p27kip1 haploinsufficiency preserves myocardial function in the early stages of myocardial infarction via Atg5‑mediated autophagy flux restoration

Zhou, Ningtian; Huang, Qiong; Cheng, Weili; Ge, Yali; Li, Dianfu; Wang, Junhong

doi:10.3892/mmr.2019.10632

Cited by 2 publications

(2 citation statements)

References 29 publications

(45 reference statements)

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“…[11][12][13] It can be regarded that p27 Kip1 may act as an important regulator in the growth of malignant tumors by regulation of CDK2 and cyclin E1. 14 Besides, downregulation of p27 Kip1 has been regarded as an independent prognostic factor in GBC. 15 In the current study, we aimed to investigate the function of miR-575 during the tumorigenesis of GBC and explore the correction between miR-575 and p27 Kip1.…”

Section: Introductionmentioning

confidence: 99%

<p>Downregulation of miR-575 Inhibits the Tumorigenesis of Gallbladder Cancer via Targeting p27 Kip1</p>

Qin

Huang

et al. 2020

OTT

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Background: Gallbladder cancer (GBC) is the most common biliary tract malignant cancer worldwide. It has been reported that microRNA-575 (miR-575) was involved in the tumorigenesis of many cancers. However, the role of miR-575 during the progression of GBC remains largely unknown. Methods: The expression of miR-575 in GBC cells was detected by quantitative real-time polymerase chain reaction. The proliferation of GBC cells was examined by CCK-8 assay and Ki-67 staining. Apoptosis of GBC cells was measured by flow cytometry, and cell invasion was tested by transwell assay. Moreover, protein expressions in GBC cells were evaluated using Western blot. The target gene of miR-575 was predicted using Targetscan and miRDB. Finally, xenograft tumor model was established to verify the function of miR-575 in GBC in vivo. Results: Our findings indicated that miR-575 antagonist decreased the proliferation and invasion of GBC cells. In addition, miR-575 antagonist significantly induced apoptosis of GBC cells via inducing G1 arrest. Meanwhile, p27 Kip1 was found to be a direct target of miR-575 with luciferase reporter assay. Moreover, miR-575 antagonist significantly decreased the expressions of CDK1 and cyclin E1 and upregulated the levels of cleaved caspase3 and p27 Kip1 in GBC cells. Finally, miR-575 antagonist notably suppressed GBC tumor growth in vivo. Conclusion: Downregulation of miR-575 significantly inhibited the tumorigenesis of GBC via targeting p27 Kip1. Thus, miR-575 might be a potential novel target for the treatment of GBC.

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Section: Introductionmentioning

confidence: 99%

<p>Downregulation of miR-575 Inhibits the Tumorigenesis of Gallbladder Cancer via Targeting p27 Kip1</p>

Qin

Huang

et al. 2020

OTT

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“…Indeed, in endometriosis, p27 appears significantly reduced, and in congenital eye alteration, p27 post-synthetic changes have been demonstrated [ 108 , 109 ]. Haploinsufficiency of CDKN1B was demonstrated to improve cardiac function in mice post-myocardial infarction [ 110 ]. Finally, a role of p27 in subarachnoid hemorrhage has been reported [ 111 ].…”

Section: Perspectives and Conclusion P27 Human Diseases And Drug Designmentioning

confidence: 99%

p27Kip1, an Intrinsically Unstructured Protein with Scaffold Properties

Bencivenga

Stampone

Roberti

et al. 2021

Cells

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The Cyclin-dependent kinase (CDK) regulator p27Kip1 is a gatekeeper of G1/S transition. It also regulates G2/M progression and cytokinesis completion, via CDK-dependent or -independent mechanisms. Recently, other important p27Kip1 functions have been described, including the regulation of cell motility and migration, the control of cell differentiation program and the activation of apoptosis/autophagy. Several factors modulate p27Kip1 activities, including its level, cellular localization and post-translational modifications. As a matter of fact, the protein is phosphorylated, ubiquitinated, SUMOylated, O-linked N-acetylglicosylated and acetylated on different residues. p27Kip1 belongs to the family of the intrinsically unstructured proteins and thus it is endowed with a large flexibility and numerous interactors, only partially identified. In this review, we look at p27Kip1 properties and ascribe part of its heterogeneous functions to the ability to act as an anchor or scaffold capable to participate in the construction of different platforms for modulating cell response to extracellular signals and allowing adaptation to environmental changes.

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p27kip1 haploinsufficiency preserves myocardial function in the early stages of myocardial infarction via Atg5‑mediated autophagy flux restoration

Cited by 2 publications

References 29 publications

<p>Downregulation of miR-575 Inhibits the Tumorigenesis of Gallbladder Cancer via Targeting p27 Kip1</p>

<p>Downregulation of miR-575 Inhibits the Tumorigenesis of Gallbladder Cancer via Targeting p27 Kip1</p>

p27Kip1, an Intrinsically Unstructured Protein with Scaffold Properties

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