot was used to detect the changes of the CCNE1 cell cycle protein. Dual luciferase activity was used to determine the potential mechanism of lncRNA OXCT1-AS1 . Results LncRNA OXCT1-AS1 was highly expressed and miR-195 was lowly expressed in NSCLC tissues and cell lines. LncBase predicted v.2.0 reported a high-scoring binding between OXCT1-AS1 and miR-195 . The luciferase reporter assay defined the regulatory relationship between OXTC1-AS1 and miR-195 . In NSCLC cells, knockdown of OXCT1-AS1 significantly increased the expression of miR-195 , decreased the proliferation and colony formation number of cancer cells, and reduced the expression of CCND1 and CCNE1 . Meanwhile, overexpression of miR-195 significantly inhibited the cell proliferation and colony formation number, and reduced the expression of CCND1 and CCNE1 . Furthermore, according to the results of the dual-luciferase activity assay, miR-195 targeted the 3' untranslated regions (3' UTRs) of CCNE1 , validating that CCNE1 is a direct target of miR-195 . Overexpression of CCNE1 restored the role of OXCR1-AS1 in NSCLC cells. Conclusions LncRNA OXCT1-AS1 can regulate the proliferation of NSCLC cells via miR-195 / CCNE1 signaling. Therefore, OXCT1-AS1 may act as a prospective biomarker and therapeutic target for patients with NSCLC.

With the acceleration of people’s life rhythm, the incidence of hypopharyngeal cancer has generally increased. This study mainly explores the clinical efficacy and toxicity of lobaplatin compared with cisplatin in the treatment of locally advanced hypopharyngeal carcinoma based on intelligent CT imaging. Group A received lobaplatin combined with docetaxel induction chemotherapy for 2 cycles after cisplatin combined with intensity-modulated radiotherapy. Lobaplatin was added to the patient, then, 200 ml of 5% glucose was added, and the patient was injected intravenously for 1.8 hours. After 2 cycles of induction chemotherapy, simultaneous lobaplatin chemotherapy was performed every week for 5 weeks (10 mg/week), and the efficacy was evaluated after 4 consecutive courses of treatment. Group B received cisplatin combined with docetaxel induction chemotherapy after 2 cycles of cisplatin combined with intensity-modulated radiotherapy. Group C was the control group and was not treated with cisplatin or docetaxel. Stomach protection treatment was given in time throughout the treatment process. All patients underwent normal CT (NCCT) and enhanced CT (CECT) examinations before treatment. We extracted 5 mm plain scan CTQNCCT and enhanced CT (CECT) digital DICOM images from the PACS system for omics feature selection. Toxic and side effects are rated in different degrees according to the evaluation criteria of the National Cancer Institute (NCD) common adverse events. Blood routine and liver and kidney function tests were checked every week, and the medication was stopped immediately if there is a serious reaction. In addition, in vitro cell culture was set up to test the inhibitory effect of cisplatin and lobaplatin on the proliferation of cancer cells. The incidence of digestive tract reaction was 13.0% in the A plan group and 58.3% in the B plan group. The A group was lower than the B group, and the difference was statistically significant ( P = 0.001  < 0.05). Compared with cisplatin, lobaplatin has a milder gastrointestinal reaction, and there is no common hepatic and renal toxicity of cisplatin. This study is helpful to provide guidance for the clinical efficacy of locally advanced hypopharyngeal cancer treatment.

To screen microRNAs (miRNAs) and analyze their role in the nasopharyngeal carcinoma (NPC) development through differential analysis and cytological validation of the nasopharyngeal carcinoma dataset. The Gene Expression Omnibus (GEO) database of NPC-related data were utilized to screen for differential miRNAs, downstream target genes and relevant pathways, and the relationships among them were verified by luciferase reporter assay and cell co-culture. To analyze the function of miRNAs and downstream target genes, a series of mimics, inhibitors or Small interfering RNAs (siRNAs) targeting the downstream target genes were transfected into NPC cells or normal epithelial cells by cell transfection techniques. Cell Counting Kit-8 (CCK8), Transwell, Enzyme-linked immunosorbent assay (ELISA) apoptosis, and western blotting were adopted to determine the changes in cell activity, invasiveness, and apoptosis after differential miRNA and target gene overexpression or downregulation. Differential analysis of miRNA dataset showed that the expression of miR-26b was significantly downregulated in NPC, in agreement with the validation results of nasopharyngeal carcinoma cell lines. And downregulation of miR-26b expression in normal nasopharyngeal epithelial cells transformed the cells to tumors. CEP135 was identified as the miR-26b downstream target gene by mRNA dataset analysis, and a luciferase reporter test revealed a direct targeting link between the two. Upregulation of CEP135 levels in nasopharyngeal cancer cell lines increased cell activity, accelerated cell migration, and inhibited apoptosis. The Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis revealed that CEP135 exerted the above effects on cells via the NF-κB pathway, and co-culture with NF-κB pathway blockers reversed cell biological behavior to the level of the control group. MiR-26b downregulation leads to CEP135 overexpression and NF-κB pathway activation in NPC, which enhances proliferation, migration, and prevents apoptosis of nasopharyngeal carcinoma cells. Therefore, the study further clarifies the biological behavior mechanism of NPC and suggests new therapeutic options for NPC.