Inhibitor of Differentiation/DNA Binding 1 (ID1) Inhibits Etoposide-induced Apoptosis in a c-Jun/c-Fos-dependent Manner

Zhao, Yahui; Luo, Aiping; Li, Sheng; Zhang, Wei; Chen, Hongyan; Li, Yang; Ding, Fang; Huang, Furong; Liu, Zhihua

doi:10.1074/jbc.m115.704361

Cited by 35 publications

(26 citation statements)

References 38 publications

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“…Temozolomide-mediated cell death appears to occur as the result of a mismatch repair response (45). ID1 has previously been shown to be involved in chemotherapeutic resistance in multiple solid cancers, including non-small cell lung cancer, colon cancer, and esophageal squamous cell carcinoma (46)(47)(48)(49). We evaluated ID1 protein expression in primary and recurrent glioblastoma patient samples using tissue microarray (TMA).…”

Section: Temozolomide Chemotherapy Results In Increased Id1 Expressiomentioning

confidence: 99%

ID1 Is Critical for Tumorigenesis and Regulates Chemoresistance in Glioblastoma

Sachdeva

Smiljanic

et al. 2019

Cancer Research

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Glioblastoma is the most common primary brain tumor in adults. While the introduction of temozolomide chemotherapy has increased long-term survivorship, treatment failure and rapid tumor recurrence remains universal. The transcriptional regulatory protein, inhibitor of DNA-binding-1 (ID1), is a key regulator of cell phenotype in cancer. We show that CRISPR-mediated knockout of ID1 in glioblastoma cells, breast adenocarcinoma cells, and melanoma cells dramatically reduced tumor progression in all three cancer systems through transcriptional downregulation of EGF, which resulted in decreased EGFR phosphorylation. Moreover, ID1positive cells were enriched by chemotherapy and drove tumor recurrence in glioblastoma. Addition of the neuroleptic drug pimozide to inhibit ID1 expression enhanced the cytotoxic effects of temozolomide therapy on glioma cells and significantly prolonged time to tumor recurrence. Conclusively, these data suggest ID1 could be a promising therapeutic target in patients with glioblastoma. Significance: These findings show that the transcriptional regulator ID1 is critical for glioblastoma initiation and chemoresistance and that inhibition of ID1 enhances the effect of temozolomide, delays tumor recurrence, and prolongs survival.

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Section: Temozolomide Chemotherapy Results In Increased Id1 Expressiomentioning

confidence: 99%

ID1 Is Critical for Tumorigenesis and Regulates Chemoresistance in Glioblastoma

Sachdeva

Smiljanic

et al. 2019

Cancer Research

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“…c-Jun is one of the downstream regulatory targets of ERK, found as the first oncogenic transcription factor [28]. e study reports that c-Jun is an important regulator of a wide range of biological processes such as cell proliferation, differentiation, invasion, migration, and apoptosis [29,30]. And its expression and activation in cancer are highly induced, providing feedback on environmental stimuli, such as DNA damage [31].…”

Section: Introductionmentioning

confidence: 99%

Curcumin Inhibits ERK/c-Jun Expressions and Phosphorylation against Endometrial Carcinoma

Zhang

et al. 2019

BioMed Research International

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Curcumin has been shown to have anticancer effects in a variety of tumors. However, there are fewer studies on the role of curcumin in endometrial carcinoma (EC). The purpose of this experiment was to examine the inhibitory effect of curcumin on endometrial carcinoma cells and ERK/c-Jun signaling pathway. We first predicted the mechanism of action of curcumin on endometrial carcinoma by network pharmacology. Then, we found that curcumin can decrease the cell viability of Ishikawa cells, inhibit the migration of cancer cells, induce apoptosis, and cause cell cycle arrest in the S phase. For molecular mechanism, curcumin reduced the mRNA expression levels of ERK2 and JUN genes and inhibited the phosphorylation of ERK and c-Jun. This suggests that curcumin inhibits the proliferation of endometrial carcinoma cells by downregulating ERK/c-Jun signaling pathway activity.

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“…Regarding apoptosis, changes in the transcriptional activity of inhibitors of this process can be observed ( BCL2 greatest after 8 hr FC = −1.96 MCL1 greatest after 2 hr FC = + 2.1) (Ashkenazi, Fairbrother, Leverson, & Souers, ) as well as programmable cell death inductors ( FOS greatest after 2 hr FC = + 2.17 TNFRSF1B greatest after 2 hr FC = + 2.1) (Zhao et al, ). Thus, an increase in the expression of both pro‐and anti‐apoptotic factors is observed.…”

Section: Discussionmentioning

confidence: 99%

“…In contrast, IL1RN gene encodes the IL-1RA protein (IL-1 receptor antagonist (Zhao et al, 2016). Thus, an increase in the expression of both pro-and anti-apoptotic factors is observed.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of changes in expression pattern of oxidative stress genes under the influence of adalimumab

Grabarek

Wcisło‐Dziadecka

Sanakiewicz

et al. 2019

Dermatologic Therapy

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The psoriasis therapy consists of the inhibition of cytokines involved in inducing and development of this disease. The aim of the study was to evaluate the changes in the expression of genes related to the oxidative stress phenomenon in the culture of normal human dermal fibroblasts of Normal Human Dermal Fibroblasts (NHDF) exposed to adalimumab. NHDF culture was exposed to adalimumab for 2‐, 8‐, and 24‐hr periods. The control consisted of the same cells not exposed to adalimumab. The oligonucleotide microarrays HG‐U133A 2.0 were used to analyze the changes in gene expression in NHDF culture. Analysis showed that there are 3,881 ID mRNA involved in the induction and development of oxidative stress, the expression of which changes significantly due to the exposure of NHDF cells to adalimumab (p < .05) among 1,369 ID mRNA of them. These include genes associated with apoptosis, the p38 MAPK pathway and the PDGF pathway, and above all with pathways not yet classified. Studies have shown that two genes: NR4A2 and IL1RN, whose expression has changed the most, expressed as Fold Change (FC) seem to be the most promising molecular markers to monitor therapy and loss of cell sensitivity to treatment.

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Inhibitor of Differentiation/DNA Binding 1 (ID1) Inhibits Etoposide-induced Apoptosis in a c-Jun/c-Fos-dependent Manner

Cited by 35 publications

References 38 publications

ID1 Is Critical for Tumorigenesis and Regulates Chemoresistance in Glioblastoma

ID1 Is Critical for Tumorigenesis and Regulates Chemoresistance in Glioblastoma

Curcumin Inhibits ERK/c-Jun Expressions and Phosphorylation against Endometrial Carcinoma

Evaluation of changes in expression pattern of oxidative stress genes under the influence of adalimumab

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