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micro-vascular invasion.Cachexia is a multifactorial disease characterized by weight loss via skeletal muscle and adipose tissue loss, an imbalance in metabolic regulation, and reduced food intake. It is caused by factors of catabolism produced by tumors in the systemic circulation as well as physiological factors such as the imbalanced inflammatory activation, proteolysis, autophagy, and lipolysis that may occur with gastric, pancreatic, esophageal, lung cancer, liver, and bowel cancer. Cancer cachexia not only negatively affects the quality of life of patients with cancer but also reduces the effectiveness of anti-cancer chemotherapy and increases its toxicity, leading to increased cancer-related mortality and expenditure of medical resources. Currently, there are no effective medical interventions to completely reverse cachexia and no approved drugs. check details Adequate nutritional support is the main method of cachexia treatment, while drugs that target the inhibition of catabolism, cell damage, and excessive activation of inflammation are under study. This article reviews recent advances in the diagnosis, staging, and evaluation of cancer cachexia.

To explore the expression and biological function of long intergenic non-protein coding RNA 1089 (LINC01089) in gastric cancer (GC) progression and its underlying mechanism.

LINC01089 and microRNA-27a-3p (miR-27a-3p) expressions were detected with the quantitative real-time polymerase chain reaction (RT-qPCR). Cell proliferation, migration and invasion were evaluated by Cell Counting Kit-8 (CCK-8) and Transwell assay. Epithelial-mesenchymal transition (EMT)-related proteins were also measured by Western blot. The relationship between LINC01089 and miR-27a-3p was revealed by a bioinformatics analysis and dual-luciferase reporter assay.

LINC01089 was significantly down-regulated in GC tissues, as well as GC cell lines. GC patients with lower LINC01089 expression were more likely to have poor outcomes. Overexpression of LINC01089 significantly suppressed GC cells growth, migration and invasion and forbade the EMT process. LINC01089 was directly targeted at miR-27a-3p. The transfection of miR-27a-3p mimics reversed the inhibitory effects on proliferative and metastatic abilities of GC cells with LINC01089 overexpression.

LINC01089 inhibits cell proliferation and metastasis in GC by targeting miR-27a-3p/EMT axis, which should be considered as a promising therapeutic target.

LINC01089 inhibits cell proliferation and metastasis in GC by targeting miR-27a-3p/EMT axis, which should be considered as a promising therapeutic target.

Osteosarcoma (OS) is the most common primary bone tumor in group of children and adolescents. Increasing studies showed that long non-coding RNAs (lncRNAs) exerted important functions in the development of tumors, including OS. LINC01535 is an lncRNA which has been studied in cervical cancer but not in OS.

This study was aimed to explore the biological function and mechanism of LINC01535 in OS.

LINC01535 expression was detected by qRT-PCR. Colony formation assay, EdU assay and CCK-8 assay were applied to check cell proliferation ability in OS. Flow cytometry analysis was conducted to measure cell apoptosis capacity. Wound healing assay and transwell assay were performed to assess cell migration and invasion. Luciferase reporter assay and RNA pull-down assay were carried out to verify the molecular mechanism.

The high expression of LINC01535 was presented in OS tissues and cell lines compared with adjacent normal tissues and human osteoblasts. Moreover, OS patients with high LINC01535 expression exhibited poor prognosis. Loss-of-function assay revealed that silenced LINC01535 significantly attenuated cell proliferation, migration and invasion, and enhanced cell apoptosis in OS. Through mechanistic exploration, we found that LINC01535 interacted with miR-214-3p, and KCNC4 was validated to be a target gene of miR-214-3p. The levels of KCNC4 mRNA and protein were positively modulated by LINC01535 and reversely mediated by miR-214-3p. Based on rescue experiments, KCNC4 overexpression reserved the suppressive function of silenced LINC01535 on OS cell growth, migration and invasion.

LINC01535, miR-214-3p and KCNC4 constituted an effective axis that exerted a pregnant regulation in OS development, which is a quite meaningful discovery for exploring potential therapeutic methods for OS patients.

LINC01535, miR-214-3p and KCNC4 constituted an effective axis that exerted a pregnant regulation in OS development, which is a quite meaningful discovery for exploring potential therapeutic methods for OS patients.

Patients with locally advanced or metastatic non-small-cell lung cancer (NSCLC) have a poor prognosis. Circular RNA circ_0016760 (circ_0016760) is associated with the development of NSCLC. At present, the role and regulatory mechanism of circ_0016760 in NSCLC have not been well explained.

Quantitative real-time polymerase chain reaction (qRT-PCR) was executed to detect the expression of circ_0016760, miR-577, and Zinc finger and BTB domain containing 7A (ZBTB7A) mRNA in NSCLC tissues and cells. The colony formation, migration, invasion, and extracellular acidification rate (ECAR) of NSCLC cells were determined through colony formation, transwell, or ECAR assays. The relationship between circ_0016760 or ZBTB7A and miR-577 was analyzed via dual-luciferase reporter and RNA pull-down or RNA immunoprecipitation (RIP) assays. Protein level of ZBTB7A was evaluated with Western blot analysis. Xenograft assay was conducted to confirm the role of circ_0016760 in vivo.

Circ_0016760 and ZBTB7A were upregulated and miR-577 was downregulated in NSCLC tissues and cells. Circ_0016760 exhaustion curbed the colony formation, migration, invasion, and ECAR of NSCLC cells in vitro and impeded tumor growth in vivo. Mechanically, circ_0016760 modulated ZBTB7A expression via sponging miR-577 in NSCLC cells. MiR-577 downregulation abolished the repressive effects of circ_0016760 silencing on colony formation, migration, invasion, and ECAR of NSCLC cells. Also, ZBTB7A upregulation overturned the repressive impacts of miR-577 elevation on colony formation, migration, invasion, and ECAR of NSCLC cells.

Circ_0016760 silencing impeded NSCLC advancement through regulation of the miR-577/ZBTB7A axis.

Circ_0016760 silencing impeded NSCLC advancement through regulation of the miR-577/ZBTB7A axis.