ABSTRACT
Gastric cancer (GC) is a serious threat to human health and an important cause of cancer-related death. Herein, we evaluated the influence of transmembrane protein 158 (TMEM158) on GC cell growth. According to Genomic Spatial Event (GSE) and The Cancer Genome Atlas (TCGA) databases, TMEM158 content is amplified in GC tissues. The diagnostic value of TMEM158 expression in GC is huge. GC sufferers with high expression of TMEM158 were associated with poor overall survival. In addition, TMEM158 content was increased in GC cells. TMEM158 promoted GC cell proliferation by modulating the PI3K/Akt signaling pathway. Lack of TMEM158 reduced GC tumor growth. Collectively, TMEM158 accelerated GC cell proliferation by modulating the PI3K/Akt signaling pathway, making it a prospective biomarker for survival in GC patients.
Subject(s)
Proto-Oncogene Proteins c-akt , Stomach Neoplasms , Humans , Proto-Oncogene Proteins c-akt/metabolism , Phosphatidylinositol 3-Kinases/metabolism , Stomach Neoplasms/genetics , Cell Proliferation/genetics , Signal Transduction , Cell Transformation, Neoplastic/genetics , Cell Line, Tumor , Gene Expression Regulation, Neoplastic , Membrane Proteins/genetics , Membrane Proteins/metabolism , Tumor Suppressor Proteins/genetics , Tumor Suppressor Proteins/metabolismABSTRACT
Gastric cancer (GC) is a serious threat to human health and an important cause of cancer-related death. Herein, we evaluated the influence of transmembrane protein 158 (TMEM158) on GC cell growth. According to Genomic Spatial Event (GSE) and The Cancer Genome Atlas (TCGA) databases, TMEM158 content is amplified in GC tissues. The diagnostic value of TMEM158 expression in GC is huge. GC sufferers with high expression of TMEM158 were associated with poor overall survival. In addition, TMEM158 content was increased in GC cells. TMEM158 promoted GC cell proliferation by modulating the PI3K/Akt signaling pathway. Lack of TMEM158 reduced GC tumor growth. Collectively, TMEM158 accelerated GC cell proliferation by modulating the PI3K/Akt signaling pathway, making it a prospective biomarker for survival in GC patients.
ABSTRACT
Neuroblastoma (NB) is one of the most common extracranial solid tumors in children, which has complex molecular mechanisms. Increasing evidence has suggested that long noncoding RNAs (lncRNAs) account for NB pathogenesis. However, the function of small nucleolar RNA host gene 16 (SNHG16) in NB is currently unclear. In the present study, publically available data and clinical specimens were employed to verify the expression of SNHG16 in NB. Colony formation, realtime cell proliferation and migration assays were performed to demonstrate the status of cellular proliferation and migration. Flow cytometry was used to examine cell cycle progression in SHSY5Y cells, and acridine orange/ethidium bromide staining and caspase3/7 activity measurements were applied to study cell apoptosis. To explore the underlying mechanism of SNHG16 function, an online database was used to identify potential RNAbinding proteins that bind SNHG16. The expression of SNHG16 was revealed to be in line with the clinical staging of NB, and high SNHG16 expression was positively associated with poor clinical outcome. Furthermore, SNHG16 silencing inhibited cell proliferation, repressed migration, and induced cell cycle arrest at the G0/G1 phase in SHSY5Y cells. Additionally, apoptosis was undetectable in SHSY5Y cells following SNHG16 silencing. Bioinformatics analysis revealed that SNHG16 regulated cell proliferation in NB through transcriptional and translational pathways. These results suggested that SNHG16 may serve important roles in the development and progression of NB, and could represent a potential target for NB therapy.
Subject(s)
Neuroblastoma/genetics , RNA, Long Noncoding/genetics , Apoptosis/genetics , Cell Cycle Checkpoints/genetics , Cell Line, Tumor , Cell Movement/genetics , Cell Proliferation/genetics , Child , Child, Preschool , Gene Silencing , Humans , Infant , Neuroblastoma/metabolism , Neuroblastoma/pathology , Oncogenes , RNA, Long Noncoding/biosynthesis , RNA, Small Interfering/administration & dosage , RNA, Small Interfering/genetics , TransfectionABSTRACT
A new 20-membered macrolide named as levantilide C was isolated from the Micromonospora strain FIM07-0019 recovered from shallow coastal waters near the island of Chiloe, Chile. The chemical structure of levantilide C was elucidated on the basis of one- and two-dimensional NMR analysis. Two known indole derivatives were also isolated from this strain. Levantilide C exhibited moderate antiproliferative activity against several tumour cell lines.