Novel miR-5088-5p promotes malignancy of breast cancer by inhibiting DBC2

Seok, Hyun Jeong; Choi, Young Eun; Choi, Jae Yeon; Yi, Joo Mi; Kim, Eun Joo; Choi, Mi Young; Lee, Su‐Jae; Bae, In Hwa

doi:10.1016/j.omtn.2021.05.004

Cited by 12 publications

(22 citation statements)

References 55 publications

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“…Experiments by our group con rmed that miR-5088-5p, a miRNA identi ed in a previous study, promotes malignancy by inhibiting the expression of Deleted in Breast Cancer 2 (DBC2) in breast cancer [32]. The current study focused on the relationship between onco-miR-5088-5p and IR-induced malignancy.…”

Section: Introductionmentioning

confidence: 69%

“…Radiotherapy is one of the most common treatment options for cancer. A previous study by our group showed that miR-5088-5p promotes tumorigenic properties in breast cancer [32]. Here, we further examined the expression patterns and mechanisms of action of miR-5088-5p in tumor malignancy during radiotherapy.…”

Section: Ir Upregulates Biogenesis Of Mir-5088-5p Through Inhibiting ...mentioning

confidence: 91%

“…1B). In our previous study, our group identi ed the mechanism of DBC2 (Deleted in Breast Cancer 2) as a target of miR-5088-5p [32]. Expression of DBC2 was dramatically decreased in the tumor tissue exposed to radiation in the xenograft mouse model (Supplementary Fig.…”

Section: Ir Upregulates Biogenesis Of Mir-5088-5p Through Inhibiting ...mentioning

confidence: 99%

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miR-5088-5p inhibitor reduces radiation-induced malignancy by decreasing Slug

Seok

Choi

et al. 2022

Preprint

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Purpose Radiotherapy is widely used for cancer treatment, but paradoxically, surviving cancer cells can become malignant, leading to tumor recurrence or metastasis. Therefore, in order to increase the effectiveness of radiotherapy, efforts to reduce radiation-induced malignancy are absolutely necessary. As a tool, microRNA simultaneously regulates the expression of multiple target mRNAs, so it has significant potential as an effective therapeutic agent. The main objective of this study is to elucidate the malignant mechanism of radiation-induced miR-5088-5p and to prove the efficacy of miR-5088-5p inhibitor for mitigating malignancy, thereby demonstrating its applicability as a therapeutic agent to increase the efficiency of radiotherapy. Methods To analyze the relationship between radiation and miR-5088-5p expression, miR-5088-5p levels were determined by qRT-PCR in the plasma of breast and lung cancer patients with or without radiotherapy. MSP and qMSP assays were used to confirm the methylation of radiation-induced miR-5088-5p. To determine whether miR-5088-5p inhibitor reduces radiation-induced malignancy by decreasing Slug, we used wound healing, invasion, sphere formation, Western blot, qRT-PCR assays, and in vivo mouse xenograft metastatic model. Results It was confirmed at both the cellular and animal model that miR-5088-5p, which showed higher expression in the plasma of breast cancer and lung cancer patients with radiotherapy, enhances tumor malignancy by enhancing its expression through hypomethylation of its promoter by radiation. On the other hand, it was shown that miR-5088-5p inhibitor reduced the mechanism of radiation-induced malignancy. Conclusions Collectively, miR-5088-5p inhibitors have shown potential as a combination therapy to enhance radiotherapy effectiveness by reducing radiation-induced malignancy.

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Section: Introductionmentioning

confidence: 69%

Section: Ir Upregulates Biogenesis Of Mir-5088-5p Through Inhibiting ...mentioning

confidence: 91%

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miR-5088-5p inhibitor reduces radiation-induced malignancy by decreasing Slug

Seok

Choi

et al. 2022

Preprint

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“…Sci. 2021, 22, 11810 2 of 21 been considered innovative biomarkers or new targets in targeted therapy in various types of cancers [7][8][9][10]. Histone proteins undergo reversible acetylation by opposite working enzymes: histone acetyltransferases (HATs) and histone deacetylases (HDACs).…”

Section: Of 20mentioning

confidence: 99%

“…Epigenetic mechanisms include modifications on histone proteins, DNA methylation, and regulation of gene expression by non-coding RNAs and microRNAs. All these mechanisms are critical for tumor initiation, progression, and metastasis [5,6], and they have been considered innovative biomarkers or new targets in targeted therapy in various types of cancers [7][8][9][10].…”

Section: Introductionmentioning

confidence: 99%

Deacetylation of Transcription Factors in Carcinogenesis

Hałasa

Adamczuk

et al. 2021

IJMS

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Reversible Nε-lysine acetylation/deacetylation is one of the most common post-translational modifications (PTM) of histones and non-histone proteins that is regulated by histone acetyltransferases (HATs) and histone deacetylases (HDACs). This epigenetic process is highly involved in carcinogenesis, affecting histone and non-histone proteins’ properties and their biological functions. Some of the transcription factors, including tumor suppressors and oncoproteins, undergo this modification altering different cell signaling pathways. HDACs deacetylate their targets, which leads to either the upregulation or downregulation of proteins involved in the regulation of cell cycle and apoptosis, ultimately influencing tumor growth, invasion, and drug resistance. Therefore, epigenetic modifications are of great clinical importance and may constitute a new therapeutic target in cancer treatment. This review is aimed to present the significance of HDACs in carcinogenesis through their influence on functions of transcription factors, and therefore regulation of different signaling pathways, cancer progression, and metastasis.

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Analysis of the subcellular location of lncRNA SLC16A1-AS1 and its interaction with premature miR-5088-5p in oral squamous cell carcinoma

Wang

Yang³

2022

Odontology

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Novel miR-5088-5p promotes malignancy of breast cancer by inhibiting DBC2

Cited by 12 publications

References 55 publications

miR-5088-5p inhibitor reduces radiation-induced malignancy by decreasing Slug

miR-5088-5p inhibitor reduces radiation-induced malignancy by decreasing Slug

Deacetylation of Transcription Factors in Carcinogenesis

Analysis of the subcellular location of lncRNA SLC16A1-AS1 and its interaction with premature miR-5088-5p in oral squamous cell carcinoma

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