Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1522282 (EMT)
 2,868 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Accumulating evidence indicates that the lncRNAs play a critical role in cancer progression and metastasis. In this study, we found that MALAT1 upregulation was associated with larger tumor size and lymph-node metastasis, and also correlated with shorter overall survival of lung adenocarcinoma patients. Furthermore, MALAT1 promotes EMT and metastasis of lung adenocarcinoma cells in vitro and in vivo. In particular, MALAT1 upregulated the expression of miR-204 target gene SLUG through competitively 'spongeing' miR-204. In summary we unveil a branch of the MALAT1/miR-204/SLUG pathway that regulates the progression of lung adenocarcinoma.
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PMID:LncRNA MALAT1 exerts oncogenic functions in lung adenocarcinoma by targeting miR-204. 2729 2

Mounting evidence shows that the long non-coding RNA MALAT1 plays a pivotal role in tumorigenesis and metastasis, but the functional significance of MALAT1 in bladder transitional cell carcinoma (BTCC) remains unclear. MALAT1 expression was measured in 56 BTCC patients and 2 BTCC cell lines by real-time PCR. The effects of MALAT1 on BTCC cells were investigated by over-expression approaches in vitro and in vivo. Insights of the mechanism of competitive endogenous RNAs (ceRNAs) were validated through bioinformatic analysis and luciferase assay. MALAT1 up-regulation positively correlated with advanced clinical pathological stage and shorter survival of BTCC patients. Furthermore, MALAT1 over-expression promoted proliferation, migration and invasion of BTCC cells in vitro and in vivo. Particularly, MALAT1 may function as a ceRNA to sponge miR-124, thus modulating the derepression of foxq1, miR-124 target gene, in post-transcriptional levels. The positive MALAT1/foxq1 interaction was confirmed by bivariate correlation analysis, and this positive correlation was of great significance in BTCC tumor growth and metastasis, also accompanied by EMT changes. Overall, this ceRNA regulatory network concerning MALAT1 and the positive MALAT1/foxq1 correlation benefit a better understanding of BTCC pathogenesis and promote the feasibility of lncRNA-directed therapy against this disease.
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PMID:LncRNA MALAT1 promotes tumor growth and metastasis by targeting miR-124/foxq1 in bladder transitional cell carcinoma (BTCC). 2973 19

Preeclampsia (PE) is a pregnancy-specific syndrome that substantially leads to maternal and fetal mortality. Multiple factors contribute to the disease, but the exact pathogenesis still remains elusive. Here we explored the roles of lncRNA MALAT1 and miR-206 in PE. qRT-PCR was applied to measure mRNA levels of MALAT1 and miR-206 in the placenta of PE patients. Scratch wound healing assay and transwell invasion assay were conducted to test the effects of MALAT1 and miR-206 on migration and invasion of trophoblast cells. In addition, we validated MALAT1/miR-206 and miR-206/IGF-1 interactions with dual luciferase reporter assay. Western bot was used to detect protein expressions of IGF-1, p-PI3K, PI3K, p-Akt and Akt. We found that MALAT1 was decreased but miR-206 was increased in the placenta of patients with PE. Inhibition of MALAT1, knockdown IGF-1, or miR-206 mimics suppressed the trophoblast cells migration and invasion, while overexpression of MALAT1, IGF-1 or miR-206 inhibitors exhibited opposite effects. Further, miR-206 was confirmed as a direct target of MALAT1. Besides, miR-206 inhibited IGF-1 expression by directly binding to the 3'UTR. Mechanistically, our study demonstrated that MALAT1 regulates IGF-1/PI3K/Akt signaling via miR-206. Together, these results suggest that MALAT1 and miR-206 play important roles in PE. MALAT1 regulates miR-206/IGF-1 axis, thereby modulating trophoblast cells migration and invasion through PI3K/Akt signal pathway. These results show light on the underlying mechanisms of PE and provide potential targets for PE therapy.Abbreviations: PE: Preeclampsia; lncRNA: Long-non-coding RNA; MALAT1: Metastasis-associated lung adenocarcinoma transcript 1; IGF-1: Insulin-like growth factor 1; PI3k: Phosphatidylinositol-4, 5-bisphosphate 3-kinase; Akt: Protein kinase B; GAPDH: Glyceraldehyde 3-phosphate dehydrogenase; qRT-PCR: Quantitative Reverse Transcription polymerase chain reaction; shRNA: Short hairpin RNA; siRNA: Small interfering RNA; EMT: Epithelial-mesenchymal transition.
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PMID:LncRNA MALAT1 regulates trophoblast cells migration and invasion via miR-206/IGF-1 axis. 3177 73

Homo sapiens metastasis associated lung adenocarcinoma transcript 1 (LncRNA MALAT1) plays an important role in many types of cancer, but its role in human lung adenocarcinoma (LAC) is still unclear. In this paper, we found that LncRNA MALAT1 had high expression in human LAC tissues (vs. paracancerous normal tissue) and human lung adenocarcinoma cells (vs. human normal lung tissue cells). The expression of lncRNA MALAT1 was significantly associated with human lung adenocarcinoma tumor size, lymph node metastasis, and TNM staging, and was negatively correlated with miR-429 expression in lung adenocarcinoma tissues. In vitro, LncRNA MALAT1 could block human LAC cells in the G1 phase to inhibit proliferation by reducing the expression of cyclin D1 protein. LncRNA MALAT1 could inhibit the invasion and migration of human LAC cells by decreasing the expression of MMP-9 and vimentin and increasing the expression of E-cadherin. We also found that Malat1 functions as a competing endogenous RNA (ceRNA) for miR-429 and directly suppressed the expression of RhoA protein. RhoA knockout and transfection of miR-429-mimic could play the same function which is to decrease the expression of cyclin D1, MMP-9, and vimentin proteins and increased E-cadherin protein expression. These results suggested that LncRNA Malat1 could promote the proliferation and EMT of human lung adenocarcinoma cells by competing with RhoA for binding to miR-429.
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PMID:Long non-coding RNA MALAT1 interaction with miR-429 regulates the proliferation and EMT of lung adenocarcinoma cells through RhoA. 3193 47

Colorectal cancer (CRC) is one of deadly malignancies that affects humans globally. Herein, the effects of MALAT1 on CRC cellular functions were investigated. RT-qPCR measured expression of MALAT1 in human cell lines for colorectal Cancer. Radiation-resistance CRC cells (CRC-IR) were generated by increasing treatments of irradiation. Cell transfection upregulated or silenced genes in CRC-IR cells so as to study the correlation between MALAT1/miR-101-3p expression and cellular resistance to irradiation through evaluation of CCK-8, FCM apoptosis, Transwell migration and invasion and western blot assays for cell viability,apoptosis, migration and invasion and EMT. MALAT1 was upregulated in radio-resistance cell lines compared to normal CRC cells and upregulation promoted cell viability. In addition, decreased MALAT1 inhibited cell proliferation and metastasis and promoted apoptosis of CRC-IR cells. The luciferase assays confirmed that MALAT1 targeted and regulated miR-101-3p expression in radio-resistance cells. MiR-101-3p counteracted the effect exerted by MALAT1 in CRC-IR cells, indicating that MALAT1 added to the radio-resistance in vitro while miR-101-3p mimics could decrease the resistance to irradiation in CRC. In this study we have demonstrated that MALAT1 could regulate the radio-resistance in colorectal cancer via sponging miR-101-3p. Eventually, these outcomes unearthed a novel axis lncRNA MALAT1/miR-101-3p,which might be a prospective treatment to regulate radio-therapy in the near future.
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PMID:Aberrant expression of lncRNA MALAT1 modulates radioresistance in colorectal cancer in vitro via miR-101-3p sponging. 3238 53