MiRNA-93: a novel signature in human disorders and drug resistance

Hussen, Bashdar Mahmud; Abdullah, Snur Rasool; Rasul, Mohammed Fatih; Jawhar, Zanko Hassan; Faraj, Goran Sedeeq Hama; Kiani, Arda; Taheri, Mohammad

doi:10.1186/s12964-023-01106-3

Cited by 18 publications

(9 citation statements)

References 138 publications

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“…Nevertheless, efficacy decreased due to the emergence of drug resistance (Cao et al, 2021;He et al, 2022). More and more studies add up to the statement that miRNAs feature in cancer development and drug resistance (Hussen et al, 2023). Here, miR-503-5p was found to be highly expressed in LUAD, indicating that it featured in the biological process of LUAD progression.…”

Section: Discussionmentioning

confidence: 84%

Hsa‐miR‐503‐5p regulates CTDSPL to accelerate cisplatin resistance and angiogenesis of lung adenocarcinoma cells

Han

Wang

2023

Chem Biol Drug Des

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The study aimed to assess the role of hsa‐miR‐503‐5p in cisplatin resistance and angiogenesis in LUAD and its underlying mechanisms. Hsa‐miR‐503‐5p expression in LUAD and the target gene downstream of hsa‐miR‐503‐5p was predicted by bioinformatics analysis. Binding relationship between the two genes was verified by dual‐luciferase reporter assay. qRT‐PCR was conducted for detecting gene expression in cells, CCK‐8 for IC50 value, angiogenesis assay for human umbilical vein endothelial cell (HUVEC) angiogenic ability, flow cytometry for apoptosis ability, transwell assay for migration ability, and western blot for detecting the protein expression of vascular endothelial growth factor receptor 1 (VEGFR1), VEGFR2, and CTD small phosphatase like (CTDSPL). The results showed that hsa‐miR‐503‐5p showed high expression, while its target gene CTDSPL presented decreased expression in LUAD. Hsa‐miR‐503‐5p also had high expression in cisplatin‐resistant LUAD cells. Knockdown of hsa‐miR‐503‐5p resensitized LUAD cells to cisplatin, inhibited angiogenesis of drug‐resistant cells, and reduced the protein expression of VEGFR1, VEGFR2, and EMT‐related targets in cisplatin‐resistant LUAD cells, but promoted the apoptosis ability. Hsa‐miR‐503‐5p bound to CTDSPL gene and promoted cisplatin resistance and malignant progression of LUAD cells by negatively regulating CTDSPL. Our results revealed that hsa‐miR‐503‐5p and CTDSPL may be novel targets for overcoming cisplatin resistance in LUAD.

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Section: Discussionmentioning

confidence: 84%

Hsa‐miR‐503‐5p regulates CTDSPL to accelerate cisplatin resistance and angiogenesis of lung adenocarcinoma cells

Han

Wang

2023

Chem Biol Drug Des

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“…During kidney injury, there can be an upregulation of miR-93, leading to decreased PTEN levels and subsequent alterations in cell mir-93/AKT/mTOR signaling pathways. These changes may impact the overall injury and repair processes in the kidney [ 58 ]. It is worth noting that the study of miRNAs in kidney injury is an active area of research, and ongoing investigations continue to shed light on their specific roles and potential therapeutic implications.…”

Section: Discussionmentioning

confidence: 99%

Renoprotective Effect of Pitavastatin against TAA-Induced Renal Injury: Involvement of the miR-93/PTEN/AKT/mTOR Pathway

Elbaset,

Mohamed,

Moustafa

et al. 2024

Advances in Pharmacological and Pharmaceutical Sciences

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This research investigated if pitavastatin (Pita) might protect rats’ kidneys against thioacetamide (TAA). By altering the PTEN/AKT/mTOR pathway, pitavastatin may boost kidney antioxidant capacity and minimize oxidative damage. Statins have several benefits, including antioxidant and anti-inflammatory characteristics. The principal hypothesis of this study was that Pita can regulate the miR-93/PTEN/AKT/mTOR pathways, which is thought to be responsible for its renoprotective effects. The experiment divided male rats into four groups. Group 1 included untreated rats as the control. Group 2 included rats which received TAA (100 mg/kg intraperitoneally thrice a week for two weeks) to destroy their kidneys. Groups 3 and 4 included rats which received Pita orally at 0.4 and 0.8 mg/kg for 14 days after TAA injections. Renal injury increased BUN, creatinine, and MDA levels and decreased glutathione (GSH) levels. Pitavastatin prevented these alterations. TAA decreased PTEN and increased miR-93, Akt, p-Akt, mTOR, and Stat3 in the kidneys. Pitavastatin also regulated the associated culprit pathway, miR-93/PTEN/Akt/mTOR. In addition, TAA induced adverse effects on the kidney tissue, which were significantly ameliorated by pitavastatin treatment. The findings suggest that pitavastatin can attenuate renal injury, likely by regulating the miR-93/PTEN/Akt/mTOR pathway. This modulation of the pathway appears to contribute to the protective effects of pitavastatin against TAA-induced renal injury, adding to the growing evidence of the pleiotropic benefits of statins in renal health.

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“…These molecules can act as either oncogenes or tumor suppressors. Ongoing studies are rapidly expanding our knowledge of these altered miRNAs in various human cancers, including lung, liver, and breast cancer ( 96 ). For example, activation of miR-31 has been identified as a mechanism that promotes mammary stem cell expansion and breast tumor development by inhibiting Wnt signaling antagonists ( 97 ).…”

Section: Interplay Between Mirna Alterations and Environmental Chemicalsmentioning

confidence: 99%

Exploring the intricate relationship between miRNA dysregulation and breast cancer development: insights into the impact of environmental chemicals

Abolhasanzadeh,

Sarabandi,

Dehghan

et al. 2024

Front. Immunol.

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Breast cancer stands as the most prevalent form of cancer among women globally, influenced by a combination of genetic and environmental factors. Recent studies have investigated changes in microRNAs (miRNAs) during breast cancer progression and the potential impact of environmental chemicals on miRNA expression. This review aims to provide an updated overview of miRNA alterations in breast cancer and to explore their potential association with environmental chemicals. We will discuss the current knowledge on dysregulated miRNAs in breast cancer, including both upregulated and downregulated miRNAs. Additionally, we will review the influence of environmental chemicals, such as endocrine-disrupting compounds, heavy metals, and air pollutants, on miRNA expression and their potential contribution to breast cancer development. This review aims to advance our understanding of the complex molecular mechanisms underlying miRNA dysregulation in breast cancer by comprehensively examining miRNA alterations and their association with environmental chemicals. This knowledge is crucial for the development of targeted therapies and preventive measures. Furthermore, identifying specific miRNAs affected by environmental chemicals may allow the prediction of individual susceptibility to breast cancer and the design of personalized intervention strategies.

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MiRNA-93: a novel signature in human disorders and drug resistance

Cited by 18 publications

References 138 publications

Hsa‐miR‐503‐5p regulates CTDSPL to accelerate cisplatin resistance and angiogenesis of lung adenocarcinoma cells

Hsa‐miR‐503‐5p regulates CTDSPL to accelerate cisplatin resistance and angiogenesis of lung adenocarcinoma cells

Renoprotective Effect of Pitavastatin against TAA-Induced Renal Injury: Involvement of the miR-93/PTEN/AKT/mTOR Pathway

Exploring the intricate relationship between miRNA dysregulation and breast cancer development: insights into the impact of environmental chemicals

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