Microrna-452 Exerts Growth-Suppressive Activity against T-Cell Acute Lymphoblastic Leukemia

Wang, Haihao; Guo, Qiannan; Zhu, Guizhi; Zhu, Shuo; Yang, Pei-Wen; Zhang, Mingsheng

doi:10.1136/jim-2017-000591

Cited by 7 publications

(3 citation statements)

References 26 publications

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“…miR-452 was epigenetically silent and targets BMI-1 to exert growth inhibitory activity in T-ALL. The restoration of miR-452 expression may provide hope and treatment strategies for the treatment of this malignant tumor (50)(51)(52)(53)(54).…”

Section: Discussionmentioning

confidence: 99%

miR-452 Reverses Abnormal Glycosylation Modification of ERα and Estrogen Resistance in TNBC (Triple-Negative Breast Cancer) Through Targeting UGT1A1

Zhou

Mao

et al. 2020

Front. Oncol.

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Background: The breast epithelial cells in patients with triple-negative breast cancer (TNBC) actually have specific estrogen receptor (ER) expression, and the abnormal glycosylation of UGT1A1 in TNBC cells resulted in abnormal expression and function of ERα through regulating the modification of ERα. Therefore, our study targets the role of UGT1A1 expression, then glycosylation modification of ERα (estrogen receptor α) and estrogen resistance in development of TNBC. Methods: The differential expression of mRNA and miRNA in TNBC tissues was tested. Luciferase activity was analyzed in TNBC cells treated with miR-452. Moreover, the human mammary gland and TNBC cell lines were dealt with estrogen and miR-452 or its inhibitors, then proliferation ability was further determined. Moreover, the role of interaction between UGT1A1 and ERα in the glycosylation modification of ERα and UGT activity, and metabolism of estrogen were assessed. The effects of miR-452 on TNBC by improving abnormal glycosylation modification of ERα by targeting UGT1A1 and estrogen resistance were studied in vitro and in vivo. Results: The expression level of UGT1A1 in TNBC tumor tissues was higher than its matched para-tumorous tissues, but the miR-452 expression was opposite. The glycosylation modification site of ERα expressed in TNBC cells was different from that of normal mammary epithelial cells. The estrogen 17β-estradiol (E2) significantly promoted mitotic entry of TNBC cells. The interaction between UGT1A1 and ERα affected the expression level of each other, as well as the UGT enzyme activity and proliferation of TNBC cells. UGT1A1 induced production of intracellular estrogens and TNBC proliferation, but it could be reversed by overexpression of ERα. Upregulation of ERα caused the downregulation of UGT1A1 and marked decrease of intracellular estrogen products, and then suppressed TNBC proliferation. Moreover, UGT1A1 was the target gene of miR-452; miR-452 antagomir restrained TNBC xenograft. Li et al. miR-452 Reverses TNBC Estrogen Resistance Conclusion: Our results demonstrated that estrogen was a positive factor in the proliferation of TNBC cells at onset of mitosis through accentuating the expression and enzyme activity of UGT1A1. However, miR-452 targeted to UGT1A1, then regulated glycosylation modification of ERα, estrogen metabolism, and TNBC development associated with estrogen resistance.

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Section: Discussionmentioning

confidence: 99%

miR-452 Reverses Abnormal Glycosylation Modification of ERα and Estrogen Resistance in TNBC (Triple-Negative Breast Cancer) Through Targeting UGT1A1

Zhou

Mao

et al. 2020

Front. Oncol.

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“… 11 miR-708-5p, miR-195-5p, miR-450b-5p, and miR-29c-5p act as oncogenes or tumor suppressors in T- or B-cell ALL progression by regulating cells proliferation, metastasis, and apoptosis. 12 miRNA-326, 13 miRNA-9, 14 miR-153-3p, 15 miRNA-452, 16 and miRNA-200c 13 are involved in ALL processes and can be used as targets for the diagnosis, prognosis, and treatment of ALL. miRNA-4500 has been recently found to be a cancer suppressor that can inhibit cell proliferation and migration in bladder cancer, 17 papillary thyroid cancer, 18 and breast cancer, 19 but its function in ALL remains unknown.…”

Section: Introductionmentioning

confidence: 99%

LINC00265/miR-4500 Axis Accelerates Acute Lymphoblastic Leukemia Progression by Enhancing STAT3 Signals

Zhao¹,

Xing²,

Song³

et al. 2021

CMAR

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Background Long noncoding RNA LINC00265 or miR-4500 is involved in the pathogenesis of many cancers. However, their functions in acute lymphoblastic leukemia (ALL) remain unknown. In this study, we investigated how LINC00265 and miR-4500 regulate the malignant characteristics of ALL. Methods Real-time PCR was used in examining the expression of LINC00265 in ALL cell lines and blood of patients with ALL. Cell proliferation, cell migration, and xenograft tumor assays were performed to verify the function of LINC00265 subjected to overexpressing and silencing experiments. The ceRNA mechanism with LINC00265/miR-4500/STAT3 was investigated through luciferase and RNA pull-down assays. Finally, the function of the LINC00265/miR-4500/STAT3 axis subjected to overexpressing and silencing assays was determined through cell proliferation, cell migration, and xenograft tumor assays. Results LINC00265 was highly expressed in ALL cell lines and blood of patients with ALL and facilitated the proliferation, migration, invasion, and growth of xenograft tumors of ALL cells. The silencing of LINC00265 expression with LINC00265 siRNA significantly inhibited the malignancy of the ALL cells. RNA pull-down and luciferase assays demonstrated that LINC00265 competitively targeted miR-4500 and enhanced STAT3 expression. Furthermore, miR-4500 inhibitors or overexpressed LINC00265 up-regulated STAT3 expression, and miR-4500 mimics or STAT3 shRNAs eliminated the LINC00265-induced malignancy of the ALL cells. Conclusion Mechanistically, LncRNA LINC00265 can competitively interact with miR-4500 and thereby up-regulates STAT3 signaling and enhances the malignancy of tumors.

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“…Similarly, it has been reported that miR‐452 promotes the EMT in neural crest cells . Wang showed that miR‐452 inhibits growth and the cell cycle against T‐cell acute lymphoblastic leukemia . Additionally, miR‐452 functions as an independent factor and has a tumor suppressive effect in colorectal cancer; however, there are few studies with a focus on miR‐452 in ccRCC, therefore we wondered about the important role of miR‐452 in cell proliferation and invasion in ccRCC.…”

Section: Introductionmentioning

confidence: 99%

miR‐452 promotes cell metastasis and the epithelial to mesenchymal by targeting SOX7 in clear‐cell renal‐cell carcinoma

Liu

Guo

Xin

et al. 2018

J of Cellular Biochemistry

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Clear‐cell renal‐cell carcinoma (ccRCC) is the most common renal cell carcinoma (RCC), representing 75%‐80% of the cases of RCC, and characterized by a high recurrence rate and poor prognosis. miR‐452 acts as a tumor promoter in several tumors, including ccRCC. The purpose of this study was to determine the role of miR‐452 in ccRCC. miR‐452 and SOX7 messenger RNA and protein levels were calculated by quantitative reverse transcription polymerase chain reaction and Western blot analysis. MTT and Transwell assays were utilized to measure proliferative and invasive abilities. The Kaplan‐Meier method was used to evaluate the association between the expression of miR‐452 or SOX7 and the overall survival of ccRCC patients. Our results showed that miR‐452 was overexpressed in ccRCC tissues and cells, and upregulation of miR‐452 predicted a poor 5‐year survival in ccRCC patients. In contrast, expression of SOX7 was low and downregulation of SOX7 predicted poor prognosis in ccRCC. In addition, miR‐452 promoted cell proliferation, invasion, and the EMT, while SOX7 reversed the function of miR‐452 on cell proliferation and invasion in 786‐O cells. In conclusion, miR‐452 was shown to inhibit cell proliferation, invasion, and the EMT through SOX7 in ccRCC, and the newly identified miR‐452/SOX7 axis provided novel insight into the pathogenesis of ccRCC.

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Microrna-452 Exerts Growth-Suppressive Activity against T-Cell Acute Lymphoblastic Leukemia

Cited by 7 publications

References 26 publications

miR-452 Reverses Abnormal Glycosylation Modification of ERα and Estrogen Resistance in TNBC (Triple-Negative Breast Cancer) Through Targeting UGT1A1

miR-452 Reverses Abnormal Glycosylation Modification of ERα and Estrogen Resistance in TNBC (Triple-Negative Breast Cancer) Through Targeting UGT1A1

LINC00265/miR-4500 Axis Accelerates Acute Lymphoblastic Leukemia Progression by Enhancing STAT3 Signals

miR‐452 promotes cell metastasis and the epithelial to mesenchymal by targeting SOX7 in clear‐cell renal‐cell carcinoma

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