Prevention of γ-Radiation-Induced DNA Damage in Human Lymphocytes Using a Serine-Magnesium Sulfate Mixture

Changizi, Vahid; Bahrami, Mona; Esfahani, Mahbod; Shetab-Boushehri, Seyed Vahid

doi:10.18295/squmj.2016.17.02.005

Cited by 4 publications

(4 citation statements)

References 24 publications

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“…Radiotherapy mainly indicates ionizing radiation which can induce damage to cellular DNA and subsequently result in cell death via direct or indirect mechanisms [ 5 ]. The efficacy of radiotherapy relies on the sensitivity of tumor cells to radiation.…”

Section: Introductionmentioning

confidence: 99%

miR-219a-5p enhances the radiosensitivity of non-small cell lung cancer cells through targeting CD164

Wei

Cheng

et al. 2020

Bioscience Reports

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Lung cancer is one of the leading causes of cancer-associated mortality. Non-small cell lung carcinoma (NSCLC) accounts for 70-85% of the total cases of lung cancer. Radioresistance frequently develops in NSCLC in the middle and later stages of radiotherapy. We investigated the role of miR-219a-5p in radioresistance of NSCLC. miR-219a-5p expression in serum and lung tissue of lung cancer patients was lower than that in control. Compared with radiosensitive NSCLC patients, miR-219a-5p expression was decreased in serum and lung tissue in radioresistant patients. miR-219a-5p expression level was negatively associated with radioresistance in NSCLC cell lines. Upregulation of miR-219a-5p increased radiosensitivity in radioresistant NSCLC cells in vitro and in vivo. Downregulation of miR-219a-5p decreased radiosensitivity in radiosensitive A549 and H358 cells. miR-219a-5p could directly bind in the 3’UTR of CD164 and negatively regulated CD164 expression. CD164 expression was higher in radioresistant NSCLC tissues than radiosensitive tissues. Upregulation of CD164 significantly inhibited miR-219a-5p-induced regulation of radiosensitivity in radioresistant A549 and H358 cells. Downregulation of CD164 significantly inhibited the effect of anti-miR-219a-5p on radiosensitive A549 and H358 cells. miR-219a-5p or downregulation of CD164 could increase apoptosis and γ-H2A histone family member X (γ-H2AX) expression in radioresistant cells in vitro and in vivo. Upregulation of CD164 could inhibit the effect of miR-219a-5p on apoptosis and γ-H2AX expression. Our results indicated that miR-219a-5p could inhibit CD164, promote DNA damage and apoptosis and enhance irradiation-induced cytotoxicity. The data highlight miR-219a-5p/CD164 pathway in the regulation of radiosensitivity in NSCLC and provide novel targets for potential intervention.

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Section: Introductionmentioning

confidence: 99%

miR-219a-5p enhances the radiosensitivity of non-small cell lung cancer cells through targeting CD164

Wei

Cheng

et al. 2020

Bioscience Reports

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“…Radiotherapy mainly involves treatment with ionizing radiation (IR), which, by direct or indirect actions, leads to the damage of cellular DNA and subsequently results in cell death (6,7). The efficacy of radiotherapy depends on the sensitivity of tumor cells to radiation; tumors can become insensitive to radiation via the radioresistance of tumor cells or the protection of the tumor microenvironment, leading to the repair of damaged cells following IR (7,8).…”

Section: Introductionmentioning

confidence: 99%

Silencing of heat shock protein 27 increases the radiosensitivity of non‑small cell lung carcinoma cells

Xu¹,

Lin²,

Zheng³

et al. 2019

Mol Med Report

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Radiotherapy is a useful treatment for malignant tumors, including lung carcinoma; however, non-small cell lung carcinoma (NSCLC) is frequently insensitive to radiation. It has been reported that heat shock protein 27 (HSPB1) is a radioresistance-associated protein in nasopharyngeal carcinoma. In the present study, the role of HSPB1 in NSCLC cells induced by irradiation was investigated. The viability of cells was determined by a Cell Counting Kit-8 assay. The apoptotic activity, cell cycle distribution and mitochondrial membrane potential (MMP) of cells were evaluated via flow cytometry. Reverse transcription-quantitative polymerase chain reaction and western blot analyses were employed to measure the expression of various genes and proteins. It was observed that knockdown of HSPB1 with small interfering RNA (si-HSPB1) markedly decreased the viability of A549 NSCLC cells and induced cell cycle arrest in the G2/M phase following exposure to 6 Gy irradiation. Furthermore, it was revealed that si-HSPB1 significantly downregulated cyclin B1 and cyclin G1 expression. Additionally, si-HSPB1 promoted apoptosis and depolarized the MMP of cells exposed to 6 Gy irradiation. The expression levels of B-cell lymphoma-2 (Bcl-2), mitochondrial cytochrome c (cyto c ) and pro-caspase-8 were downregulated, whereas those of Bcl-2 associated X protein (Bax), cytosolic cyto c and cleaved-caspase-8 were upregulated. Collectively, silencing of HSPB1 increased the radiosensitivity of NSCLC cells by reducing cell viability, depolarizing the MMP, arresting the cell cycle in the G2/M phase and promoting cell apoptosis. Therefore, HSPB1 may be a novel target for increasing radiosensitivity in the treatment of NSCLC.

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“…Transwell assay. Serum-free medium (200 µl) containing 5x10 4 cells was added to the upper compartments of Transwell inserts (8.0 µm pore size; Costar; Corning, Inc.) for the cell migration assay. As for the cell invasion assay, the chamber was coated with Matrigel (50 µl; BD Biosciences) at 37˚C for 3 h. Then, 600 µl of basal medium containing 10% FBS was added to the lower compartments.…”

Section: Rna Extraction and Reverse Transcription-quantitative Polyme...mentioning

confidence: 99%

“…Radiotherapy has developed into an important treatment modality for inoperable and postoperative patients with NSCLC (3). Radiotherapy can induce cell death via damaging the DNA of tumor cells and subsequently impede the progress of tumors (4). The sensitivity of tumor cells to radiation defines the efficacy of radiotherapy.…”

Section: Introductionmentioning

confidence: 99%

miR‑148a promotes cell sensitivity through downregulating SOS2 in radiation‑resistant non‑small cell lung cancer cells

Zhang

2022

Oncol Lett

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Non-small cell lung carcinoma (NSCLC) is the most common type of lung cancer; however, radioresistance is a significant barrier in NSCLC radiotherapy. MicroRNA (miR)-148a has been reported to be a tumor suppressor in various types of cancer, including NSCLC. In the present study, the potential role of miR-148a in regulating radiosensitivity of NSCLC cells was investigated. Serum miR-148a expression was evaluated by reverse transcription-quantitative PCR in patients with NSCLC and healthy controls. The effects of miR-148a on cell viability, migration and invasion were assessed by Cell Counting Kit-8 and Transwell assays in radiation-resistant NSCLC cells. Serum miR-148a was downregulated in patients with NSCLC compared with healthy controls and its expression was significantly increased after radiotherapy. By contrast, miR-148a expression was decreased in the radioresistant patients compared with the radiosensitivity patients. Additionally, miR-148a overexpression inhibited the cell proliferation, migration and invasion of radiation-resistant NSCLC cells. In addition, miR-148a had putative binding site with Son of Sevenless 2 (SOS2) and negatively regulated SOS2 expression. Silencing SOS2 expression significantly suppressed miR-148a inhibitor-induced increase in radiosensitivity in NSCLC. In conclusion, the results of the present study suggested that miR-148a could enhance the radiosensitivity of NSCLC cells through targeting SOS2, thus providing potential therapeutic targets to improve radiotherapy in NSCLC.

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Prevention of γ-Radiation-Induced DNA Damage in Human Lymphocytes Using a Serine-Magnesium Sulfate Mixture

Cited by 4 publications

References 24 publications

miR-219a-5p enhances the radiosensitivity of non-small cell lung cancer cells through targeting CD164

miR-219a-5p enhances the radiosensitivity of non-small cell lung cancer cells through targeting CD164

Silencing of heat shock protein 27 increases the radiosensitivity of non‑small cell lung carcinoma cells

miR‑148a promotes cell sensitivity through downregulating SOS2 in radiation‑resistant non‑small cell lung cancer cells

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