Finally, CTSB expression was evaluated in 69 resected tumor specimens, and high expression was associated with the patients' clinicopathological features and surgical outcomes. The present results suggested that CTSB is a biomarker for poor survival in patients with pancreatic cancer, which is possibly associated with P-CSLCs. This novel biomarker may also have potential as a therapeutic target.Traditional clinicopathological indices are insufficient in predicting the prognosis of patients diagnosed with oral and oropharyngeal squamous cell carcinoma (OSCC/OPSCC). Notably, autophagy and long non-coding RNAs (lncRNAs) regulate the development and progression of various types of cancer. The present study aimed to assess the association between autophagy-related lncRNAs and the prognosis of patients diagnosed with OSCC/OPSCC. Gene sequencing and clinicopathological data of patients with OSCC/OPSCC were downloaded from The Cancer Genome Atlas database, while gene set functional classification was downloaded from the Gene Set Enrichment Analysis database. Out of the 413 transcriptome data samples and 402 clinicopathological data samples retrieved, a total of nine autophagy-related lncRNAs, including PTCSC2, AC099850.3, LINC01963, RTCA-AS1, AP002884.1, UBAC2-AS1, AL512274.1, MIR600HG and AL354733.3, were screened. This was geared towards establishing a signature through gene co-expression network, univariCC. Furthermore, it promotes research on targeted diagnosis and treatment of patients diagnosed with OSCC/OPSCC.mTOR is involved in the proliferation of liver cancer. However, the clinical benefit of treatment with mTOR inhibitors for liver cancer is controversial. Protein disulfide isomerase A member 3 (PDIA3) is a chaperone protein, and it supports the assembly of mTOR complex 1 (mTORC1) and stabilizes signaling. Inhibition of PDIA3 function by a small molecule known as 16F16 may destabilize mTORC1 and enhance the effect of the mTOR inhibitor everolimus (Ev). The aim of the present study was to elucidate the usefulness of combination treatment with Ev and 16F16 in liver cancer using cultured Li-7 and HuH-6 cells. The proliferation of cultured cells was examined following treatment with 0.01 µM Ev, 2 µM 16F16 or both. The expression levels and phosphorylation of S6 kinase (S6K) and 4E-binding protein 1 (4E-BP1) were examined by western blotting. Li-7 was susceptible to Ev, and proliferation was reduced to 69.5±7.2% by Ev compared with that of untreated cells. Proliferation was reduced to 90.2±10.8% by 16F16 but to 62.3±12.2% by combination treatment with Ev and 16F16. HuH-6 cells were resistant to Ev, and proliferation was reduced to 86.7±6.1% by Ev and 86.6±4.8% by 16F16. However, combination treatment suppressed proliferation to 57.7±4.0%. Phosphorylation of S6K was reduced by Ev in both Li-7 and HuH-6 cells. Phosphorylation of 4E-BP1 was reduced by combination treatment in both Li-7 and HuH-6 cells. Immunoprecipitation assays demonstrated that PDIA3 formed a complex with 4E-BP1 but not with S6K. The small molecule 16F16 increased susceptibility to Ev in cultured liver cancer cells, which are resistant to Ev. The inhibition was associated with reduction of 4E-BP1 phosphorylation, which formed a complex with PDIA3. Combination treatment with Ev and 16F16 could be a novel therapeutic strategy for liver cancer.Fatty acid metabolism is closely associated with the occurrence and development of tumors. The aim of the present study was to investigate whether the key enzyme involved in fatty acid synthesis, fatty acid synthase (FASN), mediates fatty acid changes that affect the activity and migration of breast cancer cells, and whether specific fatty acids play a role in tumor metastasis. The difference in serum fatty acid profiles between patients with invasive ductal carcinoma (IDC) and healthy controls was evaluated by gas chromatography-mass spectrometry (GC-MS) fatty acid profile analysis, and it was revealed that five types of fatty acids may be potential tumor markers in IDC. Immunohistochemistry and GC-MS analysis revealed that FASN expression affected the serum fatty acid profiles of patients with IDC. Following FASN knockdown, the migration of SK-Br-3 breast cancer cells was inhibited, and the contents of various fatty acids both inside and outside the cell decreased, while the contents of various fatty acids inside and outside the cell increased following FASN overexpression. The results of the present study revealed that the expression level of FASN affected the content of fatty acids in IDC tissues and breast cancer cell lines, and that FASN-mediated changes in specific fatty acids promoted tumor cell migration.Histone-lysine N-methyltransferase EZH2 (EZH2) is the principle component of the polycomb repressive complex 2 (PRC2)/embryonic ectoderm development protein-EZH2 complex, which promotes tumorigenesis by repressing transcription of tumor suppressor genes. EZH2 is considered a key marker in several types of cancer, such as colorectal and prostate cancer. However, the molecular mechanisms and clinical value of EZH2 in lung cancer have not yet been fully investigated. The aim of the present study was to investigate the functions of EZH2 in lung cancer progression and to determine whether treatment with an EZH2 inhibitor enhanced the chemosensitivity of lung cancer cells to cisplatin (CDDP). At the logarithmic growth phase, A549 cells were treated with a small interfering (si)RNA-EZH2, and cell viability was detected using an MTT assay. The degree of apoptosis and cell cycle were detected using flow cytometry. Cell migration and invasion were detected via wound healing and Transwell Matrigel assays. According to iibitor may be used to increase chemosensitivity to CDDP agents in lung cancer.Colorectal cancer (CRC) is one of the most common types of human cancer. However, there is still an urgent need to identify novel treatment strategies for CRC. The present study aimed to validate the potential antitumor effects of polyphyllin VII in CRC. The present study revealed that polyphyllin VII could significantly inhibit CRC proliferation and induce cell cycle arrest and apoptosis. Moreover, the anti-metastatic effect of polyphyllin VII in CRC cells was implicated. Microarray analysis identified that polyphyllin VII could affect multiple protein coding genes and non-coding RNAs. Bioinformatics analysis revealed that polyphyllin VII regulated multiple pathways in CRC, including 'ER to Golgi vesicle-mediated transport', 'response to cAMP', 'Ras protein signal transduction', 'metabolic pathways', 'MAPK signaling pathway' and 'cell cycle'.  https://www.selleckchem.com/products/benzylpenicillin-potassium.html  Protein-Protein Interaction network analysis identified a series of key polyphyllin VII-regulating genes in CRC, including ribonucleoside-diphosphate reductase subunit M2, structural maintenance of chromosomes protein 4 and DNA replication licensing factor MCM4.