&lt;p&gt;Sp1 contributes to radioresistance of cervical cancer through targeting G2/M cell cycle checkpoint CDK1&lt;/p&gt;

Deng, Yuan-Run; Chen, Xiaojing; Chen, Wei; Wu, Lan-Fang; Jiang, Huiping; Lin, Dan; Wang, Lijing; Wang, Wei; Guo, Suiqun

doi:10.2147/cmar.s200907

Cited by 32 publications

(19 citation statements)

References 34 publications

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“…Activation of the CDK1-TFCP2L1 pathway stimulated cell proliferation, self-renewal and invasion in human aggressive bladder cancer. 31 Deng 32 reported that the up-regulation of CDK1 inhibited the G2/M phase block and promoted cervical cancer resistance to radiotherapy. CDK1 was also found to be stably activated by CDK1-KCTD12 interaction in BRAF-mutated colon cancer models resistant to Vemurafenib.…”

Section: Discussionmentioning

confidence: 99%

<p>Inhibition of CDK1 Reverses the Resistance of 5-Fu in Colorectal Cancer</p>

Zhu

Zhang

et al. 2020

CMAR

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Introduction: Although the survival rate of colorectal cancer (CRC) patients can be improved by surgery, radiotherapy, and chemotherapy, the resistance to 5-fluorouracil (5-Fu) affects the effect of chemotherapy and the prognosis of patients. An increasing number of studies showed that 5-Fu resistance was the main reason for the failure of colorectal cancer treatment. The poor prognosis of colorectal cancer greatly harms people's health. This study aimed to clarify the correlation between cyclin-dependent kinase 1 (CDK1) and 5-Fu-induced tumor resistance. Materials and Methods: Cell proliferation and invasion experiments showed that downregulation of CDK1 inhibited fluorouracil-resistant CRC cell proliferation. The expression level of CDK1 was detected in 5-Fu-resistant CRC cells in vitro. Tumor growth was inhibited by down-regulation of CDK1 in tumor xenograft mouse models. Results: We found that CDK1 was highly expressed in tumor tissues, especially in fluorouracil-resistant tissues. We also confirmed that the differential expression of 5-Fu in tumor tissues was related to tumor site, lymph node metastasis and stage. CDK1 promoted migration, invasion and inhibited apoptosis in 5-Fu-resistant CRC cells. Down-regulation of CDK1 inhibited fluorouracil-resistant CRC cell proliferation and tumorigenesis in vivo. Conclusion: High expression of CDK1 may lead to poor clinical prognosis, and inhibition of CDK1 enhances 5-Fu sensitivity in CRC. Our research suggested that CDK1 may be used to predict 5-Fu efficacy and as a therapeutic target for CRC.

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Section: Discussionmentioning

confidence: 99%

<p>Inhibition of CDK1 Reverses the Resistance of 5-Fu in Colorectal Cancer</p>

Zhu

Zhang

et al. 2020

CMAR

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“…Deng et al. showed that high Sp1 expression levels were correlated to cervical cancer progression, and that knockdown of Sp1 significantly enhanced the cellular response to radiation by inducing G2/M arrest, suggesting that Sp1 might represent a potential therapeutic target in cervical cancer [126] . Tumour hypoxia is an important contributor to radioresistance.…”

Section: Genetic Regulation Of Mitochondria Energy Metabolism and Radmentioning

confidence: 99%

Targeting cancer-cell mitochondria and metabolism to improve radiotherapy response

McCann

O’Sullivan

Marcone

2021

Translational Oncology

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Radiotherapy is a regimen that uses ionising radiation (IR) to treat cancer. Despite the availability of several therapeutic options, cancer remains difficult to treat and only a minor percentage of patients receiving radiotherapy show a complete response to the treatment due to development of resistance to IR (radioresistance). Therefore, radioresistance is a major clinical problem and is defined as an adaptive response of the tumour to radiation-induced damage by altering several cellular processes which sustain tumour growth including DNA damage repair, cell cycle arrest, alterations of oncogenes and tumour suppressor genes, autophagy, tumour metabolism and altered reactive oxygen species. Cellular organelles, in particular mitochondria, are key players in mediating the radiation response in tumour, as they regulate many of the cellular processes involved in radioresistance. In this article has been reviewed the recent findings describing the cellular and molecular mechanism by which cancer rewires the function of the mitochondria and cellular metabolism to enhance radioresistance, and the role that drugs targeting cellular bioenergetics have in enhancing radiation response in cancer patients.

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“…The induction of cell cycle arrest at the G2/M phase in tumor cells may be an effective strategy for enhancing the ionizing radiation effect against tumors [28]. Numerous recent studies have shown that increasing radiation-induced G2/M phase arrest in tumor cells can significantly increase the sensitivity of HNSCC, cervical cancer, and prostate cancer cells to ionizing radiation[29][30][31][32]. In the present study, the cell cycle detection results after irradiation showed that the proportion of cells in the G2/M phase in the CNE-2sh group was significantly higher than that in the control group cells, indicating that FANCD2 silencing significantly increased radiation-induced G2/M phase cell cycle arrest in the CNE-2 cells and enhanced their ionizing radiation sensitivity.Interestingly, in ionizing radiation sensitivity experiments involving bone marrow stromal cells and IL-3-dependent hematopoietic stem cells of FANCD2-deficient mice, Berhane et al found that the growth life of bone marrow stromal cells was shortened and showed strong radiation sensitivity and DNA damage involvement.…”

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confidence: 99%

FANCD2 knockdown with shRNA interference enhances the ionizing radiation sensitivity of nasopharyngeal carcinoma CNE-2 cells

Bao

Feng

Zhao

et al. 2021

neo

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Fanconi anemia complementation group D2 (FANCD2) has been associated with the sensitivity of tumor cells to DNA crosslinking damaging agents in certain solid tumors. However, its role in nasopharyngeal carcinoma (NPC) is still unclear. In the present study, the role of FANCD2 in the response of NPC CNE-2 cells to radiation was investigated. A CNE-2 cell model with stable FANCD2 silencing was constructed by lentiviral transfection. Fluorescence quantitative PCR and western blotting were used to evaluate FANCD2 expression in CNE-2 cells. The biological impact of FANCD2 silencing on the response of CNE-2 cells to radiation was investigated in vitro and in vivo. The microarray technology, western blotting, and immunohistochemistry were used to analyze the proteins involved in related pathways after irradiation to investigate the underlying mechanism. Lentivirus-mediated shRNA interference stably silenced the FANCD2 gene in CNE-2 cells. In vitro, in the FANCD2-silenced group, cell proliferation was significantly inhibited, apoptosis was increased, and the cell cycle was arrested at the G2/M phase after irradiation. In vivo, FANCD2 s ilencing slowed tumor growth, as the volume and weight of the xenograft tumors were significantly decreased. Both in vitro and in vivo, the differentially expressed genes NUPR1, FLI1, and FGF21 were downregulated in the FANCD2-silenced group. Our results show that FANCD2 silencing affected the sensitivity of CNE-2 cells to ionizing radiation by regulating cell proliferation, apoptosis, and cell cycle distribution. The mechanism might be associated with changes in NUPR1, FLI1, and FGF21 protein expression due to the FANCD2 silencing. This study provides a promising target for NPC radiotherapy.

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<p>Sp1 contributes to radioresistance of cervical cancer through targeting G2/M cell cycle checkpoint CDK1</p>

Cited by 32 publications

References 34 publications

<p>Inhibition of CDK1 Reverses the Resistance of 5-Fu in Colorectal Cancer</p>

<p>Inhibition of CDK1 Reverses the Resistance of 5-Fu in Colorectal Cancer</p>

Targeting cancer-cell mitochondria and metabolism to improve radiotherapy response

FANCD2 knockdown with shRNA interference enhances the ionizing radiation sensitivity of nasopharyngeal carcinoma CNE-2 cells

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