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

Qiao, Liang; Zhang, Qishu; Zhang, Weifang; Chen, Jason J.

doi:10.1111/jcmm.13806

Cited by 15 publications

(18 citation statements)

References 76 publications

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“…We have demonstrated that both WDHD1 and GCN5 play key roles in S-phase entry and G1 checkpoint control in E7 expressing cells [16,19], and our data suggest that WDHD1 regulates GCN5 expression ( Figs. 1 and 2).…”

Section: Overexpression Of Gcn5 Overrides G1 Checkpoint Activation Ansupporting

confidence: 57%

“…Our previous study demonstrated a role for WDHD1 in G1 checkpoint abrogation E7 expressing cells [ 16 ]. It was reported that GCN5 plays a role in the G1 checkpoint control while WDHD1 inhibits its degradation [ 17 – 19 ]. Moreover, our recent study revealed that GCN5 also promotes cell cycle progression in HPV E7 expressing cells [ 19 ].…”

Section: Resultsmentioning

confidence: 99%

“…It was reported that GCN5(histone acetyltransferase complex) plays a role in the G1 checkpoint control while WDHD1 inhibits degradation by disrupting its interaction with ubiquitination ligase CRL4 complex [17,18]. Our recent study revealed that GCN5 promotes HPV expressing cell proliferation by regulating E2F1 [19]. In the present study, we determined the role of GCN5 and the mechanism by which WDHD1 abrogates G1 checkpoint in E7 expressing cells.…”

mentioning

confidence: 83%

“…The concentration of the Alexis Biochemicals bleomycin used in the experiment was 4 μg/ ml. The specific experimental steps need to follow the published articles [16,19,20].…”

Section: Flow Cytometrymentioning

confidence: 99%

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WDHD1 facilitates G1 checkpoint abrogation in HPV E7 expressing cells by modulating GCN5

Yang

Pei

et al. 2020

BMC Cancer

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Background: Genomic instability is a hallmark of cancer. The G1 checkpoint allows cells to repair damaged DNA that may lead to genomic instability. The high-risk human papillomavirus (HPV) E7 gene can abrogate the G1 checkpoint, yet the mechanism is still not fully understood. Our recent study showed that WDHD1 (WD repeat and high mobility group [HMG]-box DNA-binding protein 1) plays a role in regulating G1 checkpoint of E7 expressing cells. In this study, we explored the mechanism by which WDHD1 regulates G1 checkpoint in HPV E7 expressing cells. Methods: NIKS and RPE1 derived cell lines were used. Real-time PCR, Rescue experiment, FACS and BrdU labeling experiments were performed to examine role of GCN5 in G1 checkpoint abrogation in HPV-16 E7 expressing cells. Results: In this study, we observed that WDHD1 facilitates G1 checkpoint abrogation by modulating GCN5 in HPV E7 expressing cells. Notably, depletion of WDHD1 caused G1 arrest while overexpression of GCN5 rescued the inhibitory effects of WDHD1 knockdown on G1/S progression. Furthermore, siWDHD1 significantly decreased cell cycle proliferation and DNA synthesis that was correlated with Akt phosphorylation (p-Akt), which was reversed by GCN5 overexpression in HPV E7 expressing cells. Conclusions: In summary, our data identified a WDHD1/GCN5/Akt pathway leading to the abrogation of G1 checkpoint in the presence of damaged DNA, which may cause genomic instability and eventually HPV induced tumorigenesis.

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Section: Overexpression Of Gcn5 Overrides G1 Checkpoint Activation Ansupporting

confidence: 57%

Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 83%

“…The concentration of the Alexis Biochemicals bleomycin used in the experiment was 4 μg/ ml. The specific experimental steps need to follow the published articles [16,19,20].…”

Section: Flow Cytometrymentioning

confidence: 99%

See 2 more Smart Citations

WDHD1 facilitates G1 checkpoint abrogation in HPV E7 expressing cells by modulating GCN5

Yang

Pei

et al. 2020

BMC Cancer

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“…Moreover, E2F1 has a synergistic effect with c-Myc. E2F1 has been confirmed as a target gene of c-Myc, which can reduce the expression of c-Myc by down-regulating E2F1, thereby inhibiting the proliferation of tumor cells [27]. The results of this study showed that the protein levels of c-Myc, E2F1 and NF-κB in BGC-823 cells decreased after PN treatment.…”

Section: Discussionmentioning

confidence: 60%

Anti-Tumor Effect and Mechanism of Parthenolide in Gastric Cancer Cellline BGC-823

Zhu¹,

Zhang²,

Guo³

et al. 2019

OALib

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Objective: To study the anti-tumor effect and mechanism of parthenolide in gastric cancer cell BGC-823. Methods: The cck8 assay was used to detect the changes of BGC-823 cells viability after treatment with different concentrations of parthenolide at different time points. The proliferation ability of BGC-823 cells was detected by clone formation assay. And the cell cycle and apoptosis were measured by flow cytometry. Meanwhile, to detect the difference in intracellular ROS production levels, the fluorescence assay was used. And with the help of western blotting, cell cycle-and apoptosis-related protein expression can be detected. Results: Parthenolide could inhibit the viability of BGC-823 cells in a dose-and time-dependent manner (P < 0.01). In BGC-823 cells exposed to parthenolide, the apoptosis rate was found significantly increased (P < 0.01), and the protein expression of cleaved-caspase3, cleaved-caspase8, and cleaved-caspase9 significantly increased (P < 0.01); the cell cycle was arrested at G1phase (P < 0.01); the protein levels of CyclinD1 and CyclinE1 decreased (P < 0.01), and the expression of P53 and P21 protein increased (P < 0.01); massive intracellular ROS generation was found (P < 0.01). Furthermore, the nuclear protein levels of c-Myc, E2F1, and NF-κB and the protein level of phosphorylated STAT3 decreased in BGC-823 cells exposed to parthenolide (P < 0.01). Conclusion: Parthenolide may inhibit the proliferation of BGC-823 cells and induce G1-phase cell cycle arrest and apoptosis via inhibiting STAT3-c-Myc-E2F1 axis.

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Human papillomavirus associated cervical lesion: pathogenesis and therapeutic interventions

Ye,

Zheng,

et al. 2023

MedComm

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Human papillomavirus (HPV) is the most prevalent sexually transmitted virus globally. Persistent high‐risk HPV infection can result in cervical precancerous lesions and cervical cancer, with 70% of cervical cancer cases associated with high‐risk types HPV16 and 18. HPV infection imposes a significant financial and psychological burden. Therefore, studying methods to eradicate HPV infection and halt the progression of precancerous lesions remains crucial. This review comprehensively explores the mechanisms underlying HPV‐related cervical lesions, including the viral life cycle, immune factors, epithelial cell malignant transformation, and host and environmental contributing factors. Additionally, we provide a comprehensive overview of treatment methods for HPV‐related cervical precancerous lesions and cervical cancer. Our focus is on immunotherapy, encompassing HPV therapeutic vaccines, immune checkpoint inhibitors, and advanced adoptive T cell therapy. Furthermore, we summarize the commonly employed drugs and other nonsurgical treatments currently utilized in clinical practice for managing HPV infection and associated cervical lesions. Gene editing technology is currently undergoing clinical research and, although not yet employed officially in clinical treatment of cervical lesions, numerous preclinical studies have substantiated its efficacy. Therefore, it holds promise as a precise treatment strategy for HPV‐related cervical lesions.

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

Cited by 15 publications

References 76 publications

WDHD1 facilitates G1 checkpoint abrogation in HPV E7 expressing cells by modulating GCN5

WDHD1 facilitates G1 checkpoint abrogation in HPV E7 expressing cells by modulating GCN5

Anti-Tumor Effect and Mechanism of Parthenolide in Gastric Cancer Cellline BGC-823

Human papillomavirus associated cervical lesion: pathogenesis and therapeutic interventions

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