Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Downregulation of lncRNA XR_429159.1 could promote brain metastasis in patients with limited-stage small-cell lung cancer

ABSTRACT: Downregulation of lncRNA XR_429159.1 could promote brain metastasis in patients with limited-stage small-cell lung cancer

PROVIDER: PRJNA680181 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Downregulation of lncRNA XR_429159.1 could promote brain metastasis in patients with limited-stage small-cell lung cancer

Project description:Purpose: To identify the aberrant long non-coding RNA (lncRNA) and explore the predictive value of lncRNA on the risk of brain metastases (BMs) for patients with limited-stage small cell lung cancer (SCLC). Patients and Methods: We executed an array of lncRNA and mRNA chip assays on peripheral blood mononuclear cells of SCLC patients with BM comparing to others without BMs to identify the lncRNAs relating to BMs. Then validation was conducted in clinical data to confirm the relationship of lncRNAs and BMs furtherly. We estimated the cumulative incidence of BMs using the Kaplan-Meier method and differences between the groups were analyzed using the log-rank test. Results: The expression of 67 lncRNAs (27 up, 40 down) and 47 mRNAs (20 up, 27 down) were different significantly in BM groups comparing to the group without BMs (fold change ≥ 2.0, p value ≤0.05) which were found by lncRNA and mRNA chip assays initially. Four lncRNAs were verified by qRT-PCR to confirm the accuracy of the microarray data and then the results of 11 pairs of patients (11 patients with BMs, while 11 patients without BMs) showed that low expression of LncRNA XR_429159.1 was the high-risk factor of BM. Further clinical data showed that the BM incidence of 25 patients with low level LncRNA XR_429159.1 was 31% at 1-year, and that was 14.3% in the 18 patients with high level LncRNA XR_429159.1, p = 0.035. Conclusion: Our present study identified that low expression of lncRNA XR_429159.1 was the high-risk factor of BM in patients with limited-stage SCLC.

2021-04-16 | GSE161968 | GEO

lncRNA downregulation

Project description:lncRNA downregulation

| PRJEB21799 | ENA

Glucocorticoids Promote Breast Cancer Metastasis

Project description:Glucocorticoids Promote Breast Cancer Metastasis

| PRJNA513860 | ENA

Downregulation of lncRNA XR_429159.1 Linked to Brain Metastasis in Patients With Limited-Stage Small-Cell Lung Cancer.

Project description: Not available

| S-EPMC8166247 | biostudies-literature

Myeloid-derived suppressor cells promote lung cancer metastasis

Project description:Myeloid-derived suppressor cells promote lung cancer metastasis

| PRJNA564103 | ENA

Ral GTPases promote metastasis by controlling biogenesis and organotropism of exosomes

Project description:Cancer extracellular vesicles (EVs) mainly exert pro-tumoral functions by changing the phenotypes of stromal cells to the benefit of tumor growth and metastasis. In particular, they shuttle to distant organs and seed pre-metastatic niches facilitating subsequent colonization by circulating tumor cells. The levels of tumor secreted EVs have been correlated to tumor aggressiveness, however, the link between EV secretion mechanisms, their capacity to form pre-metastatic niches and the actual formation of metastasis remains obscure. Here, we show that two GTPases RalA and RalB control, through the phospholipase PLD1, the homeostasis of multi-vesicular bodies and thereby tune the biogenesis and secretion of a subtype of (pro-metastatic) EVs. Mice experiments revealed that RalA and RalB promote lung metastasis of mammary carcinoma cells without affecting their invasive behaviors. Importantly, we show in vivo that EVs from RalA or RalB depleted cells have limited organotropic capacities and, as a consequence, are less efficient in priming lung metastasis. Furthermore, we show that such EVs lack the adhesion molecule MCAM/CD146, which is responsible for EVs organotropism. Finally, we show that RalA and RalB have increased expression in human breast cancer patients with lung metastasis. Altogether, our study identifies Ral GTPases as central molecules linking the mechanisms of EVs secretion, cargo loading to their capacity to disseminate and induce pre-metastatic niches.

2021-09-09 | PXD020180 | Pride

Downregulation of LATS kinases alters p53 to promote cell migration

Project description:p53 is a pivotal tumor suppressor and a major barrier against cancer. We now report that silencing of the Hippo pathway tumor suppressors LATS1 and LATS2 in non-transformed mammary epithelial cells reduces p53 phosphorylation and increases its association with the p52 NF-?B subunit. Moreover, it partly shifts p53âs conformation and transcriptional output towards a state resembling cancer-associated p53 mutants, and endow p53 with the ability to promote cell migration. Notably, LATS1 and LATS2 are frequently downregulated in breast cancer; we propose that such downregulation might benefit cancer by converting p53 from a tumor suppressor into a tumor facilitator. MCF10A cells transfected with siRNA against LATS1/2 alone, p53 alone or LATS1/2 and p53 together. Two independent MCF10A batches provided biological replicates

2015-12-11 | E-GEOD-74493 | biostudies-arrayexpress

Myeloid-derived suppressor cells promote lung cancer metastasis

Project description:Myeloid-derived suppressor cells (MDSCs) suppress antitumor immune activities and facilitate cancer progression. Although the concept of immunosuppressive MDSCs is well established, the mechanism that MDSCs regulate non-small cell lung cancer (NSCLC) progression through the paracrine signals is still lacking. Here, we reported that the infiltration of MDSCs within NSCLC tissues were associated with the progression of cancer status, and were positively correlated with the Patient-derived xenograft (PDX) model establishment, and poor patient prognosis. Intratumoral MDSCs directly promoted NSCLC metastasis and highly expressed chemokines that promote NSCLC cells invasion, including CCL11. CCL11 was capable of activating the AKT and ERK signaling pathways to promote NSCLC metastasis through the epithelial-mesenchymal transition (EMT) process. Moreover, high expression of CCL11 was associated with a poor prognosis in lung cancer as well as other types of cancer. Our findings underscore that MDSCs produce CCL11 to promote NSCLC metastasis via activation of ERK and AKT signaling and induction of EMT, suggesting that the MDSCs-CCL11-ERK/AKT-EMT axis contains potential targets for NSCLC metastasis treatment.

2021-01-17 | GSE136949 | GEO

Identification of endothelial derived factors that promote metastasis II

Project description:Identification of endothelial derived factors that promote metastasis II

| PRJNA606604 | ENA

Identification of endothelial derived factors that promote metastasis III

Project description:Identification of endothelial derived factors that promote metastasis III

| PRJNA606757 | ENA