scholarly journals Sesquiterpene Lactone Suppresses Vascular Smooth Muscle Cell Proliferation and Migration via Inhibition of Cell Cycle Progression

2007 ◽  
Vol 30 (9) ◽  
pp. 1754-1757 ◽  
Author(s):  
Munehiro Nakagawa ◽  
Takamasa Ohno ◽  
Rumi Maruyama ◽  
Munenori Okubo ◽  
Akito Nagatsu ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Sesquiterpene Lactone ◽  
Cell Cycle Progression ◽  
Cycle Progression ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals SKA3 overexpression promotes cell proliferation and migration in breast cancer cell lines

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Jaeyong Kang ◽  
Hansaem Kim ◽  
Hyangsoon Noh ◽  
Byung-Ha Kang ◽  
Jaejik Kim ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Cycle Progression ◽  
Breast Tumour ◽  
Breast Cancer Cell Lines ◽  
Cycle Progression ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

AbstractObjectivesBreast cancer (BC) is the most commonly diagnosed cancer in women worldwide with a high mortality rate, despite early detection and treatment. Spindle and kinetochore-associated complex subunit 3 (SKA3) is closely correlated with patient outcomes in several cancers. The present study aimed to elucidate the role of SKA3 in BC.MethodsThe biological functions of SKA3 was investigated by proliferation and migration assays in MDA-MB-231 cells with stable SKA3 knockdown and Hs578T cells ectopically expressing SKA3. Gene Expression Omnibus datasets were utilised to determine the correlation between SKA3 expression and clinical features of BC patients.ResultsWe confirmed that SKA3 mRNA expression is higher in breast tumour tissue than in normal tissue, and that higher SKA3 expression is associated with poor survival rate of BC patients. Knockdown of SKA3 reduced MDA-MB-231 cell proliferation and migration, whereas SKA3 overexpression enhanced the proliferative and migratory ability of Hs578T cells. We also found that SKA3 is involved in regulating cell cycle progression in mitotic exit.ConclusionsThese results suggest that SKA3 is correlated with BC cell proliferation and migration by promoting cell cycle progression, and could be a novel potential therapeutic target for BC treatment.

scholarly journals Loss of Canonical Insulin Signaling Accelerates Vascular Smooth Muscle Cell Proliferation and Migration Through Changes in p27Kip1 Regulation

Endocrinology ◽  
2010 ◽  
Vol 152 (2) ◽  
pp. 651-658 ◽  
Author(s):  
Daniel James Lightell ◽  
Stephanie Collier Moss ◽  
Thomas Cooper Woods
Keyword(s):  
Cell Cycle ◽  
Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Insulin Signaling ◽  
Cell Cycle Progression ◽  
Insulin Stimulation ◽  
Cycle Progression ◽  
Vsmc Proliferation ◽  
And Migration ◽  
Proliferation And Migration

Abstract Insulin resistance is associated with an accelerated rate of atherosclerosis. Vascular smooth muscle cell (VSMC) migration and proliferation are important components of atherosclerosis. To elucidate the effects of the loss of normal insulin receptor (IR) signaling on VSMC function, we compared the proliferation and migration of murine VSMCs lacking the IR (L2-VSMCs) with wild type (WT-VSMCs). We also examined changes in the response of L2-VSMCs to insulin stimulation and to inhibition of the mammalian target of rapamycin (mTOR), a kinase critical in VSMC proliferation and migration. The L2-VSMCs exhibit greater proliferation and migration rates compared with WT-VSMCs. L2-VSMCs also exhibit a resistance to the effects of rapamycin, an mTOR inhibitor, on proliferation, migration, and cell cycle progression. The resistance to mTOR inhibition is coupled with a loss of effect on the cyclin-dependent kinase inhibitor p27Kip1, an inhibitor of cell cycle progression and VSMC migration. In response to stimulation with physiological insulin, the L2-VSMCs exhibit a loss of Akt phosphorylation and a significantly increased activation of the ERK-1/2 compared with WT-VSMCs. Insulin stimulation also decreased p27Kip1 mRNA in L2-VSMCs but not in WT-VSMCs. The effect of insulin on p27Kip1 mRNA was blocked by pretreatment with an ERK-1/2 pathway inhibitor. We conclude that loss of canonical insulin signaling results in increased ERK-1/2 activation in response to physiological insulin that decreases p27Kip1 mRNA. These data demonstrate a potential mechanism where changes in IR signaling could lead to a decrease in p27Kip1, accelerating VSMC proliferation and migration.

scholarly journals Over-expression of ANP32E is associated with poor prognosis of pancreatic cancer and promotes cell proliferation and migration through regulating β-catenin

2020 ◽  
Author(s):  
Jianwei Zhang ◽  
Zhongmin Lan ◽  
Guotong Qiu ◽  
Hu Ren ◽  
Yajie Zhao ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Pancreatic Cancer ◽  
Cell Proliferation ◽  
Poor Prognosis ◽  
Cell Cycle Progression ◽  
Over Expression ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Cancer Tissues ◽  
Proliferation And Migration

Abstract Background: Pancreatic cancer is a malignant tumor with high mortality. Acidic nuclear phosphoprotein 32 family member E (ANP32E), a specific H2A.Z chaperone, has been shown to contribute to breast cancer development. However, the significance of ANP32E in pancreatic cancer is poorly understood. This study aimed to investigate the role of ANP32E in pancreatic cancer. Methods: The expression of ANP32E in 179 pancreatic cancer tissues and 171 normal tissues, and the correlation between ANP32E expression and patients’ survival were analyzed from the TCGA database. ANP32E was over-expressed and silenced using lentivirus. siRNA was used to knock down β-catenin. CCK8, colony formation, cell cycle and transwell experiments were performed to determine cell proliferation and migration. qRT-PCR and Western blot were conducted to detect mRNA and protein expression. Results: ANP32E was up-regulated in pancreatic cancer tissues and cells. Up-regulation of ANP32E predicted poor prognosis in pancreatic cancer patients. Lentivirus-mediated knockdown of ANP32E suppressed the proliferation, colony growth and migration of PANC1 and MIA cells. By contrast, ANP32E over-expression promoted the proliferation and migration of both cells. In addition, ANP32E accelerated the cell cycle progression in PANC1 and MIA cells. Molecular experiments showed that ANP32E activated β-catenin/cyclin D1 signaling. Silencing of β-catenin reduced cell proliferation and migration in ANP32E over-expressed cells. Conclusion: Our results propose that ANP32E functions as an oncogene in pancreatic cancer via activating β-catenin.

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