MicroRNA-590-5p functions as a tumor suppressor in breast cancer conferring inhibitory effects on cell migration, invasion, and epithelial-mesenchymal transition by downregulating the Wnt-β-catenin signaling pathway.

Breast cancer remains one of the foremost primary causes of female morbidity and mortality worldwide. During the current study, the effect of miR-590-5p and paired-like homeodomain transcription factor 2 (PITX2) on proliferation, invasion, migration, and epithelial-mesenchymal transition (EMT) of human breast cancer via the Wnt-β-catenin signaling pathway was investigated. Breast cancer-related genes and related signaling pathways were obtained from KEGG database.

Advances of circular RNAs in carcinoma.

Circular RNAs (circRNAs) are a type of non-coding RNAs with single-stranded closed structure. The rapid development of high-throughput sequencing technology has allowed for the widespread presence of circRNAs in transcriptomes. Moreover, increasing studies have identified a correlation between circRNAs and different cancers.

Genome-wide profiling of long non-coding RNA expression patterns in the EGFR-TKI resistance of lung adenocarcinoma by microarray.

Mutations in the epidermal growth factor receptor (EGFR) make lung adenocarcinoma cells sensitive to EGFR tyrosine kinase inhibitors (TKIs). Long-term cancer therapy may cause the occurrence of acquired resistance to EGFR TKIs. Long non-coding RNAs (lncRNAs) play important roles in tumor formation, tumor metastasis and the development of EGFR-TKI resistance in lung cancer.

Liver X receptor as a drug target for the treatment of breast cancer.

Liver X receptor (LXR) has been exploited widely as a drug target in breast cancer treatment, and various mechanisms underlying the effects of LXR in this area are well studied. The activated LXR plays important roles in estrogen receptor α (ERα) breast cancer cells, such as reducing cell proliferation and arresting cell cycle progression. Different LXR ligands have diverse effects on the development of breast cancer, such as the inhibitory effect of oxysterol, which can return cells to normocholesterol conditions and target other metabolic genes.

WITHDRAWN: The long non-coding RNA, LINC00635-001, sensitizes EGFR-TKI-resistant human lung cancer cells in vitro by inhibiting Akt activation.

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LXR ligands sensitize EGFR-TKI-resistant human lung cancer cells in vitro by inhibiting Akt activation.

Lung adenocarcinoma cells harboring epidermal growth factor receptor (EGFR) mutations are sensitive to EGFR tyrosine kinase inhibitors (TKIs). Prolonged cancer treatment will induce the development of acquired resistance to EGFR TKI. Here we investigate the effects of two novel liver x receptor (LXR) ligands (T0901317 or GW3965) on the development of acquired resistance to an EGFR TKI gefitinib.

Effect of EGFR-TKI retreatment following chemotherapy for advanced non-small cell lung cancer patients who underwent EGFR-TKI.

Objective: Non-small cell lung cancer (NSCLC) patients with epidermal growth factor receptor (EGFR)-activating mutations have higher response rate and more prolonged survival following treatment with single-agent EGFR tyrosine kinase inhibitor (EGFR-TKI) compared with patients with wild-type EGFR. However, all patients treated with reversible inhibitors develop acquired resistance over time. The mechanisms of resistance are complicated.

Circulating tumor cells and individualized chemotherapy.

Circulating tumor cells (CTC) have been identified in peripheral blood from cancer patients especially those with metastatic lesions. Recently, the analysis of CTC has been developed rapidly and showed good prospects for individualized chemotherapy. The field of CTC research is very important since gene-expression profiling becomes feasible and real time when using CTC as the sample of evaluation.