CircRAB3IP upregulates twist family BHLH transcription factor (TWIST1) to promote osteosarcoma progression by sponging miR-580-3p

Tang, Guotao; Liu, Linghua; Xiao, Zhihong; Wen, Shuo; Chen, Liangyuan; Yang, Peng

doi:10.1080/21655979.2021.1948487

Cited by 16 publications

(8 citation statements)

References 28 publications

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“…For example, miR-580-3p repressed melanoma cell malignancy through the LHFPL3-AS1/miR-580-3p/ STAT3 axis 44 . MiR-580-3p inhibited osteosarcoma cell growth and motility through the circRAB3IP/miR-580-3p/TWIST1 pathway 45 . In particular, Sun et al 46 showed that miR-580 expression was lower in patients with acute kidney injury than in patients without acute kidney injury.…”

Section: Discussionmentioning

confidence: 98%

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Circ_0068087 knockdown attenuates high‐glucose‐induced human tubular epithelial cell injury in a microribonucleic acid/progestin and adipoQ receptor 3‐dependent manner in diabetic nephropathy

Liu,

Wang,

Yang

et al. 2023

J of Diabetes Invest

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Aims/IntroductionPrevious studies have shown that circular ribonucleic acid mediates the occurrence of diabetic nephropathy. This study aimed to analyze the effects of circ_0068087 on high‐glucose (HG)‐induced human kidney 2 (HK2) cell dysfunction.Materials and MethodsCirc_0068087, miR‐580‐3p, and progestin and adipoQ receptor 3 (PAQR3) expression were detected by quantitative reverse transcription polymerase chain reaction. Cell viability and proliferation were investigated by Cell Counting Kit‐8 and EdU assays, respectively. The cell apoptotic rate was assessed by flow cytometry. Inflammatory response was assessed by enzyme‐linked immunoassays. Oxidative stress was evaluated by a superoxide dismutase activity assay kit and lipid peroxidation malondialdehyde assay kit. Molecular interaction was identified by dual‐luciferase reporter assay.ResultsCirc_0068087 and PAQR3 expression were significantly upregulated in diabetic nephropathy patients. HG treatment inhibited HK2 cell proliferation, but induced cell apoptosis, inflammation, oxidative stress and epithelial–mesenchymal transition by regulating circ_0068087. Circ_0068087 acted as a microribonucleic acid‐580‐3p (miR‐580‐3p) sponge, and miR‐580‐3p targeted PAQR3. Furthermore, circ_0068087 depletion repressed PAQR3 expression through miR‐580‐3p. MiR‐580‐3p inhibitors or PAQR3 introduction attenuated circ_0068087 silencing mediated‐effects in HG‐treated HK2 cells.ConclusionCirc_0068087 promoted HG‐induced HK2 cell injuries by the regulation of the miR‐580‐3p/PAQR3 pathway.

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Section: Discussionmentioning

confidence: 98%

“…For example, miR‐580‐3p repressed melanoma cell malignancy through the LHFPL3‐AS1/miR‐580‐3p/STAT3 axis 44 . MiR‐580‐3p inhibited osteosarcoma cell growth and motility through the circRAB3IP/miR‐580‐3p/TWIST1 pathway 45 . In particular, Sun et al 46 .…”

Section: Discussionmentioning

confidence: 99%

Circ_0068087 knockdown attenuates high‐glucose‐induced human tubular epithelial cell injury in a microribonucleic acid/progestin and adipoQ receptor 3‐dependent manner in diabetic nephropathy

Liu,

Wang,

Yang

et al. 2023

J of Diabetes Invest

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“…Overexpression of miR-580 inhibited cell motility in breast cancer by downregulating TWIST1, implying that miR-580 functioned as a tumor suppressor [ 30 ]. Moreover, circRAB3IP has been revealed to act as the sponge of miR-580-3p to promote TWIST1 expression in osteosarcoma [ 31 ]. However, the correlation between miR-580 and AML has not been explicated.…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA SATB1-AS1 contributes to the chemotherapy resistance through the microRNA-580/ 2’-5’-oligoadenylate synthetase 2 axis in acute myeloid leukemia

et al. 2021

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Acute myeloid leukemia (AML) represents a hematopoietic cancer with an invasive property. Chemoresistance blunts the therapeutic effect of chemotherapeutics in AML. Long noncoding RNAs (lncRNAs) have been implicated in chemotherapy resistance in AML. Transcriptome sequencing in the current study was applied to clarify the differentially expressed lncRNAs between peripheral blood mononuclear cells of AML and normal samples. The expression of special AT-rich sequence binding protein 1 antisense RNA 1 (SATB1-AS1) and 2 -5 -oligoadenylate synthetase 2 (OAS2) in AML patients was evaluated by qRT-PCR. The relationships among SATB1-AS1, microRNA-580 (miR-580) and OAS2 were investigated by dual-luciferase reporter assay. We observed that SATB1-AS1 and OAS2 were upregulated, while miR-580 was downregulated in AML patients. SATB1-AS1 depletion suppressed proliferation, and enhanced apoptosis and sensitivity of AML cells. Additionally, SATB1-AS1 promoted the expression of OAS2 by acting as a molecular sponge of miR-580 in AML. miR-580 downregulation, OAS2 overexpression and a selective glycogen synthase kinase (GSK)-3β inhibitor AR-A014418 abolished the effects of SATB1-AS1 deletion on the chemosensitivity of AML cells. In conclusion, SATB1-AS1 knockdown promotes the sensitivity of AML cells by upregulating miR-580 and downregulating OAS2 through the GSK3β/β-catenin pathway, providing new insights into the function of SATB1-AS1 as a miRNA sponge in AML.

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“…miR-580-3p is an inhibitor of Twist1, which reduces the malignancy of osteosarcoma cells. However, circRAB3IP reduces miR-580-3p expression to upregulate Twist1 and promote osteosarcoma malignancy [ 167 ]. CircRNA PVT1 is upregulated in cancers and stimulates the Wnt4/β-catenin axis to increase carcinogenesis [ 168 ].…”

Section: Circrnas Regulating Emt-tfs In Cancersmentioning

confidence: 99%

Circular RNAs in EMT-driven metastasis regulation: modulation of cancer cell plasticity, tumorigenesis and therapy resistance

Ashrafizadeh,

Dai,

Torabian

et al. 2024

Cell. Mol. Life Sci.

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The non-coding RNAs comprise a large part of human genome lack of capacity in encoding functional proteins. Among various members of non-coding RNAs, the circular RNAs (circRNAs) have been of importance in the pathogenesis of human diseases, especially cancer. The circRNAs have a unique closed loop structure and due to their stability, they are potential diagnostic and prognostic factors in cancer. The increasing evidences have highlighted the role of circRNAs in the modulation of proliferation and metastasis of cancer cells. On the other hand, metastasis has been responsible for up to 90% of cancer-related deaths in patients, requiring more investigation regarding the underlying mechanisms modulating this mechanism. EMT enhances metastasis and invasion of tumor cells, and can trigger resistance to therapy. The cells demonstrate dynamic changes during EMT including transformation from epithelial phenotype into mesenchymal phenotype and increase in N-cadherin and vimentin levels. The process of EMT is reversible and its reprogramming can disrupt the progression of tumor cells. The aim of current review is to understanding the interaction of circRNAs and EMT in human cancers and such interaction is beyond the regulation of cancer metastasis and can affect the response of tumor cells to chemotherapy and radiotherapy. The onco-suppressor circRNAs inhibit EMT, while the tumor-promoting circRNAs mediate EMT for acceleration of carcinogenesis. Moreover, the EMT-inducing transcription factors can be controlled by circRNAs in different human tumors.

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CircRAB3IP upregulates twist family BHLH transcription factor (TWIST1) to promote osteosarcoma progression by sponging miR-580-3p

Cited by 16 publications

References 28 publications

Circ_0068087 knockdown attenuates high‐glucose‐induced human tubular epithelial cell injury in a microribonucleic acid/progestin and adipoQ receptor 3‐dependent manner in diabetic nephropathy

Circ_0068087 knockdown attenuates high‐glucose‐induced human tubular epithelial cell injury in a microribonucleic acid/progestin and adipoQ receptor 3‐dependent manner in diabetic nephropathy

Long noncoding RNA SATB1-AS1 contributes to the chemotherapy resistance through the microRNA-580/ 2’-5’-oligoadenylate synthetase 2 axis in acute myeloid leukemia

Circular RNAs in EMT-driven metastasis regulation: modulation of cancer cell plasticity, tumorigenesis and therapy resistance

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