Dual Repressive Function by Cip1, a Budding Yeast Analog of p21, in Cell-Cycle START Regulation

Li, Pan; Liu, Xueqin; Hao, Zhimin; Jia, Yanrong; Zhao, Xiangdong; Xie, Debao; Dong, Jingao; Zeng, Fanli

doi:10.3389/fmicb.2020.01623

Cited by 11 publications

(6 citation statements)

References 23 publications

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“…p21 was first identified as a downstream gene of p53, subsequent research showed that p21 functions as an important cell cycle regulator, involved in the process of cell growth, differentiation, aging and death 21 . Previous studies have established that p21 can arrest the cell cycle in the G1 phase by interacting with cyclin D/CDK 22,23 . In our study, over‐expressed RACK1 led to p21 expression down‐regulation without affecting the expression of p53, indicating that p21 functions in an independent way on p53 in the development of CC with RACK1 dysregulation.…”

Section: Discussionsupporting

confidence: 48%

RACK1 promotes the occurrence and progression of cervical carcinoma

Yang,

Lu,

Zhang

et al. 2024

Clinical Laboratory Analysis

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BackgroundRACK1 has been identified as a multifunctional cytosolic protein, and plays a pivotal role in multiple biological responses involved in several kinds of tumors, while its effect in cervical cancer has not been well elucidated yet. The study aimed to investigate the role of RACK1 in cervical cancer occurrence and progression.MethodsThe expression of RACK1 in cervical specimens was measured by immunohistochemical staining and Western blot assay. Transgenic mice were used to detect the role of RACK1 in modulating tumorigenesis in vivo. Cervical carcinoma cell lines were used to explore the underlying mechanisms of RACK1 on the behaviors of tumor cells in vitro.ResultsWe found that RACK1 expression was upregulated in cancer tissues compared with adjacent tissues, and its expression was gradually increased from cervictis, and cervical intraepithelial neoplasis (CIN) to carcinoma. Genetic overexpression of RACK1 facilitated tumor formation and growth in nude mice. Mechanism studies disclosed that RACK1 over‐expression prolonged the G0/G1 phase by up‐regulating the expression of cyclinD1, down‐regulating p21 and p27 probably by modulating the phosphorylation of AKT.ConclusionsTaken together, we concluded that RACK1 stimulates tumorigenesis and progression of cervical cancer via modulating the proliferation of tumor cells, implying that targeting RACK1 may serve as a promising method for cervical cancer therapy.

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Section: Discussionsupporting

confidence: 48%

RACK1 promotes the occurrence and progression of cervical carcinoma

Yang,

Lu,

Zhang

et al. 2024

Clinical Laboratory Analysis

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“…S3 A ). In addition, if Cip1 were a CDK substrate, we would expect that G1 cyclin/CDK complexes would regulate its activity since Cip1 functions at the G1/S transition ( 24 , 33 , 41 ). However, G1 cyclin/CDK complexes are unable to phosphorylate Cip1 in vitro ( 42 ).…”

Section: Discussionmentioning

confidence: 99%

Cip1 tunes cell cycle arrest duration upon calcineurin activation

Flynn

Benanti

2022

Proc. Natl. Acad. Sci. U.S.A.

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Significance To ensure their survival, cells arrest the cell division cycle when they are exposed to environmental stress. The duration of this arrest is dependent upon the time it takes a cell to adapt to a particular environment. How cells adjust the amount of time they remain arrested is not known. This study investigates the role of the phosphatase calcineurin in controlling cell cycle arrest duration in yeast. We show that calcineurin lengthens arrest by prolonging Hog1-dependent activation of the poorly characterized cyclin-dependent kinase inhibitor Cip1. Cip1 only impacts cell cycle arrest in response to stressors that robustly activate calcineurin, suggesting that Cip1 is a context-specific regulator that differentially adjusts the length of arrest depending on the particular stressor.

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“…At the same time, it is associated with the occurrence of tumors and serves a role in the physiological and pathological processes. Previous studies have confirmed that p21 can form a complex with cyclin D/CDK to block the cell cycle in G1 phase and it can also interact with proliferating cell nuclear antigen (PCNA) via the C-terminus to block the activity of PCNA-activated DNA polymerase, thereby inhibiting DNA synthesis and arresting the cell cycle (55,56).…”

Section: Discussionmentioning

confidence: 99%

EGFR and ERK activation resists flavonoid quercetin‑induced anticancer activities in human cervical cancer cells in vitro

Chen

Zhang

et al. 2021

Oncol Lett

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In the present study, due to the complex and numerous targets of Sarcandrae Herb (also known as Zhong Jie Feng), network pharmacology was performed to analyze its therapeutic effect on 2 cervical cancer cell lines, which could assist with the development of novel therapies. The results suggested that the natural flavonoid quercetin (Que), the effective antitumor ingredient in SH, which is widely present in a variety of plants, may depend on the target, EGFR. Previous studies have shown that EGFR serves a crucial role in the occurrence and development of cervical cancer, but its downstream molecules and regulatory mechanisms remain unknown. The anti-cervical cancer cell properties of Que, which are present in ubiquitous plants, were examined in vitro to identify the association between Que and its underlying pathway using MTT assays, flow cytometry, western blot analysis and Transwell assays. It was found that Que reduced cervical cancer cell viability, promoted G 2 /M phase cell cycle arrest and cell apoptosis, as well as inhibited cell migration and invasion. The Tyr1068 phosphorylation site of EGFR and the corresponding ERK target were also examined and the 2 kinases were markedly activated by Que. Furthermore, the EGFR inhibitor, afatinib and the ERK inhibitor, U0126 blocked the increase of EGFR and ERK phosphorylation, and resulted in a notable enhancement of apoptosis and cell cycle arrest. Therefore, to the best of our knowledge, the current results provided the first evidence that EGFR and ERK activation induced by Que could resist Que-induced anticancer activities. On this basis, the present study determined the role of EGFR and the underlying signaling pathways involved in the anti-cervical cancer malignant behavior induced by Que and identified the negative regulatory association.

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Dual Repressive Function by Cip1, a Budding Yeast Analog of p21, in Cell-Cycle START Regulation

Cited by 11 publications

References 23 publications

RACK1 promotes the occurrence and progression of cervical carcinoma

RACK1 promotes the occurrence and progression of cervical carcinoma

Cip1 tunes cell cycle arrest duration upon calcineurin activation

EGFR and ERK activation resists flavonoid quercetin‑induced anticancer activities in human cervical cancer cells in vitro

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