scholarly journals Retracted: The Effects of Ludartin on Cell Proliferation, Cell Migration, Cell Cycle Arrest and Apoptosis Are Associated with Upregulation of p21WAF1 in Saos-2 Osteosarcoma Cells In Vitro

2021 ◽  
Vol 27 ◽  
Author(s):  
Shuang-li Zhang ◽  
Bao-lin Li ◽  
Wei Li ◽  
Ming Lu ◽  
Lin-ying Ni ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Migration ◽  
Cell Cycle Arrest ◽  
Osteosarcoma Cells ◽  
Cycle Arrest

scholarly journals REG γ knockdown suppresses proliferation by inducing apoptosis and cell cycle arrest in osteosarcoma

PeerJ ◽  
2020 ◽  
Vol 8 ◽  
pp. e8954
Author(s):  
Zhiqiang Yin ◽  
Hao Jin ◽  
Shibo Huang ◽  
Guofan Qu ◽  
Qinggang Meng
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Cycle Arrest ◽  
Cell Lines ◽  
Western Blotting ◽  
Caspase 3 ◽  
Cell Counting ◽  
Osteosarcoma Cells ◽  
Cycle Arrest

Background Osteosarcoma (OS) is the most common malignant bone tumor with high mortality in children and adolescents. REG γ is overexpressed and plays oncogenic roles in various types of human cancers. However, the expression and potential roles of REG γ in osteosarcoma are elusive. This study aims at exploring possible biological functions of REG γ in the pathogenesis of osteosarcoma and its underlying mechanism. Methods Quantitativereverse transcription-polymerase chain reaction (qRT-PCR), western blotting andimmunohistochemistry (IHC)were performed to detect the expression levels of REG γ in OS tissues and cell lines. Then, the effects of REG γ expression on OS cell proliferation in vitro were analyzed by Cell Counting Kit-8 (CCK-8), ethylene deoxyuridine (EdU), colony formation, flow cytometry. The protein levels of apoptosis and cell-cycle related proteins were evaluated using western blotting. Results In present study, we found for the first time that REG γ is overexpressed in osteosarcoma tissues and cell lines and knockdown of REG γ significantly inhibits cell proliferation and induces apoptosis and cell cycle arrest in osteosarcoma cells. Furthermore, we observed that p21, caspase-3 and cleaved caspase-3 are increased while the expression of cycinD1 and bcl-2 are decreased after REG γ depletion in osteosarcoma cells. In conclusion, REG γ may be involved in the proliferation of osteosarcoma and serve as a novel therapeutic target in patients with osteosarcoma.

scholarly journals Immortalization-Upregulated Protein Promotes Pancreatic Cancer Progression By Regulating NPM1/FHL1-Mediated Cell-Cycle-Checkpoint Protein Activity

2021 ◽  
Author(s):  
Qiankun Luo ◽  
Yanfeng Pan ◽  
Qiang Fu ◽  
Xu Zhang ◽  
Shuai Zhou ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Cycle Arrest ◽  
Cancer Progression ◽  
Cell Cycle Checkpoint ◽  
The Cancer Genome Atlas ◽  
Ductal Adenocarcinoma ◽  
Cycle Arrest ◽  
Cycle Checkpoint

Abstract Immortalization-upregulated protein (IMUP) plays a vital role in cell proliferation and tumor progression. However, its role in pancreatic ductal adenocarcinoma (PDAC) remains unclear. Here, we select IMUP as an alternative gene based on GeneChip analysis of clinical PDAC tissues and transcriptome data from The Cancer Genome Atlas. IMUP expression is upregulated in PDAC tumor tissues. Moreover, high IMUP expression correlates with poor prognosis, while IMUP depletion inhibits PDAC cell proliferation and colony formation capacity in vitro, and decreases xenograft tumor growth in vivo. IMUP downregulation leads to cell-cycle arrest in the S phase. IMUP Knockdown increases the expression of four-and-a-half LIM domain protein 1 (FHL1), which regulates the phosphorylation of cell division cycle 25A (CDC25A) by cycle checkpoint kinase 1 (CHK1) and promotes cytoplasmic distribution of CDC25A by interaction with 14-3-3ξ. Furthermore, FHL1 knockdown restores the effects induced by IMUP depletion. liquid chromatography tandem mass spectrometry and immunoprecipitation analysis further show that IMUP interacts directly with nucleophosmin (NPM1) and enhances its stability. DNA methylation sequencing shows that FHL1 promoter methylation decreases when IMUP is downregulated. Overexpression of NPM1 can increase the methylation level of FHL1, thereby decreasing its expression. Our study provides a novel perspective on IMUP/NPM1/FHL1-mediated cell-cycle arrest by regulating CDC25A phosphorylation in PDAC. These findings may provide a new therapeutic target for PDAC.

scholarly journals Sulforaphane induces cell cycle arrest and apoptosis in murine osteosarcoma cells in vitro and inhibits tumor growth in vivo

2007 ◽  
Author(s):  
Taka-aki Matsui ◽  
Hiroaki Murata ◽  
Tomoya Sakabe ◽  
Yoshihiro Sowa ◽  
Naoyuki Horie ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Tumor Growth ◽  
Cell Cycle Arrest ◽  
Osteosarcoma Cells ◽  
Cycle Arrest ◽  
Murine Osteosarcoma

scholarly journals CCT Chaperonin Complex Is Required for the Biogenesis of Functional Plk1

2005 ◽  
Vol 25 (12) ◽  
pp. 4993-5010 ◽  
Author(s):  
Xiaoqi Liu ◽  
Chin-Yo Lin ◽  
Ming Lei ◽  
Shi Yan ◽  
Tianhua Zhou ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Cycle Arrest ◽  
Mammalian Cells ◽  
Active Form ◽  
Cycle Arrest ◽  
Cdc2 Activity ◽  
Partial Depletion

ABSTRACT Experiments from several different organisms have demonstrated that polo-like kinases are involved in many aspects of mitosis and cytokinesis. Here, we provide evidence to show that Plk1 associates with chaperonin-containing TCP1 complex (CCT) both in vitro and in vivo. Silencing of CCT by use of RNA interference (RNAi) in mammalian cells inhibits cell proliferation, decreases cell viability, causes cell cycle arrest with 4N DNA content, and leads to apoptosis. Depletion of CCT in well-synchronized HeLa cells causes cell cycle arrest at G2, as demonstrated by a low mitotic index and Cdc2 activity. Complete depletion of Plk1 in well-synchronized cells also leads to G2 block, suggesting that misfolded Plk1 might be responsible for the failure of CCT-depleted cells to enter mitosis. Moreover, partial depletion of CCT or Plk1 leads to mitotic arrest. Finally, the CCT-depleted cells reenter the cell cycle upon reintroduction of the purified constitutively active form of Plk1, indicating that Plk1 might be a CCT substrate.

Sign in / Sign up

Export Citation Format

Share Document