Proteasome mediated degradation of CDC25C and Cyclin B1 in Demethoxycurcumin treated human glioma U87 MG cells to trigger G2/M cell cycle arrest

Lal, Neetika; Nemaysh, Vishal; Luthra, Pratibha Mehta

doi:10.1016/j.taap.2018.07.012

Cited by 30 publications

(17 citation statements)

References 41 publications

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“…Moreover, cell proliferation is often regulated through cell cycle [ 22 ]. Our results showed that DMC-BH induced G2/M phase cell cycle arrest in GSCs; this is consistent with a previous study demonstrating that DMC triggered G2/M cell cycle arrest in U87 MG glioma cells [ 23 ]. In addition, the DMC-BH induced cell cycle arrest was confirmed by the decreased expression of cell cycle related proteins Cdc2 and cyclin B1 in DMC-BH-exposed GSCs.…”

Section: Discussionsupporting

confidence: 93%

Demethoxycurcumin analogue DMC-BH inhibits orthotopic growth of glioma stem cells by targeting JNK/ERK signaling

Shi

Sun

Zhu³

2020

Aging

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Glioma stem cells (GSCs) play an important role in glioblastoma resistance to conventional therapies and disease recurrence. Here, we assessed the therapeutic effect of a demethoxycurcumin analogue, DMC-BH, on GSCs, and investigated the underlying mechanisms. Our in vitro data demonstrate that DMC-BH inhibits GSC proliferation, and induces apoptosis and autophagy in GSCs. In addition, our results show that DMC-BH effectively crosses the blood-brain barrier to inhibit the growth of intracranial GSC tumors in vivo. DMC-BH significantly increased phosphorylation levels of JNK, ERK and c-Jun in GSCs. Inhibition of JNK and ERK activities reversed the pro-apoptotic effect of DMC-BH in GSCs, indicating that the DMC-BH-induced apoptosis in GSCs is mediated via the JNK/ERK signaling pathway. These results suggest that DMC-BH could potentially serve as a effective therapy against GSCs that acts by targeting the JNK/ERK signaling pathway.

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Section: Discussionsupporting

confidence: 93%

Demethoxycurcumin analogue DMC-BH inhibits orthotopic growth of glioma stem cells by targeting JNK/ERK signaling

Shi

Sun

Zhu³

2020

Aging

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“…Cdc2/Cyclin B1 complex activity has been considered as an import role in G2/M phase transition. Several studies have indicated that G2/M cell cycle arrest showed decreased the expression of Cdc2/Cyclin B1 [18, 19]. Increased Cdc2/Cyclin B1 activity can promote radiation-induced cell apoptosis by inducing G2/M transition [20, 21].…”

Section: Discussionmentioning

confidence: 99%

Raltitrexed increases radiation sensitivity of esophageal squamous carcinoma cells

Ding

Liu

et al. 2019

Cancer Cell Int

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Background Radiation therapy remains an important therapeutic modality, especially for those patients who are not candidates for radical resection. Many strategies have been developed to increase the radiosensitivity of esophageal cancer, with some success. Methods This study was conducted to determine whether raltitrexed can enhance radiosensitivity of esophageal squamous cell carcinoma (ESCC). ESCC cell lines 24 h were incubated with raltitrexed or DMSO with or without subsequent irradiation. Cell Counting Kit assay-8 assay and clonogenic survival assay were used to measure the cell proliferation and radiosensitization, respectively. Flow cytometry was utilized to examine cell apoptosis and cell cycle distribution in different groups. Immunofluorescence analysis was performed to detect deoxyribonucleic acid (DNA) double-strand breaks. In addition, the expression levels of proteins that are involved in radiation induced signal transduction including Bax, Cyclin B1, Cdc2/pCdc2, and Cdc25C/pCdc25C were examined by western blot analysis. Results The results indicated that raltitrexed enhanced radiosensitivity of ESCC cells with increased DNA double-strand breaks, the G2/M arrest, and the apoptosis of ESCC cells induced by radiation. The sensitization enhancement ratio of 1.23–2.10 was detected for ESCC cells with raltitrexed treatment in TE-13 cell line. In vitro, raltitrexed also increased the therapeutic effect of radiation in nude mice. Conclusion Raltitrexed increases the radiosensitivity of ESCC. This antimetabolite drug is promising for future clinical trials with concurrent radiation in esophageal cancer.

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“…134,135 Intracellular ROS accumulation obstructs cellular proliferation and induces cell cycle arrest at the G1 and G2/M phases. 136,137 Abnormally increased levels of ischemic ROS can selectively kill malignant cells and act as an adverse factor in causing genetic instability. Thus, enhanced ROS production in the tumor bed might be one of the important strategies in ROSmediated cancer therapy.…”

Section: Ros Favor Tumor Growthmentioning

confidence: 99%

The interrelationship between cerebral ischemic stroke and glioma: a comprehensive study of recent reports

Ghosh

Chakraborty

Sarkar

et al. 2019

Sig Transduct Target Ther

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Glioma and cerebral ischemic stroke are two major events that lead to patient death worldwide. Although these conditions have different physiological incidences,~10% of ischemic stroke patients develop cerebral cancer, especially glioma, in the postischemic stages. Additionally, the high proliferation, venous thrombosis and hypercoagulability of the glioma mass increase the significant risk of thromboembolism, including ischemic stroke. Surprisingly, these events share several common pathways, viz. hypoxia, cerebral inflammation, angiogenesis, etc., but the proper mechanism behind this co-occurrence has yet to be discovered. The hypercoagulability and presence of the D-dimer level in stroke are different in cancer patients than in the noncancerous population. Other factors such as atherosclerosis and coagulopathy involved in the pathogenesis of stroke are partially responsible for cancer, and the reverse is also partially true. Based on clinical and neurosurgical experience, the neuronal structures and functions in the brain and spine are observed to change after a progressive attack of ischemia that leads to hypoxia and atrophy. The major population of cancer cells cannot survive in an adverse ischemic environment that excludes cancer stem cells (CSCs). Cancer cells in stroke patients have already metastasized, but early-stage cancer patients also suffer stroke for multiple reasons. Therefore, stroke is an early manifestation of cancer. Stroke and cancer share many factors that result in an increased risk of stroke in cancer patients, and vice-versa. The intricate mechanisms for stroke with and without cancer are different. This review summarizes the current clinical reports, pathophysiology, probable causes of co-occurrence, prognoses, and treatment possibilities.

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Proteasome mediated degradation of CDC25C and Cyclin B1 in Demethoxycurcumin treated human glioma U87 MG cells to trigger G2/M cell cycle arrest

Cited by 30 publications

References 41 publications

Demethoxycurcumin analogue DMC-BH inhibits orthotopic growth of glioma stem cells by targeting JNK/ERK signaling

Demethoxycurcumin analogue DMC-BH inhibits orthotopic growth of glioma stem cells by targeting JNK/ERK signaling

Raltitrexed increases radiation sensitivity of esophageal squamous carcinoma cells

The interrelationship between cerebral ischemic stroke and glioma: a comprehensive study of recent reports

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