CREB‐binding protein regulates lung cancer growth by targeting MAPK and CPSF4 signaling pathway

Tang, Zhipeng; Yu, Wei; Zhang, Changlin; Zhao, Shilei; Yu, Zhenlong; Xiao, Xia; Tang, Ranran; Yang, Xuan; Yang, Wenjing; Hao, Jie; Xu, Tingting; Zhang, Qianyi; Huang, Wenlin; Deng, Wuguo; Guo, Wei

doi:10.1016/j.molonc.2015.10.015

Cited by 38 publications

(25 citation statements)

References 45 publications

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“…CBP is a coactivator that interacts with the cAMP response element binding protein (CREB), a process dependent on the cAMP‐dependent protein kinase A and its phosphorylation of CREB . CBP was shown to interact with various cellular transcriptional factors, including CREB / ATF, c‐oo Jun, c‐Myb, Myo‐D, c‐Fos, β‐catenin/TCFs, and cleavage and polyadenylation specific factor 4 . The hematopoietic transcription factors such as EKLF, GATA‐1, NF‐E2, and viral proteins, such as the adenovirus E1A, the simian virus 40 T antigen, and the Epstein‐Barr virus Zta also interacted with CBP .…”

Section: Resultsmentioning

confidence: 99%

Comprehensive Profiling of Lysine Acetylome in Baculovirus Infected Silkworm (Bombyx mori) Cells

Xue

Zhao

et al. 2018

Proteomics

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Section: Resultsmentioning

confidence: 99%

Comprehensive Profiling of Lysine Acetylome in Baculovirus Infected Silkworm (Bombyx mori) Cells

Xue

Zhao

et al. 2018

Proteomics

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“…5c). Based on our previous research, we conjectured that the combination treatment could influence the binding of cleavage and polyadenylation specific factor 4 (CPSF4) at hTERT promoter and thereby regulate the transcription and expression of hTERT [23, 32, 33]. Pulldown assay indicated that the binding of CPSF4 to the hTERT promoter was almost undetectable after combination treatment with BKM120 and Prima-1 Met (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…The ChIP assay was done as described previously [22, 23]. Briefly, cells were fixed with 1% formaldehyde for 10 minutes and cross-linking was quenched with 0.125 M glycine for 10 minutes.…”

Section: Methodsmentioning

confidence: 99%

Synergistic Antitumor Effect of BKM120 with Prima-1Met Via Inhibiting PI3K/AKT/mTOR and CPSF4/hTERT Signaling and Reactivating Mutant P53

Xu²,

Li³

et al. 2018

Cell Physiol Biochem

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Background/Aims: PI3KCA and mutant p53 are associated with tumorigenesis and the development of cancers. NVP-BKM120, a selective pan-PI3K inhibitor, exerts the antitumor activity by suppressing the PI3K signaling pathway. Prima-1^Met, a low molecular weight compound, can rescue the gain-of-function of mutant p53 by restoring its transcriptional function. In this study, we investigated whether PI3K inhibition combined with mutant p53 reactivation could enhance the antitumor effect in thyroid cancer cells. Methods: The effects of BKM120 and Prima-1^Met on the proliferation, apoptosis, migration and invasion of thyroid cancer cells were measured by MTT, colony formation, flow cytometry, wound-healing and transwell assays, respectively. Thyroid differentiation was assessed by detecting the expression levels of specific markers using RT-PCR and Western blot. The in vivo antitumor efficacy was analyzed in a mouse xenograft model. Results: The combinational treatment of BKM120 and Prima-1^Met significantly enhanced the inhibitions of cell viability, colony formation, migration and invasion, and the induction of apoptosis in thyroid cell lines, and synergistically suppressed tumor xenograft growth by inhibiting the PI3K/Akt/mTOR and EMT signaling pathways, up-regulating p53 targeted genes, and triggering the release of cytochrome c. Moreover, the combination of BKM120 and Prima-1^Met suppressed the stemlike traits of thyroid cancer cells and promoted their differentiation by upregulating the expression of thyroid-specific differentiation markers and repressing the expression of cancer stem cell markers. Furthermore, the mechanism study demonstrated that the combinational treatment synergistically abrogated the binding of CPSF4 at the promoter of hTERT and thus suppressed hTERT expression. Consistently, overexpression of hTERT rescued the inhibitions of cell viability, invasion and stem-like traits mediated by the combination of BKM120 and Prima-1^Met. Conclusion: Our results showed that the combination of BKM120 with Prima-1^Met synergistically suppressed the growth of thyroid cancer cells and tumor xenografts via inhibiting PI3K/Akt/mTOR and CPSF4/hTERT signaling and reactivating mutant p53.

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“…CREB-binding protein (CREBBP) plays a role during development and has been implicated in cancer formation. [62][63][64][65][66][67] Indeed, germline mutations in the gene cause Rubinstein-Taybi syndrome, characterized by increased risk of malignancy, especially childhood brain cancer and leukemia, as well as other symptoms such as mental retardation. 62,68 Pouponnot et al 69 found CREBBP to interact with SMAD1 in HaCat human keratinocyte cells, but there was little to no interaction with SMAD4.…”

Section: Commonly Implicated Smad-interacting Tfsmentioning

confidence: 99%

“…CREB‐binding protein (CREBBP) plays a role during development and has been implicated in cancer formation . Indeed, germline mutations in the gene cause Rubinstein‐Taybi syndrome, characterized by increased risk of malignancy, especially childhood brain cancer and leukemia, as well as other symptoms such as mental retardation .…”

Section: Introductionmentioning

confidence: 99%

Transcription factors—Intricate players of the bone morphogenetic protein signaling pathway

Ampuja

Kallioniemi

2017

Genes Chromosomes & Cancer

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CREB‐binding protein regulates lung cancer growth by targeting MAPK and CPSF4 signaling pathway

Cited by 38 publications

References 45 publications

Comprehensive Profiling of Lysine Acetylome in Baculovirus Infected Silkworm (Bombyx mori) Cells

Comprehensive Profiling of Lysine Acetylome in Baculovirus Infected Silkworm (Bombyx mori) Cells

Synergistic Antitumor Effect of BKM120 with Prima-1Met Via Inhibiting PI3K/AKT/mTOR and CPSF4/hTERT Signaling and Reactivating Mutant P53

Transcription factors—Intricate players of the bone morphogenetic protein signaling pathway

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