Low dose radiation regulates BRAF-induced thyroid cellular dysfunction and transformation

Kaushik, Neha; Kim, Min Jung; Kaushik, Nagendra Kumar; Myung, Jae Kyung; Choi, Mi Young; Kang, Jae Hyeok; Cha, Hyuk‐Jin; Kim, Cha Soon; Nam, Sang Yong; Lee, Su Jae

doi:10.1186/s12964-019-0322-x

Cited by 6 publications

(4 citation statements)

References 43 publications

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“…Bibby et al reported that silencing miR-330-5p increases MMP1 expression and promotes an invasive phenotype in esophageal adenocarcinoma [ 22 ]. It is also found that loss of miR-330-5p leads to PAX8 upregulation by LDR and suppression of thyroid carcinogenesis [ 23 ]. However, the biological functions and potential molecular mechanisms of miR-330-5p in the proliferation and metastasis of TC remain to be further elucidated.…”

Section: Discussionmentioning

confidence: 99%

Hsa-miR-330-5p Aggravates Thyroid Carcinoma via Targeting FOXE1

Wang

Liu

Ren

et al. 2021

Journal of Oncology

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Background. Thyroid carcinoma (TC) is one of the frequent endocrine malignancies, and growing evidence suggests that aberrant microRNA (miRNA) expression contributes to TC development and progression. Nevertheless, the function of miR-330-5p in the progression of TC remains unknown. Methods. The expression levels of miR-330-5 in patients with thyroid carcinoma and healthy controls were detected, and their potential diagnostic and prognostic values were analyzed. Results. In this study, we firstly found that miR-330-5p expression was markedly upregulated in TC tissue and cell lines. Functionally, the downregulation of miR-330-5p suppressed TC cell proliferation, migration, and invasion. Further studies revealed that miR-330-5p negatively regulated the expression of forkhead box E1 (FOXE1). More importantly, the results of rescue experiments suggested that FOXE1 overexpression reduced the positive effects of miR-330-5p overexpression in TPC-1 and K-1 cells. Conclusions. This work revealed that miR-330-5p facilitated the TC progression through targeting FOXE1, which may offer novel therapeutic options for TC.

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Section: Discussionmentioning

confidence: 99%

Hsa-miR-330-5p Aggravates Thyroid Carcinoma via Targeting FOXE1

Wang

Liu

Ren

et al. 2021

Journal of Oncology

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“…Furthermore, as reported by Lau et al [69], thiocyanate, an antioxidant related to the immune system, was increased in adults' saliva treated with low doses by cone beam computed tomography [105]. A low dose of 100 mGy γ-irradiation reduced BRAF V600E virus transformation of human thyroid normal follicular cells, and it also suppressed thyroid transformation in mice by restoring the thyroid metabolizing gene expression of PAX and, in addition, suppressed thyroid cancer carcinogenesis through inhibition of STAT3-miRNA-330-5p pathways [106]. As also seen by the previously reported low-dose IR effects on neoplastic transformation [107], the reduction of spontaneous lung cancers in mice [108], and immunogenic effects [109], typical low-dose hormetic effects exhibit beneficial outcomes.…”

Section: Hormesismentioning

confidence: 98%

Low-Dose Non-Targeted Effects and Mitochondrial Control

Averbeck

2023

IJMS

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Non-targeted effects (NTE) have been generally regarded as a low-dose ionizing radiation (IR) phenomenon. Recently, regarding long distant abscopal effects have also been observed at high doses of IR) relevant to antitumor radiation therapy. IR is inducing NTE involving intracellular and extracellular signaling, which may lead to short-ranging bystander effects and distant long-ranging extracellular signaling abscopal effects. Internal and “spontaneous” cellular stress is mostly due to metabolic oxidative stress involving mitochondrial energy production (ATP) through oxidative phosphorylation and/or anaerobic pathways accompanied by the leakage of O2− and other radicals from mitochondria during normal or increased cellular energy requirements or to mitochondrial dysfunction. Among external stressors, ionizing radiation (IR) has been shown to very rapidly perturb mitochondrial functions, leading to increased energy supply demands and to ROS/NOS production. Depending on the dose, this affects all types of cell constituents, including DNA, RNA, amino acids, proteins, and membranes, perturbing normal inner cell organization and function, and forcing cells to reorganize the intracellular metabolism and the network of organelles. The reorganization implies intracellular cytoplasmic-nuclear shuttling of important proteins, activation of autophagy, and mitophagy, as well as induction of cell cycle arrest, DNA repair, apoptosis, and senescence. It also includes reprogramming of mitochondrial metabolism as well as genetic and epigenetic control of the expression of genes and proteins in order to ensure cell and tissue survival. At low doses of IR, directly irradiated cells may already exert non-targeted effects (NTE) involving the release of molecular mediators, such as radicals, cytokines, DNA fragments, small RNAs, and proteins (sometimes in the form of extracellular vehicles or exosomes), which can induce damage of unirradiated neighboring bystander or distant (abscopal) cells as well as immune responses. Such non-targeted effects (NTE) are contributing to low-dose phenomena, such as hormesis, adaptive responses, low-dose hypersensitivity, and genomic instability, and they are also promoting suppression and/or activation of immune cells. All of these are parts of the main defense systems of cells and tissues, including IR-induced innate and adaptive immune responses. The present review is focused on the prominent role of mitochondria in these processes, which are determinants of cell survival and anti-tumor RT.

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“…In a recent study, thiocyanate (SCN − ), a biomolecule that acts as a natural antioxidant in the immune system, was found to be increased in the saliva of 10 healthy orthodontic patients (age 12-17 years) subsequent to exposure to LDIR effective doses of 0.174-0.256 mSv, delivered during cone beam computed tomography (CBCT), inferring that LDIR may exert protective effects by activating the natural antioxidant system [54]. In addition, LDIR (0.1 Gy, γ-radiation) has also demonstrated a bio-positive effect in reducing the transformation of thyroid cancer cells by restoring the thyroid metabolising genes expression, PAX8 and suppressing thyroid cancer carcinogenesis by inhibiting STAT3-miR-330-5p pathways in both cells and a mouse model [55]. Moreover, other experimental studies have demonstrated that the hormetic effects of LDIR only occur in normal cells or tissues and not in malignant cells [56][57][58].…”

Section: Ldir-induced Hormetic Effectsmentioning

confidence: 99%

Low Dose Ionising Radiation-Induced Hormesis: Therapeutic Implications to Human Health

et al. 2021

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The concept of radiation-induced hormesis, whereby a low dose is beneficial and a high dose is detrimental, has been gaining attention in the fields of molecular biology, environmental toxicology and radiation biology. There is a growing body of literature that recognises the importance of hormetic dose response not only in the radiation field, but also with molecular agents. However, there is continuing debate on the magnitude and mechanism of radiation hormetic dose response, which could make further contributions, as a research tool, to science and perhaps eventually to public health due to potential therapeutic benefits for society. The biological phenomena of low dose ionising radiation (LDIR) includes bystander effects, adaptive response, hypersensitivity, radioresistance and genomic instability. In this review, the beneficial and the detrimental effects of LDIR-induced hormesis are explored, together with an overview of its underlying cellular and molecular mechanisms that may potentially provide an insight to the therapeutic implications to human health in the future.

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Low dose radiation regulates BRAF-induced thyroid cellular dysfunction and transformation

Cited by 6 publications

References 43 publications

Hsa-miR-330-5p Aggravates Thyroid Carcinoma via Targeting FOXE1

Hsa-miR-330-5p Aggravates Thyroid Carcinoma via Targeting FOXE1

Low-Dose Non-Targeted Effects and Mitochondrial Control

Low Dose Ionising Radiation-Induced Hormesis: Therapeutic Implications to Human Health

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