scholarly journals Human papillomavirus 16/18 E5 promotes cervical cancer cell proliferation, migration and invasion in vitro and accelerates tumor growth in vivo

2012 ◽  
Vol 29 (1) ◽  
pp. 95-102 ◽  
Author(s):  
SHUJIE LIAO ◽  
DONGRUI DENG ◽  
WEINA ZHANG ◽  
XIAOJI HU ◽  
WEI WANG ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Human Papillomavirus ◽  
Tumor Growth ◽  
Cancer Cell ◽  
Migration And Invasion ◽  
Cancer Cell Proliferation ◽  
Human Papillomavirus 16

Growth factor progranulin contributes to cervical cancer cell proliferation and transformation in vivo and in vitro

2014 ◽  
Vol 134 (2) ◽  
pp. 364-371 ◽  
Author(s):  
Yi Lu ◽  
Lin Zheng ◽  
Wen Zhang ◽  
Tingting Feng ◽  
Juan Liu ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Growth Factor ◽  
Cancer Cell ◽  
Cervical Cancer Cell ◽  
Cancer Cell Proliferation

Inhibition of Cancer Cell Proliferation in vitro and Tumor Growth in vivo by Hydrophis spiralis Sea Snake Venom

2007 ◽  
Vol 3 (4) ◽  
pp. 186-190
Author(s):  
R. Karthikeya ◽  
S. Karthigaya ◽  
M. Sri Balasubash ◽  
S. Vijayalaks ◽  
S.T. Somasundar ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Tumor Growth ◽  
Cancer Cell ◽  
Snake Venom ◽  
Cancer Cell Proliferation ◽  
Sea Snake ◽  
Proliferation In Vitro

scholarly journals MiR-212-3p functions as a tumor suppressor gene in group 3 medulloblastoma via targeting nuclear factor I/B (NFIB)

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Naveenkumar Perumal ◽  
Ranjana K. Kanchan ◽  
David Doss ◽  
Noah Bastola ◽  
Pranita Atri ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Tumor Suppressor ◽  
Cancer Cell ◽  
Migration And Invasion ◽  
Stem Cell Markers ◽  
Cancer Cell Proliferation ◽  
Group 3

AbstractHaploinsufficiency of chromosome 17p and c-Myc amplification distinguish group 3 medulloblastomas which are associated with early metastasis, rapid recurrence, and swift mortality. Tumor suppressor genes on this locus have not been adequately characterized. We elucidated the role of miR-212-3p in the pathophysiology of group 3 tumors. First, we learned that miR-212-3p undergoes epigenetic silencing by histone modifications in group 3 tumors. Restoring its expression reduced cancer cell proliferation, migration, colony formation, and wound healing in vitro and attenuated tumor burden and improved survival in vivo. MiR-212-3p also triggered c-Myc destabilization and degradation, leading to elevated apoptosis. We then isolated an oncogenic target of miR-212-3p, i.e. NFIB, a nuclear transcription factor implicated in metastasis and recurrence in various cancers. Increased expression of NFIB was confirmed in group 3 tumors and associated with poor survival. NFIB silencing reduced cancer cell proliferation, migration, and invasion. Concurrently, reduced medullosphere formation and stem cell markers (Nanog, Oct4, Sox2, CD133) were noted. These results substantiate the tumor-suppressive role of miR-212-3p in group 3 MB and identify a novel oncogenic target implicated in metastasis and tumor recurrence.

scholarly journals Lentivirus-Mediated VEGF Knockdown Suppresses Gastric Cancer Cell Proliferation and Tumor Growth in vitro and in vivo

2020 ◽  
Vol Volume 13 ◽  
pp. 1331-1341 ◽  
Author(s):  
Jong-Hyung Park ◽  
Jin-Hee Seo ◽  
Hee-Yeon Jeon ◽  
Sun-Min Seo ◽  
Han-Kyul Lee ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Tumor Growth ◽  
Cancer Cell ◽  
Gastric Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Gastric Cancer Cell Proliferation

scholarly journals miR-506 suppresses cervical cancer cell proliferation both in vitro and in vivo

Neoplasma ◽  
2018 ◽  
Vol 65 (03) ◽  
pp. 331-338 ◽  
Author(s):  
M. GONG ◽  
C. CHEN ◽  
H. ZHAO ◽  
M. SUN ◽  
M. SONG
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
Cervical Cancer Cell ◽  
Cancer Cell Proliferation

scholarly journals Silencing VDAC1 Expression by siRNA Inhibits Cancer Cell Proliferation and Tumor Growth In Vivo

2017 ◽  
Vol 8 ◽  
pp. 493 ◽  
Author(s):  
Tasleem Arif ◽  
Lilia Vasilkovsky ◽  
Yael Refaely ◽  
Alexander Konson ◽  
Varda Shoshan-Barmatz
Keyword(s):  
Cell Proliferation ◽  
Tumor Growth ◽  
Cancer Cell ◽  
Cancer Cell Proliferation

scholarly journals LINC00511 is associated with the malignant status and promotes cell proliferation and motility in cervical cancer

2019 ◽  
Vol 39 (9) ◽  
Author(s):  
Chun-Ling Yu ◽  
Xiao-Ling Xu ◽  
Fang Yuan
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Cancer Patients ◽  
Cancer Cell ◽  
Clinical Stage ◽  
Cervical Cancer Cell ◽  
Migration And Invasion ◽  
Epithelial Cell Line ◽  
Cancer Cell Proliferation ◽  
Poor Overall Survival

Abstract LINC00511 is a newly identified lncRNA that is up-regulated in many types of human cancers and may serve as an oncogenic lncRNA. However, there was no report about the role of LINC00511 in cervical cancer. Therefore, we investigated the clinical value of LINC00511 in cervical cancer patients via analyzing the correlation between LINC00511 expression and clinicopathological features. Moreover, we performed loss-of-function study to estimate the effect of LINC00511 on cervical cancer cell proliferation, migration, and invasion. In our study, we found LINC00511 expression levels were increased in cervical cancer tissues and cell lines compared with adjacent normal tissues and normal cervical epithelial cell line, respectively. High LINC00511 expression was correlated with advanced clinical stage, large tumor size, histological type of adenocarcinoma, and present lymph node metastasis, distant metastasis, and poor overall survival in cervical cancer patients. The in vitro studies indicated that knockdown of LINC00511 inhibited cervical cancer cell proliferation, migration, and invasion. In conclusion, LINC00511 acts as oncogenic lncRNA in cervical cancer, and may be a novel biomarker and potential therapeutic target for cervical cancer patients.

scholarly journals PRMT1-mediated EZH2 methylation promotes breast cancer cell proliferation and tumorigenesis

2021 ◽  
Vol 12 (11) ◽  
Author(s):  
Zhongwei Li ◽  
Diandian Wang ◽  
Xintian Chen ◽  
Wenwen Wang ◽  
Pengfei Wang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cell Cycle Progression ◽  
Cancer Cell Proliferation ◽  
Breast Cancer Cell Proliferation ◽  
Ezh2 Expression

AbstractProtein arginine methyltransferase 1 (PRMT1) is able to promote breast cancer cell proliferation. However, the detailed mechanisms of PRMT1-mediated breast cancer cell proliferation are largely unknown. In this study, we reveal that PRMT1-mediated methylation of EZH2 at the R342 site (meR342-EZH2) has a great effect on PRMT1-induced cell proliferation. We also demonstrate that meR342-EZH2 can accelerate breast cancer cell proliferation in vitro and in vivo. Further, we show that meR342-EZH2 promotes cell cycle progression by repressing P16 and P21 transcription expression. In terms of mechanism, we illustrate that meR342-EZH2 facilitates EZH2 binding with SUZ12 and PRC2 assembly by preventing AMPKα1-mediated phosphorylation of pT311-EZH2, which results in suppression of P16 and P21 transcription by enhancing EZH2 expression and H3K27me3 enrichment at P16 and P21 promoters. Finally, we validate that the expression of PRMT1 and meR342-EZH2 is negatively correlated with pT311-EZH2 expression. Our findings suggest that meR342-EZH2 may become a novel therapeutic target for the treatment of breast cancer.

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