Long Non-coding RNA LINC01503 Promotes Gastric Cancer Cell Proliferation and Invasion by Regulating Wnt Signaling.

BACKGROUND: Previous studies have indicated that the dysregulation of long non-coding RNAs plays an important role in tumors. LINC01503 is a newly discovered lncRNA that promotes development of various tumor types. However, the function of LINC01503 in gastric cancer has not been reported yet. AIMS: To explore the function of LINC01503 in gastric cancer development and the underlying molecular biological regulatory mechanisms. METHODS: LINC01503 expression in tissues and cell lines of gastric cancer were determined through qRT-PCR. Transwell assay and cell number counting experiments were employed to detect the cell invasion and proliferation. C-myc, cyclin D1, and ß-catenin expressions were analyzed through Western blot and qRT-PCR. RESULTS: LINC01503 was highly expressed in gastric cancer tissues and cell lines, which was correlated with poor prognosis. Knockdown of LINC01503 suppressed gastric cancer cell proliferation and invasion, whereas overexpression of LINC01503 showed a reverse trend. Silencing LINC01503 significantly inhibited the expression of c-myc, cyclin D1, and ß-catenin. Overexpressing ß-catenin rescued the inhibitory effects, induced by LINC01503 silencing, on gastric cancer cell proliferation and metastasis. CONCLUSIONS: This research reported that the elevated expression of LINC01503 could promote proliferation and metastasis of gastric cancer through positively regulating the Wnt/ß-catenin pathway.

Integration of whole-genome sequencing and functional screening identifies a prognostic signature for lung metastasis in triple-negative breast cancer.

Lung metastasis is one of the leading causes of death for triple-negative breast cancer (TNBC). We sought to characterize the genetic alterations underlying TNBC lung metastases by integrating whole-genome sequencing and functional screening. Furthermore, we aimed to develop a metastasis-related gene signature for TNBC patients to improve risk stratification. In this prospective observational study, we first conducted whole-genome sequencing of paired primary tumor and lung metastasis from one TNBC patient to identify potential genetic driver alterations. An in vivo gain-of-function screening using an amplified open reading frame library was then employed to screen candidate genes promoting lung metastasis. Finally, we applied Cox proportional hazard regression modeling to develop a prognostic gene signature from 14 candidate genes in TNBC. Compared to the primary tumor, copy number amplifications of chromosomes 3q and 8q were identified in the lung metastasis. We discovered an enrichment of 14 genes from chromosomes 3q and 8q in mouse lung metastases model. We further developed and validated a four-gene signature (ENY2, KCNK9, TNFRSF11B and KCNMB2) that predicts recurrence-free survival and lung metastasis in TNBC. Our data also demonstrated that upregulated expression of ENY2 could promote invasion and lung metastasis of TNBC cells both in vitro and in vivo. In conclusion, our study reveals functional genes with copy number amplifications among chromosome 3q and 8q in lung metastasis of TNBC. And we develop a functional gene signature that can effectively stratify patients into low- and high-risk subgroups of recurrence, helping frame personalized treatments for TNBC.

Gastric Cancer Growth Modulated by circSNTB2/miR-6938-5p/G0S2 and PDCD4.

BACKGROUND: Gastric cancer (GC) is the third most common cause of cancer-related death worldwide. Increasing studies have indicated that circular RNAs (circRNAs) play critical roles in cancer progression. However, the precise mechanism and functions of most circRNAs are still unknown in gastric cancer. METHODS: In the present study, we aim to uncover the mechanism by which circRNAs regulate gastric cancer tumorigenesis. By analyzing the microarray data, we screened differential expressed circRNAs in the gastric cancer group and identified a down-regulated circRNA, hsa_circ_0040039 (circSNTB2). Mechanically, circSNTB2 served as a sponge for the miR-6938-5p and up-regulated its expression. RESULTS: Meanwhile, G0/G1 switch gene 2 (G0S2) and programmed cell death gene 4 (PDCD4) were identified to be the aim genes of miR-6938-5p, constructing circSNTB2/miR-6938-5p/G0S2 and PDCD4 pathways. CONCLUSION: Taken together, our findings demonstrated that circSNTB2 plays an essential role in gastric cancer by regulating miR-6938-5p through G0S2 and PDCD4 genes. CircSNTB2 could be a promising biomarker for GC diagnosis and targeted therapy.

Laparoscopic resection of a rare diaphragmatic haemangioma: a case report.

This case report describes the laparoscopic resection of a rare diaphragmatic haemangioma. A 45-year-old male patient was diagnosed incidentally with a left subphrenic mass by computed tomography. Laparoscopic left subphrenic mass excision was performed under general anaesthesia. A phrenic haemangioma was confirmed by postoperative pathology. Tumours originating in the diaphragm are rare, with only approximately 200 cases reported in the past century. The diaphragmatic tumour was determined to be primary because intraoperative imaging showed that the tumour was relatively isolated and had no obvious relationship with the surrounding tissues and organs.

Epidemiology and survival outcomes of mucinous adenocarcinomas: A SEER population-based study.

To investigate the epidemiology, demographics and survival of mucinous adenocarcinomas (MACs), we identified 80,758 MAC patients in the Surveillance, Epidemiology and End Results (SEER) database. The reported incidence of MACs ebbed and flowed over time; however, a significant increase in reported annual age-adjusted incidences of MACs in the appendix, lung and bronchus was observed from 1981 to 2014. The demographics and outcomes of MACs differed by anatomic sites. MACs of the stomach had the largest percentage of poorly differentiated or undifferentiated tumors (41.2%), while MACs of the appendix and pancreas were associated with more advanced tumor stage (P < 0.001). MACs of the pancreas, lung and bronchus and stomach showed worse survival than other sites, despite localized, regional or distant stage (P < 0.001). In univariate and multivariate analysis, site, tumor grade, tumor stage, regional nodes, sex, race, surgery and year of diagnosis were identified as independent prognostic factors of cancer-specific survival. In conclusion, the incidence of MACs of certain specific sites, such as the appendix, lung and bronchus, is rapidly increasing. We also revealed a series of prognostic factors of MACs, including tumor sites, tumor grade and tumor stage, which may improve the current understanding of the clinical and biological patterns of MACs.