Enhancement of myogenic differentiation and inhibition of rhabdomyosarcoma progression by miR-28-3p and miR-193a-5p regulated by SNAIL

Skrzypek, Klaudia; Nieszporek, Artur; Badyra, Bogna; Lasota, Małgorzata; Majka, Marcin

doi:10.1016/j.omtn.2021.04.013

Cited by 10 publications

(11 citation statements)

References 50 publications

(122 reference statements)

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“…miR-127-3p is expressed at significantly higher level in proliferating rather than differentiating cells [ 10 ]. The miR-28-3p is a crucial regulator of myogenic differentiation of rhabdomyosarcoma cells and myoblasts [ 12 ]. The expression of miR-30b-5p was associated with differentiation of both skeletal and vascular smooth muscles via interaction with MBNL1 and/or MBNL2 [ 13 , 14 ].…”

Section: Discussionmentioning

confidence: 99%

“…Second, no direct interaction between miRs and protein expression was identified. Previous studies suggested that increased miRs such as miR-181a-5p, 28-3p and let-7 family may represent new therapeutic targets in various diseases [ 8 , 12 , 32 ]. Further studies are needed to validate the significance of the miRs as diagnostic or therapeutic targets.…”

Section: Discussionmentioning

confidence: 99%

“…RT-qPCR was performed to validate the expression of miRs using 38 samples including 19 pairs of myometrium and leiomyoma ( S1 Fig ). After a database search and literature review, miR-181a-5p [ 6 – 8 ], miR-127-3p [ 9 – 11 ], miR-28-3p [ 12 ], miR-30b-5p [ 13 , 14 ] and let-7c-5p [ 15 , 16 ] were selected for further validation ( S1 Table ). MicroRNA TaqMan ® Reverse Transcription Kit and TaqMan MicroRNA Assays were used (Applied Biosystems, Foster City,CA, USA).…”

Section: Methodsmentioning

confidence: 99%

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MicroRNAs as potential indicators of the development and progression of uterine leiomyoma

et al. 2022

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Recent studies demonstrated a significant role of several microRNAs (miRs) in the development of leiomyoma. Here, we investigated miR expression profiles using microarray and found a significantly higher expression of miRs in leiomyoma than in adjacent myometrium. We also confirmed the upregulation of five selected miRs including miR-181a-5p, 127-3p, 28-3p, 30b-5p and let-7c-5p in cellular proliferation, extracellular matrix turnover, and angiogenesis by RT-qPCR. Interestingly, the miRs showed a higher expression in cases of large leiomyoma or in patients with a history of transfusion due to anemia. We then analyzed the expression of the miR target molecules including Transforming Growth Factor Beta Receptor 2 (TGFBR2) and Insulin-like Growth Factor 2 mRNA Binding Protein 1 (IGF2BP1) via immunohistochemistry. TGFBR2 and IGF2BP1 were positively stained in 81% and 62.5% of leiomyoma tissues but not in adjacent myometrium. Both were more frequently positive in patients with ≥ 6 cm leiomyoma and mass effect. The mean expression levels of miR-181a-5p, 127-3p, 28-3p, 30b-5p and let-7c-5p were higher in cases with TGFBR2 and IGF2BP1 positive leiomyoma. We observed several miRs were overexpressed in leiomyoma tissues, and these results provide insight into the role of miRs in the development and progression of leiomyoma and underscore the need to validate their utility as diagnostic or therapeutic targets.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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MicroRNAs as potential indicators of the development and progression of uterine leiomyoma

et al. 2022

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“…miR-28, a miRNA, is located within the gene on chromosome 3q28. It is a tumor suppressor and a viral suppressor [ 31 ] gene, which is regulated through the binding of STAT5 and p53 to its promoter [ 32 ]. In humans, the miR-28 family is divided into subtypes miR-28-3p and miR-28-5p, named after the 3′ and 5′ ends of the pre-miR-28, respectively.…”

Section: Discussionmentioning

confidence: 99%

Effects of hsa-miR-28-5p on Adriamycin Sensitivity in Diffuse Large B-Cell Lymphoma

Yan

Shang

Hai-peng

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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Background. Adriamycin (doxorubicin) is an important traditional drug that exhibits cytotoxicity in Diffuse Large B-cell Lymphoma (DLBCL). Doxorubicin affects the DLBCL cells at all stages of their cell cycle. Combined with our previous results, this study discovered that the overexpression of hsa-miR-28-5p inhibited the proliferation, promoted apoptosis, and triggered cell cycle arrest at the S-phase in DLBCL cells. However, the effect of (Homo sapiens, hsa)-microRNA (miR)-28-5p on doxorubicin sensitivity in DLBCL has not been investigated. This study aims to reveal the effects of hsa-miR-28-5p on doxorubicin sensitivity at the level of DLBCL cells. Methods. To determine the optimal concentration of doxorubicin, different concentrations of doxorubicin were used to treat DLBCL cells. CCK-8 assay was used to detect the proliferation of DLBCL cells. The hsa-miR-28-5p-mimic NC and hsa-miR-28-5p mimic were transfected to doxorubicin-mediated DLBCL cells. Simultaneously, blank control groups were set up. The cells were cultured and transfected for 24 h. Next, each group was administered with different concentrations of doxorubicin and cultured again for 24 h to observe the effects of hsa-miR-28-5p on doxorubicin sensitivity at different times. The proliferation, early apoptosis, and late apoptosis in DLBCL cells were determined using soft agar colony-forming assay, mitochondrial membrane potential assay, and caspase-3 activity assay, respectively. The apoptosis and cell cycle were explored using Annexin V-PE/7-AAD and PI/RNase staining buffer, respectively. We speculated that PD-L1 might be involved in the effect of hsa-miR-28-5p on the sensitivity of adriamycin (doxorubicin) in the DLBCL cells. Hence, we performed immunohistochemistry (IHC) to determine PD-L1 expression within formalin-fixed paraffin-embedded (FFPE) samples from 52 DLBCL cases. Results. The optimal concentration of doxorubicin targeting DLBCL cells was found to be 3.028 μmol/l. The effect of doxorubicin on DLBCL cells was time- and concentration-dependent. hsa-miR-28-5p mimic + doxorubicin remarkably decreased proliferation of DLBCL. DLBCL cell apoptosis rate was the highest in hsa-miR-28-5p mimic + doxorubicin group. Apart from that, hsa-miR-28-5p mimic plus doxorubicin had the best effect in promoting DLBCL cell apoptosis. After the intervention of hsa-miR-28-5p mimic + doxorubicin on DLBCL cells, the cell cycle was arrested in the S-phase and DNA synthesis was blocked. hsa-miR-28-5p mimic + doxorubicin could regulate the cycle of DLBCL cells. As a result, overexpression of hsa-miR-28-5p combined with doxorubicin is possibly involved in the development of DLBCL by affecting the proliferation, apoptosis, and cycle of DLBCL cells. PD-L1 showed an association with the prognosis of DLBCL patients. Combining with the literature, this suggested hsa-miR-28-5p may influence DLBCL occurrence and therapeutic effect by regulating the PD-L1 level. Conclusion. The combination of hsa-miR-28-5p mimic and doxorubicin may be considered more effective in inhibiting growth, arresting the cell cycle, and promoting cell apoptosis of DLBCL cells compared to using doxorubicin alone. The effects of doxorubicin on DLBCL cells were found to be time- and concentration-dependent. The overexpression of hsa-miR-28-5p enhanced the effect of doxorubicin on DLBCL cells, which may be attributed to the regulation of PD-L1 levels.

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“…Several RMS subtypes are distinguished, including the embryonic subtype (ERMS), which accounts for approximately 70% of all RMS cases, and the alveolar (ARMS) subtype which is usually associated with poor prognosis. Important factors regulating RMS progression include surface receptors, such as the CXCR4 [10] and c-MET [11][12][13], SNAIL transcription factor [14][15][16], and microRNAs that may post transcriptionally regulate expression of many genes [17][18][19]. Moreover, in 80% of ARMS there are two characteristic translocations: PAX3-FOXO1 and PAX7-FOXO1, which account for approximately 75% and 25% of all translocations appearing in RMS, respectively [1].…”

Section: Introductionmentioning

confidence: 99%

Progression and Differentiation of Alveolar Rhabdomyosarcoma Is Regulated by PAX7 Transcription Factor—Significance of Tumor Subclones

Skrzypek¹,

Adamek²,

Kot³

et al. 2021

Cells

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Rhabdomyosarcoma (RMS), is the most frequent soft tissue tumor in children that originates from disturbances in differentiation process. Mechanisms leading to the development of RMS are still poorly understood. Therefore, by analysis of two RMS RH30 cell line subclones, one subclone PAX7 negative, while the second one PAX7 positive, and comparison with other RMS cell lines we aimed at identifying new mechanisms crucial for RMS progression. RH30 subclones were characterized by the same STR profile, but different morphology, rate of proliferation, migration activity and chemotactic abilities in vitro, as well as differences in tumor morphology and growth in vivo. Our analysis indicated a different level of expression of adhesion molecules (e.g., from VLA and ICAM families), myogenic microRNAs, such as miR-206 and transcription factors, such as MYOD, MYOG, SIX1, and ID. Silencing of PAX7 transcription factor with siRNA confirmed the crucial role of PAX7 transcription factor in proliferation, differentiation and migration of RMS cells. To conclude, our results suggest that tumor cell lines with the same STR profile can produce subclones that differ in many features and indicate crucial roles of PAX7 and ID proteins in the development of RMS.

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Enhancement of myogenic differentiation and inhibition of rhabdomyosarcoma progression by miR-28-3p and miR-193a-5p regulated by SNAIL

Cited by 10 publications

References 50 publications

MicroRNAs as potential indicators of the development and progression of uterine leiomyoma

MicroRNAs as potential indicators of the development and progression of uterine leiomyoma

Effects of hsa-miR-28-5p on Adriamycin Sensitivity in Diffuse Large B-Cell Lymphoma

Progression and Differentiation of Alveolar Rhabdomyosarcoma Is Regulated by PAX7 Transcription Factor—Significance of Tumor Subclones

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