Browse
Submit Data
Databases
API
Help

Dataset Information

32 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MiR-501 promotes tumor proliferation and metastasis by targeting HOXD10 in endometrial cancer.

ABSTRACT:

Background

Several studies have shown the crucial role of miR-501 in regulating cellular pathology in various cancers. However, the function and expression of miR-501 in endometrial cancer (EC) remain obscure.

Methods

The expression of miR-501 was determined using quantitative real-time PCR. MTT assay, colony formation assay and cell cycle analysis were used to evaluate the proliferation ability. Migration and invasion were assessed using transwell assay. Tumor formation in nude mice was used to observe the effects of miR-501 on cell proliferation and migration in vivo. Luciferase assay, quantitative real-time PCR and western blot were applied to determine that HOXD10 was the target gene of miR-501.

Results

In this study, we observed significantly up-regulated expression of miR-501 in endometrial cancer, which correlated with higher pelvic lymph node metastasis and shorter overall survival in high-grade endometrial cancer. High expression of miR-501 was also found in the copy-number-high group than other groups. Moreover, in vitro and in vivo assay showed that overexpression of miR-501 can promote proliferation and metastasis. Mechanistically, we found that miR-501 promotes tumor progression by directly targeting HOXD10. Further study also indicated that miR-501 overexpression can activate the AKT/mTOR pathway.

Conclusions

MiR-501, which functions as an oncomir in endometrial cancer, might be a potential therapeutic target in high grade endometrial cancer.

SUBMITTER: Sun X

PROVIDER: S-EPMC8141179 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Similar Datasets

miR-501 promotes hemangioma progression by targeting <i>HOXD10</i>.

Project description:MicroRNAs (miRNAs) are often abnormally expressed in human cancers to act as either oncogenes or tumor suppressor genes. MiRNA-501 (miR-501) has been found to be abnormally expressed in certain types of cancer, but its expression and biological role in hemangioma remain to be fully elucidated. In this study, the expression of miR-501 in hemangioma cell lines was analyzed by quantitative real-time polymerase chain reaction (qRT-PCR). The TargetScan algorithm, luciferase activity reporter assay, and Western blot analysis were conducted to validate homeobox D10 (HOXD10) as a direct target of miR-501. The results revealed that miR-501 expression was upregulated in hemangioma cell lines. Downregulation of miR-501 inhibited hemangioma cell proliferation, cell cycle progression, colony formation, migration, and invasion in vitro. Bioinformatics analysis indicated that HOXD10 was a putative target of miR-501. In addition, in a luciferase reporter system, it was confirmed that HOXD10 is a direct target of miR-501. It was also demonstrated HOXD10 downregulation reversed the effects of the miR-501 inhibitor on hemangioma cell activities. These findings indicated that miR-501 targeted HOXD10 to promote hemangioma cell processes, suggesting that miR-501 has an oncogenic role in the pathogenesis of hemangioma.

| S-EPMC6511771 | biostudies-literature

miR-600 promotes ovarian cancer cells stemness, proliferation and metastasis via targeting KLF9.

Project description:Previous studies have revealed that miRNAs participate in the pathogenesis of ovarian cancer; however, whether miR-600 is also involved remains unclear. In this study, we aimed to investigated the role of miR-600 in ovarian cancer progression. Here, miR-600 expression was significantly upregulated in ovarian cancer tissues and stem cells. Functional studies showed that miR-600 promoted ovarian cancer cell stemness, proliferation and metastasis. Mechanistic studies revealed that Kruppel like factor 9 (KLF9) was indicated as the target of miR-600. The luciferase reporter assay suggested that miR-600 directly bound to the 3'-untranslated region of KLF9. Additionally, miR-600 expression was negatively associated with KLF9 expression in human ovarian cancer tissues. Si-KLF9 partially abolished the discrepancy of self-renewal, growth and metastasis capacity between miR-600 knockdown ovarian cancer cells and control cells. In conclusion, our results suggest that miR-600 promotes ovarian cancer cell stemness, proliferation and metastasis via directly downregulating KLF9, and impairing miR-600 levels may be a new treatment strategy for ovarian cancer in the future.

| S-EPMC9063371 | biostudies-literature

miR-224 enhances invasion and metastasis by targeting HOXD10 in non-small cell lung cancer cells.

Project description:Increasing number of studies have indicated aberrant microRNA (miRNA) expression could affect normal biological progress in non-small cell lung cancer (NSCLC) cells. This study was performed to evaluate the biologic functions of microRNA-224 (miR-224) in NSCLC. Real-time PCR was performed to evaluate the expression of miR-224 and Homeobox D10 (HOXD10) in NSCLC cell lines and tissues. Transwell assays were performed to investigate the function of miR-224 on NSCLC cell migration and invasion. Moreover, western blotting and luciferase assays were used to investigate HOXD10 as miR-224 downstream targets. miR-224 is increased in NSCLC metastatic tissues and cell lines. Increased miR-224 expression promoted NSCLC cell migration and invasion, while low miR-224 expression suppressed NSCLC cell migration and invasion. Furthermore, HOXD10 was targeted directly by miR-224 in NSCLC cells. Moreover, we found that HOXD10 was a functional target and influenced tumour-inductive functions of miR-224 on progression of NSCLC. These findings suggest that miR-224 may be used in the treatment of NSCLC. Targeting this novel strategy, miR-224/HOXD10 axis may be helpful as promising biomarker and therapeutic method to control NSCLC cell metastasis.

| S-EPMC5920555 | biostudies-literature

MiR-126-5p Promotes Tumor Cell Proliferation, Metastasis and Invasion by Targeting TDO2 in Hepatocellular Carcinoma.

Project description:TDO2 is a key enzyme in the kynurenine metabolic pathway, which is the most important pathway of tryptophan metabolism. It has been shown that miRNAs are involved in cell metastasis through interaction with target mRNAs. In this study, we found 645 miRNAs that could be immunoprecipitated with TDO2 through the RNA-immunoprecipitation experiment. miR-126-5p was selected as the research target, which was also confirmed by dual-luciferase reporter assay. Through qRT-PCR analysis, it was verified that the overexpression of miR-126-5p promoted the expression of TDO2, PI3K/AKT and WNT1. Meanwhile, it was verified that overexpression of miR-126-5p can promote intracellular tryptophan metabolism by HPLC. We also verified the effects of miR-126-5p on cell proliferation, migration, and invasion by cck-8, cell colony formation and trans-well assay in both HCCLM3 cells and HepG2 cells. In vivo experiments were also conducted to verify that miR-126-5p promoted tumor formation and growth via immunohistochemical detection of cell infiltration and proliferation to generate markers Ki-67, BAX, and VEGF. In conclusion, our results suggest that miR-126-5p is a biomarker and a potential new treatment target in the progression of HCC via promoting the expression of TDO2.

| S-EPMC8779717 | biostudies-literature

miR-552 promotes the proliferation and metastasis of cervical cancer cells through targeting MUC15 pathway.

Project description:Accumulating evidence shows that microRNAs (miRNAs) play key roles in tumorigenesis, progression, recurrence and drug resistance of malignant tumors. The tumor-promoting role of miR-552 has been evidenced in multiple tumors. Yet, the relevance of miR-552 in cervical cancer remains undetermined. This study aimed to investigate the role of miR-552 in cervical cancer proliferation and metastasis. Herein, we for first found that miR-552 expression was upregulated in cervical cancer tissues compared with their normal controls. Functional assays revealed that miR-552 promoted the proliferation and metastasis of cervical cancer cells. Mechanically, bioinformatics and luciferase reporter analysis identified MUC15 as a direct target of miR-552. Reduced MUC15 expression was detected in cervical cancer, and MUC15 overexpression exhibited a tumor-suppressive effect. MUC15 restoration partially abolished the discrepancy of growth and metastasis capacity between miR-552 overexpression cervical cancer cells and control cells. Taken together, these data demonstrate that miR-552 acts as a potential oncogene miRNA in cervical cancer, which exerts its function through targeting MUC15.

| S-EPMC8425207 | biostudies-literature

miR-552 promotes laryngocarcinoma cells proliferation and metastasis by targeting p53 pathway.

Project description:Numerous researches show that MicroRNAs (miRNAs) participate in tumorigenesis, progression, recurrence and drug resistance of malignant tumors, including laryngocarcinoma. miR-552 works as an oncogene in both colorectal cancer and liver cancer. However, the potential role of miR-552 in laryngocarcinoma is unknown. Herein, we for first found that miR-552 expression was upregulated in laryngocarcinoma tissues compared with their normal controls. Moreover, miR-552 expression was also increasing in the laryngocarcinoma cells. miR-552 interference inhibited the proliferation and metastasis of laryngocarcinoma cells in vitro and in vivo. Mechanically, bioinformatics and luciferase reporter analysis identified p53 as a direct target of miR-552. miR-552 knockdown upregulated the p53 mRNA and protein expression in laryngocarcinoma cells. miR-552 expression was negatively associated with p53 expression in laryngocarcinoma tissues. More importantly, the p53 siRNA or p53 overexpression virus abrogated the discrepancy of growth and metastasis capacity between miR-552 interference laryngocarcinoma cells and control cells.

| S-EPMC7217371 | biostudies-literature

MiR-371 promotes proliferation and metastasis in hepatocellular carcinoma by targeting PTEN.

Project description:Hepatocellular carcinoma (HCC) is the leading cause of cancer-related mortality worldwide. MiR-371 has recently emerged as an important regulator in tumorigenesis, and may serve as a biomarker for malignant tumors. We transfected miR-371 or its inhibitor in two human HCC cell lines, then used 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, soft agar colony formation, and transwell migration assays to evaluate the effects on cell proliferation, migration, and invasion. We found that miR-371 was positively correlated with HCC metastasis and poor prognosis in the inflicted patients, and the high expression of miR-371 was promoted, whereas a low level of miR-371 depressed cell proliferation and invasion. We found PTEN to be a direct target of miR-371. The overexpression or knockdown of PTEN exhibited the opposite effects from those of miR-371 on cell proliferation and migration. Our study demonstrates that miR-371 promotes proliferation and metastasis in HCC by targeting PTEN. [BMB Reports 2019; 52(5): 312-317].

| S-EPMC6549920 | biostudies-literature

Elevated MiR-222-3p promotes proliferation and invasion of endometrial carcinoma via targeting ERα.

Project description:MicroRNAs play key roles in tumor proliferation and invasion. Here we show distinct expression of miR-222-3p between ERα-positive and ERα-negative endometrial carcinoma (EC) cell lines and primary tumors, and investigation of its relationship with ERα and other clinical parameters. In vitro, the function of miR-222-3p was examined in RL95-2 and AN3CA cell lines. MiR-222-3p expression was negatively correlated with ERα. Over-expressed miR-222-3p in RL95-2 cells promoted cell proliferation, enhanced invasiveness and induced a G1 to S phase shift in cell cycle. Furthermore, the miR-222-3p inhibitor decreased the activity of AN3CA cells to proliferate and invade. In vivo, down-regulated miR-222-3p of AN3CA cells inhibited EC tumor growth in a mouse xenograft model. Additionally, miR-222-3p increased raloxifene resistance through suppressing ERα expression in EC cells. In conclusion, miR-222-3p plays a significant role in the regulation of ERα expression and could be potential targets for restoring ERα expression and responding to antiestrogen therapy in a subset of ECs.

| S-EPMC3909214 | biostudies-literature

Tumor-derived endomucin promotes colorectal cancer proliferation and metastasis.

Project description:BackgroundEndomucin (EMCN) is a type I transmembrane glycoprotein and a mucin-like component of the endothelial cell glycocalyx. The mechanism of EMCN action in colorectal cancer (CRC) remains unclear.AimsOur aim was to explore the role of EMCN in the progression of CRC.Materials & methodsWe examined EMCN expression in CRC tissues and normal para-carcinoma tissues. The function and mechanisms of EMCN were checked in CRC cell lines and in mouse xenograft. Additionally, we used co-immunoprecipitation and mass spectrometry to identify the potential EMCN-binding proteins. Functional annotation analysis showed where these genes were enriched.ResultsWe found that EMCN was overexpressed in tumor tissues compared with that in normal para-carcinoma tissues. We also found that overexpression of EMCN induced CRC proliferation and metastasis both in vitro and in vivo. EMCN knockdown prevents epithelial-mesenchymal transition in vitro. We identified 178 potential EMCN-binding partners. Furthermore, functional annotation analysis indicated that these genes were considerably enriched in carcinogenic-related functions and pathways. Collectively, the identification of EMCN-binding partners enhanced our understanding of the mechanism of EMCN-mediated malignant phenotypes, and this research may provide valuable insights into the molecular mechanisms underlying CRC.ConclusionTumor-derived endomucin promotes colorectal cancer proliferation and metastasis. We identified 178 EMCN-binding proteins and initially screened three potential EMCN-interacting proteins: NALCN, and TPM2, ANKK1. Our study provides valuable insights into the molecular mechanisms underlying CRC development.

| S-EPMC9939191 | biostudies-literature

miR-196a-5p promotes metastasis of colorectal cancer via targeting I?B?.

Project description:BACKGROUND:MicroRNA-196a-5p (miR-196a-5p) has been reported to be involved in the metastatic process of several cancers. In present work, we aimed to investigate the effects of miR-196a-5p and its potential target I?B? on migration, invasion and epithelial-mesenchymal transition (EMT) of colorectal cancer (CRC) cells. METHODS:CCK-8 assay, wound healing assay and cell invasion assay were performed to evaluate the cell proliferation, migration and invasion. In vivo metastasis models were used to investigate the tumor metastasis ability. Real-time PCR, immunofluorescence staining or western blot were utilized to detect the expression of miR-196a-5p, I?B?, p-I?B?, nuclear p65 and EMT markers including E-cadherin, N-cadherin and fibronectin. Dual luciferase reporter assay was carried out to determine whether there is a direct interaction between miR-196a-5p and I?B? mRNA. RESULTS:Using SW480 cell with miR-196-5p over-expressed plus SW620 and HCT116 cells with miR-196a-5p knockdown, we found that miR-196a-5p promoted cell proliferation, migration and invasion in vitro and facilitated liver metastasis in vivo. We also observed that miR-196a-5p knockdown or NF-?B pathway inhibition up-regulated E-cadherin while down-regulated N-cadherin and fibronectin. By contrast, miR-196a-5p over-expression promoted EMT process of CRC. Data of dual luciferase reporter assay indicated that miR-196a-5p targeted the I?B?. Moreover, miR-196a-5p down-regulated I?B? expression while up-regulated nuclear p65 expression. Additionally, over-expression of I?B? in CRC cells attenuated the effects of miR-196a-5p on cell migration, invasion and EMT. CONCLUSIONS:miR-196a-5p may play a key role in EMT, invasion and metastasis of CRC cells via targeting the I?B?.

| S-EPMC6325824 | biostudies-other

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data