Identification of Tumor-Suppressive Regulated Genes: as a Therapeutic Target in Lung Adenocarcinoma.

Analyses of our microRNA (miRNA) expression signature combined with The Cancer Genome Atlas (TCGA) data revealed that both strands of pre- (, the guide strand, and , the passenger strand) are significantly downregulated in lung adenocarcinoma (LUAD) clinical specimens. Functional analyses of LUAD cells ectopically expressing showed significant suppression of their aggressiveness (e.g.

Minichromosome maintenance proteins in lung adenocarcinoma: Clinical significance and therapeutic targets.

Lung cancer is the most common cause of cancer-related death worldwide, accounting for 1.8 million deaths annually. Analysis of The Cancer Genome Atlas data showed that all members of the minichromosome maintenance (MCM) family (hexamers involved in DNA replication: MCM2-MCM7) were upregulated in lung adenocarcinoma (LUAD) tissues.

MicroRNA signature of small-cell lung cancer after treatment failure: impact on oncogenic targets by miR-30a-3p control.

Small-cell lung cancer (SCLC) is associated with a high mortality rate and limited treatment efficacy. We created a microRNA (miRNA) expression signature by RNA sequencing using specimens from patients with SCLC who had failed treatment. Forty-nine miRNAs were downregulated in SCLC tissues and were candidate tumor-suppressive miRNAs.

Regulation of Oncogenic Targets by Tumor-Suppressive in Lung Squamous Cell Carcinoma.

Several recent studies have shown that both strands of certain miRNAs derived from miRNA duplexes are involved in cancer pathogenesis. Our own recent studies revealed that both strands of the duplex act as tumor-suppressive miRNAs in lung adenocarcinoma (LUAD) through the targeting of several oncogenes. The aim of the study here was to further investigate the tumor-suppressive roles of (the passenger strand) in lung squamous cell carcinoma (LUSQ) and its control of cancer-promoting genes in LUSQ cells.

Molecular Signature of Small Cell Lung Cancer after Treatment Failure: The Complex as Therapeutic Target.

Small cell lung cancer (SCLC) is a highly aggressive cancer, and patients who become refractory to first-line treatment have a poor prognosis. The development of effective treatment regimens is urgently needed. In this study, we identified a gene expression signature of SCLC after treatment failure using SCLC clinical specimens (GEO accession number: GSE162102).

: A Novel Oncogenic Target of Lung Adenocarcinoma Regulated by Both Strands of ( and ).

Lung adenocarcinoma (LUAD) is the most aggressive cancer and the prognosis of these patients is unfavorable. We revealed that the expression levels of both strands of ( and ) were significantly suppressed in several cancer tissues. Analyses of large The Cancer Genome Atlas (TCGA) datasets showed that reduced or expression is associated with worse prognoses in LUAD patients (disease-free survival (DFS): = 0.

Involvement of Dual Strands of ( and ) and Their Target Oncogenes in the Molecular Pathogenesis of Lung Adenocarcinoma.

Our analyses of tumor-suppressive microRNAs (miRNAs) and their target oncogenes have identified novel molecular networks in lung adenocarcinoma (LUAD). Moreover, our recent studies revealed that some passenger strands of miRNAs contribute to cancer cell malignant transformation. Downregulation of both strands of the duplex was observed in LUAD clinical specimens.

Effect of bevacizumab on brain radiation necrosis in anaplastic lymphoma kinase-positive lung cancer.

Central nervous system (CNS) metastases from anaplastic lymphoma kinase (ALK)-positive lung cancer often results in failure of ALK-tyrosine kinase inhibitor (TKI) therapy. Patients with uncontrolled CNS metastases receive radiation therapy, which sometimes causes brain radiation necrosis. We added bevacizumab (15 mg/kg, every 3-4 weeks) to the regimen of four ALK-positive lung cancer patients with brain radiation necrosis who were receiving ALK-TKI therapy.

Aberrantly expressed PLOD1 promotes cancer aggressiveness in bladder cancer: a potential prognostic marker and therapeutic target.

Bladder cancer (BC) is the ninth most malignant tumor worldwide. Some BC patients will develop muscle-invasive BC (MIBC), which has a 5-year survival rate of approximately 60% due to metastasis. As such, there is an urgent need for novel therapeutic and diagnostic targets for MIBC.

Molecular Pathogenesis of Gene Regulation by the Duplex: Regulates in Lung Adenocarcinoma.

Based on our miRNA expression signatures, we focused on (the guide strand) and (the passenger strand) to investigate their functional significance in lung adenocarcinoma (LUAD). Downregulation of duplex was confirmed in LUAD clinical specimens. In vitro assays revealed that ectopic expression of and inhibited cancer cell malignancy.

Regulation of by Antitumor Inhibits Cancer Cell Aggressiveness Features in Lung Squamous Cell Carcinoma.

In the human genome, is encoded close to the on chromosome region 17q11.2. Our previous study showed that both strands of pre- acted as antitumor miRNAs and were involved in lung squamous cell carcinoma (LUSQ) pathogenesis.

Involvement of dual-strand of the miR-144 duplex and their targets in the pathogenesis of lung squamous cell carcinoma.

The prognosis of patients with advanced-stage lung squamous cell carcinoma (LUSQ) is poor, and effective treatment protocols are limited. Our continuous analyses of antitumor microRNAs (miRNAs) and their oncogenic targets have revealed novel oncogenic pathways in LUSQ. Analyses of our original miRNA expression signatures indicated that both strands of miR-144 (miR-144-5p, the passenger strand; miR-144-3p, the guide strand) showed decreased expression in cancer tissues.

Dual strands of the miR-145 duplex (miR-145-5p and miR-145-3p) regulate oncogenes in lung adenocarcinoma pathogenesis.

Our original microRNA (miRNA) expression signatures (based on RNA sequencing) revealed that both strands of the miR-145 duplex (miR-145-5p, the guide strand, and miR-145-3p, the passenger strand) were downregulated in several types of cancer tissues. Involvement of passenger strands of miRNAs in cancer pathogenesis is a new concept in miRNA biogenesis. In our continuing analysis of lung adenocarcinoma (LUAD) pathogenesis, we aimed here to identify important oncogenes that were controlled by miR-145-5p and miR-145-3p.

Downregulation of matrix metalloproteinase 14 by the antitumor miRNA, miR-150-5p, inhibits the aggressiveness of lung squamous cell carcinoma cells.

In the present study, in order to elucidate the aggressive nature of lung squamous cell carcinoma (LUSQ), we investigated the oncogenic RNA networks regulated by antitumor microRNAs (miRNAs or miRs) in LUSQ cells. The analysis of our original miRNA expression signatures of human cancers revealed that microRNA‑150‑5p (miR‑150‑5p) was downregulated in various types of cancer, indicating that miR‑150‑5p acts as an antitumor miRNA by targeting several oncogenic genes. Thus, the aims of this study were to investigate the antitumor roles of miR‑150‑5p in LUSQ cells and to identify oncogenes regulated by miR‑150‑5p that are involved in the aggressive behavior of LUSQ.

IL-13 enhances mesenchymal transition of pulmonary artery endothelial cells via down-regulation of miR-424/503 in vitro.

Pulmonary arterial hypertension (PAH) has a major effect on life expectancy with functional degeneracy of the lungs and right heart. Interleukin-13 (IL-13), one of the type 2 cytokines mainly associated with allergic diseases, has recently been reported to be associated with Schistosomiasis-associated PAH which shares pathological features with other forms of PAH, such as idiopathic PAH and connective tissue disease-associated PAH. But a direct pathological role of IL-13 in the development of PAH has not been explored.