The oncoprotein HBXIP promotes migration of breast cancer cells via GCN5-mediated microtubule acetylation

Li, Leilei; Liu, Bowen; Zhang, Xiaodong; Ye, Lihong

doi:10.1016/j.bbrc.2015.02.036

Cited by 22 publications

(16 citation statements)

References 36 publications

(49 reference statements)

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“…In recent years, GCN5 has also been implicated a function in certain oncogenic processes. In breast cancer cells, HBXIP (hepatitis B X‐interacting protein) oncoprotein promotes the migration of breast cancer cells through modulating microtubule acetylation mediated by GCN5 . GCN5 is required for invariant natural killer T (iNKT)‐cell development through EGR2 acetylation .…”

Section: Introductionmentioning

confidence: 99%

The lysine acetyltransferase GCN5 contributes to human papillomavirus oncoprotein E7‐induced cell proliferation via up‐regulating E2F1

Qiao

Zhang

et al. 2018

J Cellular Molecular Medi

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General control nondepressible 5 (GCN5), the first identified transcription‐related lysine acetyltransferase (KAT), is an important catalytic component of a transcriptional regulatory SAGA (Spt‐Ada‐GCN5‐Acetyltransferase) and ATAC (ADA2A‐containing) complex. While GCN5 has been implicated in cancer development, its role in cervical cancer is not known. The human papillomavirus (HPV) oncoprotein E7 abrogates the G1 cell cycle checkpoint and induces genomic instability, which plays a central role in cervical carcinogenesis. In this study, we observed that GCN5 was up‐regulated in HPV E7‐expressing cells, knockdown of GCN5 inhibited cell cycle progression and DNA synthesis in HPV E7‐expressing cells. Notably, GCN5 knockdown reduced the steady‐state levels of transcription factor E2F1. Depletion of E2F1 caused G1 arrest while overexpression of E2F1 rescued the inhibitory effects of GCN5 knockdown on G1/S progression in HPV E7‐expressing cells. Results from chromatin immunoprecipitation (ChIP) assays demonstrated that GCN5 bound to the E2F1 promoter and increased the extent of histone acetylation within these regions. GCN5 also acetylated c‐Myc and increased its ability to bind to the E2F1 promoter. Knockdown of c‐Myc reduced the steady‐state levels of E2F1 and caused G1 arrest. These results revealed a novel mechanism of E7 function whereby elevated GCN5 acetylates histones and c‐Myc to regulate E2F1 expression and cell cycle progression.

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Section: Introductionmentioning

confidence: 99%

The lysine acetyltransferase GCN5 contributes to human papillomavirus oncoprotein E7‐induced cell proliferation via up‐regulating E2F1

Qiao

Zhang

et al. 2018

J Cellular Molecular Medi

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“…Extensive efforts have been made towards a better understanding of human breast cancer oncogenic events, and many biomarkers have been reported to be an indicator for initiation and invasion of breast cancer. These may include among others; proline rich inositol polyphosphate 5-phosphatase (PIPP), which when depleted inhibits PI3K/AKT signaling, enhanced the transformation ability of breast cancer cells, but reduced cell migration and invasion thus indicating that PIPP is a potential suppressor of oncogenic PI3K/AKT signaling in breast cancer (8); bone marrow stromal antigen 2 which is expressed in cancer cells and facilitates the emergence of neoplasia and malignant progression of breast cancer (9) and others such as oncoprotein hepatitis B X-interacting protein which when mediated by general control non-derepressible 5 promotes the migration of breast cancer cells and therapeutically could act as a novel target in breast cancer (10).…”

Section: Introductionmentioning

confidence: 99%

PEG10 promotes human breast cancer cell proliferation, migration and invasion

Xiao

Tembo

et al. 2016

International Journal of Oncology

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Abstract. Paternally expressed imprinted gene 10 (PEG10), derived from the Ty3/Gypsy family of retrotransposons, has been implicated as a genetic imprinted gene. Accumulating evidence suggests that PEG10 plays an important role in tumor growth in various cancers, including hepatocellular carcinoma, lung cancer and prostate cancer. However, the correlation between PEG10 and breast cancer remains unclear.In the present study, we evaluated and characterized the role of PEG10 in human breast cancer proliferation, cell cycle, clone formation, migration and invasion. The expression level of PEG10 was significantly elevated in breast cancer tissues and associated with distant metastasis and poor clinical outcome. Gene set enrichment analysis indicated that high expression of PEG10 could enrich cell cycle-related processes in breast cancer tissues. Ectopic overexpression of PEG10 in breast cancer cells enhanced cell proliferation, cell cycle, clone formation along with migration and invasion. Cell-to-cell junction molecule E-cadherin was downregulated and matrix degradation proteases MMP-1, MMP-2, MMP-9 were up regulated after PEG10 overexpression. Our results demonstrated that PEG10 is a crucial oncogene and has prognostic value for breast cancer, which could be applied in breast cancer diagnosis and targeting therapy in future.

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“…The positive role of GCN5 in the development of various tumors was gradually elucidated, we next questioned whether GCN5 was associated with PFKFB4‐mediated TC cells development (Li, Liu, Zhang, & Ye, ; Liu et al, ; Shao et al, ; Yin et al, ). It is intriguing that GCN5 expression was inhibited by shPFKFB4‐transfected (Figure ).…”

Section: Resultsmentioning

confidence: 99%

“…was associated with PFKFB4-mediated TC cells development (Li, Liu, Zhang, & Ye, 2015;Liu et al, 2015;Shao et al, 2018;Yin et al, 2015). It is intriguing that GCN5 expression was inhibited by shPFKFB4-transfected ( Figure 4).…”

Section: Downregulation Of Pfkfb4 Inhibited Gcn5 Expression and Phomentioning

confidence: 91%

PFKFB4 negatively regulated the expression of histone acetyltransferase GCN5 to mediate the tumorigenesis of thyroid cancer

Chen

You

et al. 2020

Dev Growth Differ

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Thyroid cancer (TC) is the most common malignant endocrine tumor, and its incidence has progressively increased over several decades. Accumulating evidence has suggested that PFKFB4, a critical regulatory enzyme of glycolysis, has been implicated in various solid cancers. However, the exact effect of PFKFB4 on TC remains unclear. Hence, the objective of this work was to investigate the role of PFKFB4 in TC and explore the underlying regulatory mechanisms. Here, we provide evidence that mRNA levels of PFKFB4 were upregulated in TC patients’ thyroids and cell lines. Downregulation of PFKFB4 reduced TC cell viability and inhibited colony formation. In addition, the migration and invasion of TC cells were suppressed by PFKFB4 knockdown, suggesting that PFKFB4 is positively correlated with tumorigenesis of TC. Molecularly, knockdown of PFKFB4 significantly inhibited expression of GCN5 and phosphorylation of PI3K/AKT. Moreover, the suppressive role of shPFKFB4 in TC cell growth was reversed by upregulation of GCN5. Finally, the in vivo experiment indicated that downregulation of PFKF4B suppressed tumor growth in xenografts TC model mice. In total, our results suggested that PFKFB4‐mediated TC tumorigenesis by positively regulating GCN5 and PI3K/AKT signaling. These findings provide new research directions and therapeutic options considering PFKF4B as a novel diagnosis marker and therapeutic target.

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The oncoprotein HBXIP promotes migration of breast cancer cells via GCN5-mediated microtubule acetylation

Cited by 22 publications

References 36 publications

The lysine acetyltransferase GCN5 contributes to human papillomavirus oncoprotein E7‐induced cell proliferation via up‐regulating E2F1

The lysine acetyltransferase GCN5 contributes to human papillomavirus oncoprotein E7‐induced cell proliferation via up‐regulating E2F1

PEG10 promotes human breast cancer cell proliferation, migration and invasion

PFKFB4 negatively regulated the expression of histone acetyltransferase GCN5 to mediate the tumorigenesis of thyroid cancer

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