Chk2-mediated G2/M cell cycle arrest maintains radiation resistance in malignant meningioma cells

Gogineni, Venkateswara Rao; Nalla, Arun Kumar; Gupta, Rohit; Dinh, Dzung H.; Klopfenstein, Jeffrey D.; Rao, Jasti S.

doi:10.1016/j.canlet.2011.08.022

Cited by 68 publications

(55 citation statements)

References 51 publications

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“…In human leukemic cell lines the long cell cycle arrest in G2 phase is responsible for relative radioresistance of these cells, because it allows time for repair of radiation damage (Vávrová et al, 2004). In meningioma cells the radioresistance is closely correlated with the induction of G2-M arrest (Gogineni et al, 2011). Thus, we propose that the G2-M arrest could be another important factor involved in the acquired radioresistance.…”

Section: Discussionmentioning

confidence: 89%

Involvement of Cdc25c in Cell Cycle Alteration of a Radioresistant Lung Cancer Cell Line Established with Fractionated Ionizing Radiation

Li¹,

Yang²,

Mei³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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Cancer patients often suffer from local tumor recurrence after radiation therapy. Cell cycling, an intricate sequence of events which guarantees high genomic fidelity, has been suggested to affect DNA damage responses and eventual radioresistant characteristics of cancer cells. Here, we established a radioresistant lung cancer cell line, A549R , by exposing the parental A549 cells to repeated γ-ray irradiation with a total dose of 60 Gy. The radiosensitivity of A549 and A549R was confirmed using colony formation assays. We then focused on examination of the cell cycle distribution between A549 and A549R and found that the proportion of cells in the radioresistant S phase increased, whereas that in the radiosensitive G1 phase decreased. When A549 and A549R cells were exposed to 4 Gy irradiation the total differences in cell cycle redistribution suggested that G2-M cell cycle arrest plays a predominant role in mediating radioresistance. In order to further explore the possible mechanisms behind the cell cycle related radioresistance, we examined the expression of Cdc25 proteins which orchestrate cell cycle transitions. The results showed that expression of Cdc25c increased accompanied by the decrease of Cdc25a and we proposed that the quantity of Cdc25c, rather than activated Cdc25c or Cdc25a, determines the radioresistance of cells.

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Section: Discussionmentioning

confidence: 89%

Involvement of Cdc25c in Cell Cycle Alteration of a Radioresistant Lung Cancer Cell Line Established with Fractionated Ionizing Radiation

Li¹,

Yang²,

Mei³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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“…We have designed different concentration and different time of SKF96365 administrated in vitro, and we chose 5 μM and 8 h after SKF96365 treated. At this concentration and time, Eca109 cells were mostly arrest at G2/M phase, which was the best condition for radiotherapy (25).…”

Section: Discussionmentioning

confidence: 99%

Study on the role of transient receptor potential C6 channels in esophageal squamous cell carcinoma radiosensitivity

Zhang

Fan

et al. 2017

J. Thorac. Dis.

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“…Interfering with the process of cell cycle and apoptosis contributes to the tumor radiation response either [115, 116]. Cell cycle checkpoints are pivotal for safeguarding genome stability, and if they are defect in cells, there will be an increasingly rate of genome instability and neoplastic transformation.…”

Section: Mirna and The Downstream Effector Genes Of Radiation Relamentioning

confidence: 99%

MicroRNA and signal transduction pathways in tumor radiation response

Zhao

Cao

2013

Cellular Signalling

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Tumor radiation response is an essential issue in radiotherapy and a core determining factor of tumor radioresistance or radiosensitivity. Multiple factors can influence tumor radiation response, and among them tumor genetic and epigenetic background, tumor microenvironment and tumor blood flow status may take a leading role. During the whole process of tumor radiation response, tumor radiosensitivity can be regulated in an orderly manner through some classical signal transduction pathways. Although these pathways have already owned multiple biological functions and involved in the process of carcinogenesis, their regulatory roles in tumor radiation response can not be ignored. MicroRNA (miRNA) is a class of non-coding RNA of about 22 nucleotides in length, which binds to the 3’-untranslated region (3’-UTR) of target gene and controls the expression of it at the post-transcriptional level. MiRNA participates in numerous physiology and pathology processes and acts as oncogene or tumor suppressor to affect cancer progression. Through interplaying with the key components in radiation related signal transduction pathways, miRNA could effectively activate the expression of DNA damage response genes and cell cycle related genes in nucleus, and play a critical role in the modulation of radiation response and radiosensitivity in tumor cells. In this review, we mainly elucidate the regulatory mechanisms and functions of miRNA in these radiation related signal transduction pathways from three different aspects which include the upstream receptors, midstream transducer pathways, and downstream effector genes.

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Chk2-mediated G2/M cell cycle arrest maintains radiation resistance in malignant meningioma cells

Cited by 68 publications

References 51 publications

Involvement of Cdc25c in Cell Cycle Alteration of a Radioresistant Lung Cancer Cell Line Established with Fractionated Ionizing Radiation

Involvement of Cdc25c in Cell Cycle Alteration of a Radioresistant Lung Cancer Cell Line Established with Fractionated Ionizing Radiation

Study on the role of transient receptor potential C6 channels in esophageal squamous cell carcinoma radiosensitivity

MicroRNA and signal transduction pathways in tumor radiation response

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