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Background: Cardiovascular diseases (CVDs) are the leading cause of death globally, taking an estimated 17.9 million lives each year. More evidence has shown that gut microbiota influences the three diseases through metabolites, the observational association between the gut microbiome, cardiovascular and cerebrovascular diseases has been well documented. However, whether there is a causal relationship with this association remains unclear. Methods: Basing publicly available GWAS aggregated data, a two-sample Mendelian randomization (MR) was used to examine the causal relationship between the gut microbiome, cardiovascular and cerebrovascular diseases. Two sets of MR analyses were performed. A set of single nucleotide polymorphisms (SNPs) less than the genome-wide statistical significance threshold (5×10-5) is used as the instrumental variable. Results: Based on the significance level of locus range, the results showed that there was a causal effect of gut microbial composition on the risk of MI, CI, and CAD. The inverse variance weighted (IVW) method shows that Alphaproteobacteria, Clostridialesvadin-BB60groupand Oxalobacteraceae were risk factors for MI, yet FamilyXIII was protective factor. Coriobacteriales, Verrucomicrobiales，ClostridialesvadinBB60groupwere risk factors for CI, while Actinobacteria, Gammaproteobacteria, Verrucomicrobiae, Enterobacteriales, Enterobacteriaceae, Methanobacteriaceae, Prevotellaceae were protective factors. And Actinomycetaceae was positively related with the risk of CAD, while Gammaproteobacteria and Actinomycetaleswere negatively related with it. Actinobacteria, Proteobacteria and ClostridialesvadinBB60group could casually related with CVDs. Conclusion: Our MR Analysis showed a causal relationship between gut microbiome and CVDs, which may help provide new insights into mechanisms underlying of CVDs.

Takotsubo syndrome (TTS) is characterized by acute and transient dysfunction of the apical segment of the left ventricle. In recent years, there have been increasing numbers of case reports about TTS; however, it is still being neglected and misdiagnosed in many primary hospitals in China. We present a case of a 68-year-old female who presented to our hospital with one month of paroxysmal cough. Here severe cough would sometimes induce headache, chest pain, nausea, and vomiting. She had an unexplained cardiogenic shock approximately 4 months prior and gradually developed orthopnea. Cardiac biomarkers were mildly elevated, and electrocardiogram (ECG) displayed diffuse and deep T-waves inversion in leads I, II, AVL, and V2-V9, like acute myocardial infarction. However, coronary angiography was performed and showed the absence of obstructed coronary atherosclerosis or acute plaque rupture. The patient was successively treated in four hospitals and was eventually diagnosed with TTS in our hospital (the fourth hospital) due to noncardiogenic discomfort. Physicians at some primary hospitals require additional clinical experience to deeply understand TTS. Many doctors could learn about TTS from a medical textbook but remain unfamiliar with the disease. We hope that through analysis of this case, primary doctors will have a deeper understanding of TTS, avoid misdiagnosing the typical cases that occur in their patients.

Objective: Previous studies have shown that parental attachment was associated with higher levels of posttraumatic growth (PTG) in individuals who have experienced traumatic events. The aim of the current longitudinal study is to investigate resilience as one pathway through which parental attachment is related to PTG among Chinese adolescents following the Yancheng tornado. Methods: A total of 351 adolescent survivors participated in this longitudinal study. Participants completed the revised version of Inventory of Parent and Peer Attachment (IPPA-R) at 12 months (T1), and the revised Chinese version of the Post-Traumatic Growth Inventory (PTGI-R) and the Connor and Davidson’s Resilience Scale (CD-RISC) at 18 months (T2) after the tornado, respectively. Results: It indicated that parental attachment at T1 has direct and positive effect on PTG at T2, and resilience at T2 fully mediated the relationship between parental attachment at T1 and PTG at T2. Conclusion: The findings revealed that parental attachment and resilience are two key resources that promote adolescent’s PTG, and parental attachment acts through resilience to promote PTG in adolescents.

Diet-induced obesity (OB) is usually accompanied by hypertriglyceridemia, which is characterized by the accumulation of triglyceride (TG)-rich lipoprotein (TRL) particles in the circulation. We previously found that postprandial TRL combined with insulin induced the adipogenic differentiation of 3T3-L1 preadipocytes, which may represent a key mechanism underlying obesity. However, the specific mechanism and signaling pathway involved in this process remain to be fully elucidated. In this study, we found that, in the postprandial state, patients with obesity had significantly higher levels of TG and remnant cholesterol (RC) than normal-weight controls. In vitro, we found that postprandial TRL, together with insulin, promoted the adipogenic differentiation of adipose-derived mesenchymal stem cells (AMSCs), as evidenced by the increased expression of lipogenesis-related genes and their protein products, including low-density lipoprotein related protein 1 (LRP1). Besides, caveolin-1 (Cav-1) expression was also significantly upregulated under this condition. Cav-1 and LRP1 were observed to interact, and then led to the activation of the PI3K/AKT1 signaling pathway. Meanwhile, the inhibition of LRP1 or Cav-1 significantly attenuated the adipogenic differentiation of AMSCs and downregulated AKT1 phosphorylation levels. Moreover, treatment with a selective AKT1 inhibitor significantly suppressed postprandial TRL and insulin-induced adipogenesis in AMSCs. Combined, our results demonstrated that, in association with insulin, postprandial TRL can promote the adipogenic differentiation of AMSCs in a manner that is dependent on the LRP1/Cav-1-mediated activation of the PI3K/AKT1 signaling pathway. Our findings indicated that a postprandial increase in TRL content is a critical factor in the pathogenesis of hypertriglyceridemia and diet-induced obesity.

Home quarantine may lead to families developing a variety of psychological distress. The purpose of this study was to examine the psychological status of children and their parent during 2019 coronavirus disease (COVID-19) outbreak in China. Data were collected from children (n = 1360) and their parent (n = 1360) in China using online survey during February 2020. Demographic information, media exposure, and psychological status including anxiety, depression and posttraumatic stress disorder (PTSD) symptoms were assessed using self-report measures. The results indicated that, for children, 1.84% experienced moderate anxiety, 2.22% experienced depression and 3.16% met the diagnostic criteria for PTSD; for parent, 1.18%, 0.01% and 3.60% experienced moderate anxiety, severe depression, and moderate depression, respectively, and 3.53% met the diagnostic criteria for PTSD. Moreover, excessive media exposure (β = −0.08 ~ 0.13, ps

Background: Hypertension (HBP) often occurs together with hypertriglyceridemia that indicates elevated triglyceride (TG) and remnant cholesterol (RC) levels. Non-fasting (i.e. postprandial) blood lipid test after a daily meal has been recommended by the European Atherosclerosis Society (EAS). However, little is known about the difference between fasting and non-fasting cut-off values in assessing high TG (HTG) and high RC (HRC) in HBP outpatients.Methods: Two hundred and twenty-five Chinese outpatients with HBP were enrolled in this study. According to the time of blood lipid test, they were divided into two groups, i.e. the fasting group (n=119) and the non-fasting group (n=139). Non-fasting levels of blood lipids at 2 h after a daily breakfast were also tested in 33 patients among the fasting group. Venous blood samples were collected. Serum levels of blood lipids were measured by the enzymatic and direct methods on a HITACHI 7170A analyzer or estimated via related formulas. Results: The non-fasting group had significantly higher levels of TG and RC while lower levels of total cholesterol, low-density lipoprotein cholesterol and non-high-density lipoprotein cholesterol than the fasting group (P＜0.05). According to TG and RC cut-off values of the EAS, the percentages of HTG and HRC in the non-fasting group were 67.6% and 65.6%, respectively, while those in the fasting group were 57.1% and 52.9%, respectively. However, the percentages of HTG in the fasting state and at 2 h after a daily breakfast in 33 outpatients did not reach statistical significance (57.6% v.s. 51.5%). So did the fasting and at 2 h non-fasting percentages of HRC in them.Conclusion: Non-fasting blood lipid test could find more HBP outpatients with HTG in Chinese outpatients with HBP. However, the percentage of HTG at 2h after a daily breakfast seemed to be close to that in the fasting state.

Background Circular RNAs (circRNAs) play important roles in cancer development and progression. The purpose of this study is to identify aberrantly expressed circRNAs in gastric cancer (GC), unravel their roles in GC progression, and provide new targets for GC diagnosis and therapy. Methods Bioinformatic analyses were performed to identify the aberrantly expression of hsa_circ_0061137 (termed as circDIDO1) in GC. Gain- and loss-of-function studies were performed to examine the biological roles of circDIDO1 in GC progression. Tagged RNA affinity purification, mass spectrometry, immunofluorescence, co-immunoprecipitation, and Western blot were used to identify circRNA-interacting and circRNA-encoded proteins. RNA sequencing, qRT-PCR, and Western blot were performed to analyze circRNA-regulated downstream target genes and signaling pathways. Mouse tumor models were used to analyze the effects of circDIDO1 on GC growth and metastasis. Results CircDIDO1 was transcribed from human DIDO1 (death-inducer obliterator 1) gene and formed by back-splicing of exons 2–6 of the linear transcript. circDIDO1 was down-regulated in GC tissues and its low levels were associated with larger tumor size, distal metastasis, and poor prognosis. CircDIDO1 overexpression inhibited while knockdown promoted GC cell proliferation, migration and invasion. CircDIDO1 overexpression suppressed GC growth and metastasis in mouse tumor models. Mechanistically, circDIDO1 encoded a novel 529aa protein that directly interacted with poly ADP-ribose polymerase 1 (PARP1) and inhibited its activity. CircDIDO1 also specifically bound to peroxiredoxin 2 (PRDX2) and promoted RBX1-mediated ubiquitination and degradation of PRDX2, which led to the inactivation of its downstream signaling pathways. Conclusions CircDIDO1 is a new circRNA that has tumor suppressor function in GC and it may serve as a potential prognostic biomarker and therapeutic target for GC.

Long non-coding RNAs (lncRNAs) have been suggested as important regulators of cancer development and progression in hepatocellular carcinoma (HCC). Nevertheless, the clinical value and biological roles of LINC00978 in HCC remain unclear. In this study, we detected the expression of LINC00978 in tumor tissues and serum of HCC patients, examined the roles of LINC00978 in HCC progression and elucidated the underlying molecular mechanisms. We found that LINC00978 expression was upregulated in tumor tissues and serum of HCC patients. Higher serum levels of LINC00978 could distinguish HCC patients from hepatitis and liver cirrhosis patients and healthy controls. LINC00978 knockdown inhibited HCC cell proliferation, migration and invasion while promoted cell cycle arrest and apoptosis. Overexpression of LINC00978 led to the opposite effects. LINC00978 knockdown also inhibited HCC growth and metastasis in mouse tumor models. Mechanistically, LINC00978 bound to EZH2 and mediated its accumulation at the promoter region of p21 and E-cadherin genes, leading to the trimethylation of H27K3 and the inhibition of p21 and E-cadherin expression. Moreover, the simultaneous depletion of p21 and E-cadherin expression reversed the inhibitory effects of LINC00978 knockdown on HCC cell proliferation, migration, and invasion. Taken together, these findings suggest that LINC00978 promotes HCC progression by inhibiting p21 and E-cadherin expression via EZH2-mediated epigenetic silencing. LINC00978 may represent a novel biomarker for HCC diagnosis, prognosis, and therapy.

Background: Tumor-associated stromal cells have been widely recognized for their tumor-promoting capability involving paracrine signaling. However, the underlying mechanism and the effects of the molecules in the glycolysis pathway in gastric cancer-associated mesenchymal stem cells (GCMSCs) and gastric cancer cells on tumor progression remain unclear.Methods: The expression of hepatocyte growth factor (HGF) in GCMSCs and bone marrow mesenchymal stem cells (BMMSCs) was detected by enzyme-linked immunosorbent assay (ELISA). The effect of HGF derived from GCMSCs on the proliferation, metastasis, and HK2 expression of gastric cancer cells was evaluated in vitro and in vivo. The effects of G6PD on the production of HGF in mesenchymal stem cells (MSCs) were analyzed by immunoblotting.Results: HGF derived from GCMSCs promoted glycolysis, proliferation, and metastasis of gastric cancer by upregulating c-Myc-HK2 signal. The progression of the disease induced by GCMSCs decelerated in the absence of HK2. The expression of G6PD activated NF-κB signaling and stimulated the production of HGF in GCMSCs. Blocking HGF derived from GCMSCs decreased proliferation, metastasis, and angiogenesis of gastric cancer cells in vivo.Conclusions: GCMSCs highly expressed G6PD and facilitated the progression of gastric cancer through the G6PD-NF-κB-HGF axis coordinates. Blocking HGF derived from GCMSCs is a potential new therapeutic target for the treatment of gastric cancer.

Background Increasing evidence indicates that circular RNAs (circRNAs) are dysregulated in human cancers. The biological roles of circRNAs in gastric cancer (GC) have not been well‐characterized. Methods The GEO database was used to analyze circRNA expression profile in GC. The expression level of target circRNA in tumor tissues and adjacent non‐tumor tissues was detected by reverse transcription‐quantitative PCR. Gene transfection was used to manipulate the expression of circRNAs. The biological roles of circRNAs in cell proliferation, migration, and invasion were determined by cell counting, colony formation, transwell migration, Matrigel invasion, and mouse xenograft tumor assays. The interactions between circRNAs and miRNAs were verified by RNA immunoprecipitation and luciferase reporter assays. Results We found that circHN1 was upregulated in GC tissues and cell lines compared to adjacent non‐tumor tissues and normal gastric epithelial cells. Additionally, circHN1 silencing significantly promoted GC cell growth, colony formation, migration, and invasion, whereas circHN1 overexpression had the opposite effects. CircHN1 overexpression also suppressed gastric cancer growth in the mouse xenograft tumor model. CircHN1 was mainly localized in the cytoplasm of GC cells and could bind to AGO2. MiR‐1248 and miR‐375 were predicted to interact with circHN1 by bioinformatic analyses. MiR‐1248 and miR‐375 overexpression inhibited the activity of the circHN1 luciferase reporter. Conclusion CircHN1 is aberrantly expressed in GC and affects the proliferation and migration of gastric cancer cells by acting as miRNA sponge.

Long non-coding RNAs (LncRNAs) have been suggested as important regulators of cancer development and progression in non-small cell lung cancer (NSCLC). Nevertheless, the biological roles and clinical significance of lncRNA UFC1 in NSCLC remain unclear. We detected the expression of UFC1 in tumor tissues, serum, and serum exosomes of NSCLC patients by qRT-PCR. Gene overexpression or silencing were used to examine the biological roles of UFC1 in NSCLC. RNA immunoprecipitation and ChIP assays were performed to evaluate the interaction between UFC1 and enhancer of zeste homolog 2 (EZH2) and the binding of EZH2 to PTEN gene promoter. Rescue study was used to access the importance of PTEN regulation by UFC1 in NSCLC progression. UFC1 expression was upregulated in tumor tissues, serum, and serum exosomes of NSCLC patients and high level of UFC1 was associated with tumor infiltration. UFC1 knockdown inhibited NSCLC cell proliferation, migration and invasion while promoted cell cycle arrest and apoptosis. UFC1 overexpression led to the opposite effects. Mechanistically, UFC1 bound to EZH2 and mediated its accumulation at the promoter region of PTEN gene, resulting in the trimethylation of H3K27 and the inhibition of PTEN expression. UFC1 knockdown inhibited NSCLC growth in mouse xenograft tumor models while the simultaneous depletion of PTEN reversed this effect. NSCLC cells derived exosomes could promote NSCLC cell proliferation, migration and invasion through the transfer of UFC1. Moreover, Exosome-transmitted UFC1 promotes NSCLC progression by inhibiting PTEN expression via EZH2-mediated epigenetic silencing. Exosome-mediated transmit of UFC1 may represent a new mechanism for NSCLC progression and provide a potential marker for NSCLC diagnosis.

Background Long non-coding RNAs (lncRNAs) have emerged as important regulators of human cancers. However, the functional roles of lncRNAs and the mechanisms responsible for their aberrant expression in gastric cancer (GC) have not been well characterized. Methods In this study, we examined the expression of lncRNA UFC1 in GC by qRT-PCR and explored its correlation with clinicopathological parameters. In vitro cell functional assays and in vivo animal studies were performed to determine the roles of UFC1 in GC progression. Results UFC1 was elevated and predicted poorer prognosis in GC. UFC1 knockdown inhibited while UFC1 overexpression promoted GC cell proliferation, migration, and invasion. UFC1 bound to miR-498 to antagonize its tumor suppressive effect on Lin28b. Suppression of Lin28b by miR-498 could be rescued by UFC1 overexpression, whereas Lin28b overexpression partially rescued UFC1 knockdown-mediated inhibition of GC cell function. Lin28b expression was increased in GC and suggested a co-expression pattern with UFC1. Conclusions UFC1 has a promoting role in GC progression, at least in part, by acting as a miR-498 sponge and derepressing Lin28b expression, which would provide a novel biomarker for GC diagnosis and prognosis and offer a potential target for GC therapy. Electronic supplementary material The online version of this article (10.1186/s13046-018-0803-6) contains supplementary material, which is available to authorized users.

Background: CircRNAs play important roles in cancer development and progression and have the potential to serve as cancer biomarkers. The aim of this study was to investigate the role of circular RNA CCDC66 (circCCDC66) in gastric cancer and to reveal the underlying mechanisms. Methods: The expression of circCCDC66 in GC tissues and cell lines was examined by qRT-PCR. The correlation between circCCDC66 expression level and clinicopathological characteristics was analyzed. The biological roles of circCCDC66 in GC cell apoptosis, proliferation, migration and invasion were determined by flow cytometry, cell counting, cell colony formation, wound healing, transwell migration and matrigel invasion assays. The role of circCCDC66 in GC growth was further confirmed by mouse xenograft tumor model. Western blot and qRT-PCR were used to explore the effects of circCCDC66 on epithelial-mesenchymal transition (EMT)-related gene and protein expression. Results: CircCCDC66 expression was elevated in both GC tissues and cell lines compared to adjacent normal tissues and normal gastric epithelial cell line. The upregulation of circCCDC66 in GC tissues was related to tumor stage and lymphatic metastasis. CircCCDC66 knockdown significantly inhibited GC cell proliferation, migration and invasion and induced cell apoptosis in GC cells. On the contrary, circCCDC66 overexpression had the opposite effects. In addition, circCCDC66 knockdown suppressed the tumorigenesis of GC cells in nude mice. Furthermore, circCCDC66 knockdown inhibited the activation of c-Myc and TGF-β signaling pathways and reversed EMT in GC cells. c-Myc and TGF-β interference blocked circCCDC66-mediated promotion of gastric cancer cell proliferation, migration and invasion. Conclusion: CircCCDC66 promotes GC growth and metastasis by activating c-Myc and TGF-β signaling pathways, suggesting that it may serve as a potential biomarker for GC.

MicroRNAs (miRNAs) play critical roles in the growth, metastasis and therapeutic resistance of liver cancer. Accumulating evidence suggests that miR‑498 is aberrantly expressed in several human malignancies. However, the role and underlying mechanism of miR‑498 in liver cancer remain unclear. In the present study, we investigated the potential roles and clinical value of miR‑498 in liver cancer. We found that the miR‑498 expression level was significantly lower in liver cancer patient tissues than that in healthy control tissues. The expression of miR‑498 was also decreased in liver cancer cell lines compared to that noted in a normal human normal liver cell line. miR‑498 overexpression markedly inhibited liver cancer cell proliferation, migration and invasion. miR‑498 overexpression induced cell cycle arrest and apoptosis while it suppressed epithelial‑mesenchymal transition (EMT) in liver cancer cells. Bioinformatic analysis and luciferase reporter assay further identified zinc finger E‑box binding homeobox 2 (ZEB2) as a novel target of miR‑498. Furthermore, ZEB2 knockdown recapitulated the inhibitory effects of miR‑498 overexpression in liver cancer cells. ZEB2 overexpression rescued the inhibition of liver cancer cell proliferation, migration, and invasion by miR‑498, indicating that ZEB2 acts as a downstream effector of miR‑498 in liver cancer cells. Thus, we demonstrated that miR‑498 suppresses the growth and metastasis of liver cancer cells, partly at least, by directly targeting ZEB2, suggesting that miR‑498 may serve as a potential biomarker for the diagnosis and therapy of liver cancer.

Xu Zhang,1,2,* Peng Zhang,1,* Meng Shao,1 Xueyan Zang,1 Jiayin Zhang,1 Fei Mao,1 Hui Qian,1,2 Wenrong Xu1,2 1Jiangsu Key Laboratory of Medical Science and Laboratory Medicine, School of Medicine, Jiangsu University, Zhenjiang, Jiangsu 212013, China; 2Zhenjiang Key Laboratory of Gastrointestinal Cancer, Jiangsu University, Zhenjiang, Jiangsu 212013, China *These authors contributed equally to this work Background: Increasing evidence suggests that SALL4 plays oncogenic roles in cancer development and progression. We have previously shown that SALL4 is highly expressed in gastric cancer, and its upregulation is associated with lymph node metastasis and poor prognosis. The role of SALL4 in gastric cancer metastasis and the underlying mechanism remain unclear.Materials and methods: The biological roles of SALL4 in gastric cancer cell mobility, migration, and invasion were investigated by wound healing, transwell migration assay, and Matrigel invasion assay. The effects of SALL4 on epithelial–mesenchymal transition (EMT) in gastric cancer cells were examined by quantitative real-time PCR and Western blot. The downstream target genes of SALL4 were identified by microarray. The regulation of TGF-β1 by SALL4 in gastric cancer cells was analyzed by luciferase reporter assay and chromatin immunoprecipitation assay.Results: SALL4 knockdown inhibited, while SALL4 overexpression promoted the motility, migration, and invasion abilities of gastric cancer cells in vitro. SALL4 knockdown also suppressed the peritoneal metastasis of gastric cancer cells in nude mice. SALL4 knockdown suppressed, while SALL4 overexpression induced the activation of TGF-β/SMAD signaling pathway and triggered EMT in gastric cancer cells. TGF-β1 was identified as a direct target gene of SALL4. The results of chromatin immunoprecipitation study and luciferase reporter assay further confirmed that SALL4 bound to the promoter of TGF-β1 gene and activated its expression. TGF-β1 knockdown reversed SALL4-mediated promotion of gastric cancer cell motility, migration, and invasion, indicating that TGF-β1 acts as a downstream effector of SALL4. Furthermore, the expression of TGF-β1 was found to be closely associated with that of SALL4 in gastric cancer tissues.Conclusion: SALL4 promotes the metastasis of gastric cancer, at least partly, by directly activating TGF-β1, suggesting that SALL4 may serve as a new target for gastric cancer therapy. Keywords: gastric cancer, SALL4, TGF-β1, EMT, metastasis

Figure S1. UFC1 knockdown inhibits gastric cancer cell proliferation, migration and invasion. Figure S2. UFC1 overexpression enhances gastric cancer cell proliferation, migration and invasion. Figure S3. Bioinformatic prediction of UFC1-binding miRNAs and target genes of miR-498. Figure S4. Relative expression levels of miR-498 and Lin-28b in gastric cancer cells and gastric cancer tissues. Figure S5. UFC1 overexpression antagonizes miR-498-medited inhibition of gastric cancer cell proliferation, migration and invasion. Figure S6. Lin28b knockdown inhibits gastric cancer cell proliferation, migration and invasion. Figure S7. Lin28b overexpression promotes gastric cancer cell proliferation, migration and invasion. Figure S8. UFC1 promotes gastric cancer cell proliferation, migration and invasion via the upregulation of Lin28b. (DOCX 19 kb)

Table S1. The sequences of primers for qRT-PCR. Table S2 The sequences of control and UFC1 shRNAs. Table S3. The association between UFC1 expression levels (–ΔCt) in tumor tissues and the clinicopathological features of gastric cancer patients. Table S4. The correlation between serum UFC1 expression levels (–ΔCt) and the clinicopathological characteristics of gastric cancer patients. Table S5. The correlation between exosomal UFC1 expression levels (–ΔCt) and the clinicopathological parameters of gastric cancer patients. (DOCX 25 kb)

Objectives Long noncoding RNAs (lncRNAs) play important roles in cancer development and progression. The deregulated expression of LINC00978 has been reported in human cancers. However, the expression pattern and biological roles of LINC00978 in gastric cancer (GC) remain unclear. In this study, we investigated the potential roles and clinical value of LINC00978 in gastric cancer. Materials and methods QRT-PCR was performed to investigate the expression of LINC00978 in gastric cancer cell lines, tissues and serum samples. Cell counting, colony formation, transwell migration and matrigel invasion assays were performed to determine the effects of shRNA-mediated knockdown of LINC00978 on gastric cancer cell functions. In vivo tumour growth assay was also conducted. Flow cytometry, immunohistochemistry, western blot and qRT-PCR were used for potential mechanism study. Results LINC00978 expression level was elevated in GC tumour tissues, serum samples and cell lines. The expression level of LINC00978 was significantly correlated with tumour size (P = 0.02), lymphatic metastasis (P = 0.009) and TNM stage (P = 0.009). LINC00978 knockdown inhibited the proliferation of GC cells by suppressing cell cycle progression and inducing apoptosis. LINC00978 knockdown also inhibited the migration and invasion of GC cells. In addition, LINC00978 knockdown inhibited the activation of TGF-β/SMAD signalling pathway and the process of epithelial-mesenchymal transition (EMT) in GC cells. Moreover, the in vivo tumorigenicity of LINC00978 knockdown GC cells in mice was significantly decreased. Conclusions LINC00978 promotes gastric cancer progression and may serve as a potential biomarker for GC.

Long noncoding RNAs (LncRNAs) play important roles in tumor development and progression. The expression of lncRNAs is frequently dysregulated in human cancer. DANCR (anti-differentiation noncoding RNA) is a newly identified lncRNA in human cancer, however, its functional roles and clinical value in gastric cancer (GC) remains unknown. In this study, we investigated the expression of DANCR in the tumor tissues and serum of GC patients and analyzed the correlation between DANCR expression levels and the clinicopathological characteristics. Our results showed that the expression of DANCR was higher in the tumor tissues than that in the adjacent non-cancerous tissues. The expression level of DANCR was also elevated in the serum of GC patients compared to that of healthy controls. The expression levels of DANCR were significantly associated with tumor size, TNM stage, lymphatic metastasis and invasion depth. DANCR knockdown inhibited the proliferation of GC cells by inducing cell cycle arrest and cell apoptosis. In addition, DANCR knockdown suppressed gastric cancer growth in vivo. Moreover, DANCR knockdown inhibited the migration and invasion of GC cells via the suppression of epithelial-mesenchymal transition (EMT). However, DANCR overexpression had the opposite effect. DANCR is activated by SALL4 in gastric cancer cells and exerted its oncogenic activities through the activation of β-catenin pathway. Taken together, our findings suggest that DANCR promotes the progression of gastric cancer and have the potential to serve as a novel diagnostic biomarker.