miR-650 promotes motility of anaplastic thyroid cancer cells by targeting PPP2CA

Background Aberrant expression of microRNAs (miR) has been proposed as non-invasive biomarkers for breast cancers. The aim of this study was to analyse the miR-622 level in the plasma and in tissues of breast cancer patients and to explore the role of miR-622 and its target, the NUAK1 kinase, in this context. Methods miR-622 expression was analysed in plasma and in tissues samples of breast cancer patients by q-RT-PCR. Bioinformatics programs, luciferase assay, public dataset analysis and functional experiments were used to uncover the role of miR-622 and its target in breast cancer cells. Results miR-622 is downregulated in plasma and in tissues of breast cancer patients respect to healthy controls and its downregulation is significantly associated with advanced grade and high Ki67 level. Modulation of miR-622 affects the motility phenotype of breast cancer cells. NUAK1 kinase is a functional target of miR-622, it is associated with poor clinical outcomes of breast cancer patients and is inversely correlated with miR-622 level. Conclusions miR-622/NUAK1 axis is deregulated in breast cancer patients and affects the motility phenotype of breast cancer cells. Importantly, miR-622 and NUAK1 hold promises as biomarkers and as targets for breast cancers.

show abstract

“…Wound healing and Transwell assays were performed to evaluate the effect of miR-622 on cell migration ability as previously described. 27 …”

Section: Methodsmentioning

confidence: 99%

miR-622 is a novel potential biomarker of breast carcinoma and impairs motility of breast cancer cells through targeting NUAK1 kinase

et al. 2020

Self Cite

View full text Add to dashboard Cite

show abstract

“…During the past few decades, the expression profiles of miRNAs in different subtypes of thyroid cancer have been analyzed ( 32 ). A large number of mammalian miRNAs are upregulated in thyroid tumors, such as miR-650 ( 33 ), miR-340-5p ( 34 ), miR-424-5p ( 35 ) and miR-155 ( 36 ); while a number of miRNAs have been reported to be downregulated, such as miR-26a ( 37 ), miR-215 ( 38 ), miR-34a ( 39 ) and miR-206 ( 40 ). In addition, a previous study indicated that the expression levels of numerous miRNAs exhibit significant differences in MTC ( 41 ).…”

Section: Discussionmentioning

confidence: 99%

miR‑592 acts as an oncogene and promotes medullary thyroid cancer tumorigenesis by targeting cyclin‑dependent kinase 8

2020

View full text Add to dashboard Cite

Medullary thyroid carcinoma (MTC) is a relatively rare subtype of thyroid cancer, accounting for 5–10% of all cases of thyroid cancer worldwide. Due to the current lack of knowledge regarding the tumorigenesis of MTC, the clinical treatment of MTC remains a challenge. It has been reported that microRNAs (miRNAs) regulate the progression of MTC; however, the regulatory network of miRNAs and the exact underlying mechanisms are not completely understood. In the present study, an miRNA expression profile (GSE40807), consisting of 80 samples, was downloaded and analyzed using Gene Expression Omnibus-2R to identify differentially expressed miRNAs between MTC and normal samples. miR-592 expression levels were significantly increased in MTC tissues and cell lines compared with normal tissues and cell lines. Patients with high miR-592 expression levels exhibited a less favorable prognosis compared with patients with low miR-592 expression. The results suggested that miR-592 overexpression promoted TT and MZ-CRC-1 cell proliferation in vitro . In addition, miR-592 negatively regulated cyclin-dependent kinase 8 (CDK8) via targeted binding in MTC cells. Moreover, co-transfection of CDK8 overexpression plasmid and miR-592 mimic reversed miR-592-mediated MTC cell proliferation. In conclusion, miR-592 may serve as an oncogene in MTC by decreasing the expression of CDK8, indicating that the miR-592/CDK8 axis might serve as a promising therapeutic target for MTC.

show abstract

“…Various functional roles of miR-650 are regarded in different tumors, which are dependent on the target genes in a particular histological type ( 28). An elevated miR-650 expression is observed in hepatocellular cancer, lung adenocarcinoma, and prostate cancer, which correlates with tumor metastasis and poor prognosis (29)(30)(31)(32). Nevertheless, the overexpression of miR-650 also indicates favorable survival estimation in chronic lymphocytic leukemia and colorectal cancer (33,34).…”

Section: Discussionmentioning

confidence: 99%

LncRNA POU3F3 Contributes to Dacarbazine Resistance of Human Melanoma Through the MiR-650/MGMT Axis

Wang

Liu

et al. 2021

Front. Oncol.

View full text Add to dashboard Cite

Background: Alkylating agents are critical therapeutic options for melanoma, while dacarbazine (DTIC)-based chemotherapy showed poor sensitivity in clinical trials. Long non-coding RNAs (lncRNAs) were highlighted in the progression of malignant tumors in recent years, whereas little was known about their involvement in melanoma.Methods: The functional role and molecular mechanism of lncRNA POU3F3 were evaluated on DTIC-resistant melanoma cells. Further studies analyzed its clinical role in the disease progression of melanoma.Results: We observed elevated the expression of lncRNA POU3F3 in the DTIC-resistant melanoma cells. Gain-of-function assays showed that the overexpression of lncRNA POU3F3 maintained cell survival with DTIC treatment, while the knockdown of lncRNA POU3F3 restored cell sensitivity to DTIC. A positive correlation of the expression O6-methylguanine-DNA-methyltransferase (MGMT) was observed with lncRNA POU3F3 in vitro and in vivo. Bioinformatic analyses predicted that miR-650 was involved in the lncRNA POU3F3-regulated MGMT expression. Molecular analysis indicated that lncRNA POU3F3 worked as a competitive endogenous RNA to regulate the levels of miR-650, and the lncRNA POU3F3/miR-650 axis determined the transcription of MGMT in melanoma cells to a greater extent. Further clinical studies supported that lncRNA POU3F3 was a risk factor for the disease progression of melanoma.Conclusion: LncRNA POU3F3 upregulated the expression of MGMT by sponging miR-650, which is a crucial way for DTIC resistance in melanoma. Our results indicated that lncRNA POU3F3 was a valuable biomarker for the disease progression of melanoma.

show abstract

miR-650 promotes motility of anaplastic thyroid cancer cells by targeting PPP2CA

Cited by 27 publications

References 50 publications

miR-622 is a novel potential biomarker of breast carcinoma and impairs motility of breast cancer cells through targeting NUAK1 kinase

miR-622 is a novel potential biomarker of breast carcinoma and impairs motility of breast cancer cells through targeting NUAK1 kinase

miR‑592 acts as an oncogene and promotes medullary thyroid cancer tumorigenesis by targeting cyclin‑dependent kinase 8

LncRNA POU3F3 Contributes to Dacarbazine Resistance of Human Melanoma Through the MiR-650/MGMT Axis

Contact Info

Product

Resources

About