p53 Retards cell-growth and suppresses etoposide-induced apoptosis in Pin1-deficient mouse embryonic fibroblasts

Shimazaki, K; Uchida, Takafumi; Komine, Akihiko; Takahashi, K.

doi:10.1016/j.bbrc.2012.04.121

Cited by 4 publications

(4 citation statements)

References 26 publications

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“…This defect depends on a tumor suppressor, p 53 [8]. These results suggest that both Pin1 and p53 might be essential for cell-cycle regulation [7][8][9]. With aging, Pin 1-/-mice showed immature germ cells, mammary gland impairment, and retinal dystrophy, i.e., decreased levels of cyclin D1 that resulted in cyclin D1-/-mice phenotypes.…”

Section: Introductionmentioning

confidence: 89%

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L-balenine inhibits the catalytic activity of Pin1, a peptidyl prolyl <i>cis/trans</i>-isomerase

et al. 2020

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Purpose: Pin1 is a peptidyl prolyl cis/trans-isomerase (PPIase) that regulates phosphorylated protein function by cistrans-isomerization. Pin1 catalytic activity has been associated with the pathogenesis of cancer, asthma, neurodegenerative diseases, nonalcoholic steatohepatitis, and viral infections. Recently, imidazole dipeptide molecules from natural products have attracted interest as functional food components. Here, we evaluated the effects of natural imidazole dipeptides on the PPIase activity of Pin1 to identify novel Pin1 inhibitors. Methods: PPIase catalytic activity of Pin1 was measured using chymotrypsin-coupled isomer specific protein degradation. The test substance was preincubated with recombinant Pin1 to form their complex. Results: Our results showed that among the imidazole dipeptide molecules, L-balenine, and not L-anserine and Lcarnosine, reduced the PPIase activity of Pin1. Both β-alanine and 1-methyl-L-histidine obtained by hydrolysis of Lbalenine did not affect Pin1 PPIase activity. These results suggested that the structure of L-balenine allows it to occupy the active site of the Pin1 enzyme. Conclusion: Among imidazole dipeptides from natural products, L-balenine inhibited the PPIase catalytic activity of Pin 1.

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Section: Introductionmentioning

confidence: 89%

“…Although embryonic Pin1-/-fibroblasts grew normally, they proved significantly deficient in their ability to restart proliferation in response to serum stimulation after G0 arrest [7]. This defect depends on a tumor suppressor, p 53 [8]. These results suggest that both Pin1 and p53 might be essential for cell-cycle regulation [7][8][9].…”

Section: Introductionmentioning

confidence: 92%

L-balenine inhibits the catalytic activity of Pin1, a peptidyl prolyl <i>cis/trans</i>-isomerase

et al. 2020

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“…The prolyl isomerase Pin1 is a P53 binding protein [105]. It participates in the cell cycle progression through regulation of cell cycle-related proteins such as CDK1, CDC25C, Wee1, Myt1, and PLK1, and regulates G2/M progression.…”

Section: Pin1 Catalyzes Conformational Change Of Cdc25c and Promotes ...mentioning

confidence: 99%

The role of CDC25C in cell cycle regulation and clinical cancer therapy: a systematic review

et al. 2020

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One of the most prominent features of tumor cells is uncontrolled cell proliferation caused by an abnormal cell cycle, and the abnormal expression of cell cycle-related proteins gives tumor cells their invasive, metastatic, drug-resistance, and anti-apoptotic abilities. Recently, an increasing number of cell cycle-associated proteins have become the candidate biomarkers for early diagnosis of malignant tumors and potential targets for cancer therapies. As an important cell cycle regulatory protein, Cell Division Cycle 25C (CDC25C) participates in regulating G2/M progression and in mediating DNA damage repair. CDC25C is a cyclin of the specific phosphatase family that activates the cyclin B1/CDK1 complex in cells for entering mitosis and regulates G2/M progression and plays an important role in checkpoint protein regulation in case of DNA damage, which can ensure accurate DNA information transmission to the daughter cells. The regulation of CDC25C in the cell cycle is affected by multiple signaling pathways, such as cyclin B1/CDK1, PLK1/Aurora A, ATR/CHK1, ATM/CHK2, CHK2/ERK, Wee1/Myt1, p53/Pin1, and ASK1/JNK-/38. Recently, it has evident that changes in the expression of CDC25C are closely related to tumorigenesis and tumor development and can be used as a potential target for cancer treatment. This review summarizes the role of CDC25C phosphatase in regulating cell cycle. Based on the role of CDC25 family proteins in the development of tumors, it will become a hot target for a new generation of cancer treatments.

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“…The expression levels of ARF, p53, and p21 were elevated in senescent MEFs cells and during senescence induced by the oncogenic signal H-ras. Mouse fibroblasts with humanized p53 (Hupki cells, derived from a human p53 knock-in mouse model) first senesce ( 111 , 112 ).In addition, telomeres become progressively shorter in length, and once the length reaches a critical threshold, the telomeres signal to p53 for growth arrest via the ATM pathway, and upregulate p21 to lead to G1 arrest via the p19ARF/p53/p21 pathway, ultimately leading to cell senescence ( 113 , 114 ).…”

Section: Cell Senescence Related Factorsmentioning

confidence: 99%

The role of oxidative stress in intervertebral disc cellular senescence

et al. 2022

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With the aggravation of social aging and the increase in work intensity, the prevalence of spinal degenerative diseases caused by intervertebral disc degeneration(IDD)has increased yearly, which has driven a heavy economic burden on patients and society. It is well known that IDD is associated with cell damage and degradation of the extracellular matrix. In recent years, it has been found that IDD is induced by various mechanisms (e.g., genetic, mechanical, and exposure). Increasing evidence shows that oxidative stress is a vital activation mechanism of IDD. Reactive oxygen species (ROS) and reactive nitrogen species (RNS) could regulate matrix metabolism, proinflammatory phenotype, apoptosis, autophagy, and aging of intervertebral disc cells. However, up to now, our understanding of a series of pathophysiological mechanisms of oxidative stress involved in the occurrence, development, and treatment of IDD is still limited. In this review, we discussed the oxidative stress through its mechanisms in accelerating IDD and some antioxidant treatment measures for IDD.

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p53 Retards cell-growth and suppresses etoposide-induced apoptosis in Pin1-deficient mouse embryonic fibroblasts

Cited by 4 publications

References 26 publications

L-balenine inhibits the catalytic activity of Pin1, a peptidyl prolyl <i>cis/trans</i>-isomerase

L-balenine inhibits the catalytic activity of Pin1, a peptidyl prolyl <i>cis/trans</i>-isomerase

The role of CDC25C in cell cycle regulation and clinical cancer therapy: a systematic review

The role of oxidative stress in intervertebral disc cellular senescence

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