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Breast cancer is the most commonly diagnosed cancer and the leading cause of cancer death in females worldwide. Chemoresistance has been a major reason for the drug therapy failure. The present study performed a microarray analysis between MCF-7 and MCF-7/adriamycin (ADR) cells, and intended to identify long non-coding (lnc)RNA expression character in drug resistant breast cancer cells. MCF-7/ADR cells were induced from MCF-7 cells via pulse-selection with doxorubicin for 4 weeks, and the resistance to doxorubicin of ADR cells was confirmed by MTT assay. Microarray analysis was performed between MCF-7 and MCF-7/ADR cells. Total RNA was extracted from the two cell lines respectively and was transcribed into cDNA. The results of the microarray were verified by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Gene Ontology (GO) and pathways analysis were conducted to enrich the dysregulated lncRNAs presented in the microarray results. Compared to the MCF-7 cells, 8,892 lncRNAs were differentially expressed in MCF/ADR cells (absolute fold-change >2.0). A total of 32 lncRNAs were selected for RT-qPCR by fold-change filtering, standard Student's t-test, and multiple hypothesis testing. Among the dysregulated lncRNAs, AX747207 was prominent because its associated gene RUNX3 was previously reported to be relative to malignant tumor chemoresistance. GO analysis results also indicated some biological processes and molecular functions linked to chemoresistance. The pathway enrichment results provided some potential pathways associated with chemoresistance. In the present study, the authors intended to identify lncRNA expression character in drug resistant cell line MCF-7/ADR, corresponding to the parental MCF-7 cell line. In addition, the study identified the lncRNA AX747207, and its potential targeted gene RUNX3, may be related to chemoresistance in breast cancer. These results may new insights into exploring the mechanisms of chemoresistance in breast cancer. [ABSTRACT FROM AUTHOR]

Human gastric cancer is a common malignant neoplasm of the digestive system and represents a threat to human health worldwide. The mechanisms underlying gastric cancer germination and development are not yet fully understood. Circular RNAs (circRNAs) serve crucial roles in various physiological and pathological processes, particularly cancer. However, few studies have focused on the mechanisms involving circRNAs in gastric cancer. Therefore the present study set out to identify the differentially expressed circRNAs in gastric cancer. Three specimens of gastric cancer and normal gastric tissue were selected and circRNA microarray analysis was performed to detect the differentially expressed circRNAs. The changes in circRNAs were confirmed by reverse transcription‑quantitative polymerase chain reaction analysis. A total of 347 upregulated and 603 downregulated circRNAs (fold‑change, >2.0) were identified in gastric cancer compared with the normal gastric tissue. A total of 20 selected circRNAs were dysregulated during gastric cancer, which suggests their potential role in gastric cancer. The present study identified circRNAs in the expression profile of human gastric cancer that were potentially involved in the underlying molecular mechanisms of its development. [ABSTRACT FROM AUTHOR]

Tongue squamous epithelial cells are the main component of tongue coating, with proliferation, differentiation and apoptosis being the root cause of the formation and maintenance of tongue coating. The present study aimed to explore the molecular mechanism by which serum influences tongue coating, to enable a better understanding for future investigations. Tongue carcinoma squamous cells were exposed to serum‑starvation in vitro. Cellular proliferation and apoptosis were observed by using 3‑[4,5‑dimethyl‑2‑thiazolyl]‑2,5‑ diphenyl‑2‑H‑tetrazolium bromide (MTT) assay, flow cytometry, Hoechst staining, scanning electron microscope (SEM), transmission electron microscope (TEM), and by measuring the expression ratio of B‑cell lymphoma 2 apoptosis regulator (Bcl‑2)/Bcl‑2 associated protein X apoptosis regulator (Bax) mRNA and protein by reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) and western blotting, respectively. MTT assays revealed that serum‑starvation results in suppression of cellular proliferation, while flow cytometry data revealed that serum‑starvation induces cell cycle arrest at G1 phase and increases apoptosis. In addition, chromatin condensation and membrane blebbing were observed through Hoechst staining, TEM and SEM. The Bcl‑2/Bax ratio was found to be significantly decreased in cells that had undergone serum‑starvation by both RT‑qPCR and western blotting analysis, further indicating that serum‑starvation induces apoptosis. Therefore, tongue carcinoma squamous cells in a serum‑free medium can simulate apoptosis related to the formation of tongue coating, which may offer guidance for future investigations about other factors. [ABSTRACT FROM AUTHOR]

In patients with triple-negative breast cancer (TNBC), high tumour mutation burden and aberrant oncogene expression profiles are some of the causes of poor prognosis. Therefore, it is necessary to identify aberrantly expressed oncogenes, since they have the potential to serve as therapeutic targets. Transient receptor potential channel 5 opposite strand (TRPC5OS) has been previously shown to function as a novel tumour inducer. However, the underlying mechanism of TRPC5OS function in TNBC remain to be elucidated. Therefore, in the present study TRPC5OS expression was first measured in tissue samples of patients with TNBC and a panel of breast cancer cell lines (ZR-75-1, MDA-MB-453, SK-BR-3, JIMT-1, BT474 and HCC1937) by using qRT-PCR and Western blotting. Subsequently, the possible effects of TRPC5OS on MDA-MB-231 cells proliferation were determined using Cell Counting Kit-8 and 5-Ethynyl-2′-deoxyuridine assays after Lentiviral transfection of MDA-MB-231. In addition, potential interaction partners of TRPC5OS were explored using liquid chromatography-mass spectrometry (LC-MS)/MS. Gene expression patterns following TRPC5OS overexpression were also detected in MDA-MB-231 cells by using High-throughput sequencing. Gene Ontology (GO) and Kyoto Encyclopaedia of Genes and Genomes (KEGG) analysis were then used to systematically verify the potential interactions among the TRPC5OS-regulated genes. The potential relationship between TRPC5OS-interacting proteins and gene expression patterns were studied using Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) analysis. TRPC5OS expression was found to be significantly higher in TNBC tumour tissues and breast cancer cell lines compared with luminal tumour tissues and ZR-75-1. In addition, the overexpression of TRPC5OS significantly increased cell proliferation. High-throughput sequencing results revealed that 5,256 genes exhibited differential expression following TRPC5OS overexpression, including 3,269 upregulated genes and 1,987 downregulated genes. GO analysis results indicated that the functions of these differentially expressed genes were enriched in the categories of 'cell division' and 'cell proliferation' regulation. KEGG analysis showed that the TRPC5OS-regulated genes were associated with processes of 'homologous recombination' and 'TNF signalling pathways'. Subsequently, 17 TRPC5OS-interacting proteins were found using LC-MS/MS and STRING analysis. The most important protein among interacting proteins was ENO1 which was associated with glycolysis and regulated proliferation of cancer. In summary, data from the present study suggest that TRPC5OS overexpression can increase TNBC cell proliferation and ENO1 may be a potential target protein mediated by TRPC5OS. Therefore, TRPC5OS may serve as a novel therapeutic target for TNBC. [ABSTRACT FROM AUTHOR]

Cancer cells undergo metabolic reprogramming, including increased glucose metabolism, fatty acid synthesis and glutamine metabolic rates. These enhancements to three major metabolic pathways are closely associated with glycolysis, which is considered the central component of cancer cell metabolism. Increasing evidence suggests that dysfunctional glycolysis is commonly associated with drug resistance in cancer treatment, and aberrant glycolysis plays a significant role in drug-resistant cancer cells. Studies on the development of drugs targeting these abnormalities have led to improvements in the efficacy of tumor treatment. The present review discusses the changes in glycolysis targets that cause drug resistance in cancer cells, including hexokinase, pyruvate kinase, pyruvate dehydrogenase complex, glucose transporters, and lactate, as well the underlying molecular mechanisms and corresponding novel therapeutic strategies. In addition, the association between increased oxidative phosphorylation and drug resistance is introduced, which is caused by metabolic plasticity. Given that aberrant glycolysis has been identified as a common metabolic feature of drug-resistant tumor cells, targeting glycolysis may be a novel strategy to develop new drugs to benefit patients with drug-resistance. [ABSTRACT FROM AUTHOR]

A correction is presented to the article "Chemoresistance‑related long non‑coding RNA expression profiles in human breast cancer cells" which was published in a 2019 issue of the periodical.