scholarly journals microRNA-1296 Inhibits Glioma Cell Growth by Targeting ABL2

2021 ◽  
Vol 20 ◽  
pp. 153303382199000
Author(s):  
Gaolian Zhang ◽  
Meng Xia ◽  
Jianhui Guo ◽  
Yi Huang ◽  
Jianrong Huang ◽  
...  
Keyword(s):  
Glioma Cell ◽  
Karnofsky Performance Scale ◽  
The Novel ◽  
Inhibitory Effects ◽  
Aberrant Expression ◽  
Who Grade ◽  
Glioma Cell Proliferation ◽  
Mrna And Protein Expression ◽  
Induced Apoptosis ◽  
Tumor Suppressive Function

Aberrant expression of microRNAs (miRNAs) has been reported to play a role in tumorigenesis. Dysfunction of miR-1296 was found in a variety of cancers, however, the function of miR-1296 in the progression of glioma remains largely understood. Here, our results showed that miR-1296 was significantly down-regulated in glioma tissues and cell lines. Decreased expression of miR-1296 was associated with the tumor size, WHO grade and karnofsky performance scale (KPS) of glioma patients. Low expression of miR-1296 was significantly correlated with the shorter 5-year overall survival of glioma patients. Overexpression of miR-1296 inhibited the proliferation, colony formation, migration and induced apoptosis of glioma cells. MiR-1296 was found to bind the 3’-untranslated region (UTR) of ABL proto-oncogene 2 (ABL2) and subsequently repressed both the mRNA and protein expression of ABL2. ABL2 was overexpressed in glioma tissues and inversely correlated with that of miR-1296. Ectopic expressed ABL2 could reverse the inhibitory effects of miR-1296 on glioma cell proliferation. Our results illustrated the novel tumor-suppressive function of miR-1296 in glioma via repressing ABL2, suggesting a potential application of miR-1296 in the treatment of glioma.

scholarly journals TRPV2 channel negatively controls glioma cell proliferation and resistance to Fas-induced apoptosis in ERK-dependent manner

2010 ◽  
Vol 31 (5) ◽  
pp. 794-803 ◽  
Author(s):  
Massimo Nabissi ◽  
Maria Beatrice Morelli ◽  
Consuelo Amantini ◽  
Valerio Farfariello ◽  
Lucia Ricci-Vitiani ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Glioma Cell ◽  
Dependent Manner ◽  
Glioma Cell Proliferation ◽  
Induced Apoptosis

Isoliquiritigenin Inhibits Proliferation and Induces Apoptosis in Tongue Squamous Cell Carcinoma by Modulating miR-21/FOXG1 Pathway

2019 ◽  
Vol 17 (4) ◽  
pp. 463-469
Author(s):  
Hou Deqiang ◽  
Gao Yufeng ◽  
Bai Ning ◽  
Dong Yu
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Carcinoma Cells ◽  
Tongue Squamous Cell Carcinoma ◽  
Luciferase Assay ◽  
Forkhead Box ◽  
Proliferation And Apoptosis ◽  
Mrna And Protein Expression ◽  
Induced Apoptosis

Isoliquiritigenin is a flavonoid commonly found in liquorice and has been identified as a potent anti-tumor agent. The aim of this study was to investigate whether isoliquiritigenin regulates the proliferation and apoptosis of tongue squamous cell carcinoma cells by regulating forkhead box G1 expression via miR-21. MTT assay and flow cytometry were used to analyze cell proliferation and apoptosis, respectively. Quantitative real time polymerase chain reaction and western blotting were used to detect mRNA and protein expression levels, respectively. The relationship between miR-21 and forkhead box G1 was detected by dual luciferase assay. Isoliquiritigenin inhibited proliferation and induced apoptosis of tongue squamous cell carcinoma cells, and decreased miR-21 levels and promoted forkhead box G1 expression. Forkhead box G1 was then identified as a target of miR-21 and ISL could promote forkhead box G1 expression by inhibiting miR-21. Further analysis suggested that upregulation of miR-21 improved proliferation and suppressed apoptosis of tongue squamous cell carcinoma cells by inhibiting forkhead box G1 expression. Finally, our results revealed that isoliquiritigenin inhibited proliferation and induced apoptosis of tongue squamous cell carcinoma cells by regulating miR-21. Isoliquiritigenin might act as a novel therapeutic treatment for tongue squamous cell carcinoma cells through up-regulation of forkhead box G1 expression via inhibiting miR-21expression.

Discovery of N-Phenyl-4-(1H-pyrrol-3-yl)pyrimidin-2-amine Derivatives as Potent Mnk2 Inhibitors: Design, Synthesis, SAR Analysis, and Evaluation of in vitro Anti-leukaemic Activity

2019 ◽  
Vol 15 (6) ◽  
pp. 602-623 ◽  
Author(s):  
Ahmed M. Abdelaziz ◽  
Sarah Diab ◽  
Saiful Islam ◽  
Sunita K.C. Basnet ◽  
Benjamin Noll ◽  
...  
Keyword(s):  
Proliferative Activity ◽  
Myeloid Cell ◽  
Structural Diversity ◽  
Translation Initiation Factor ◽  
Initiation Factor ◽  
Cell Leukaemia ◽  
Aberrant Expression ◽  
Design Synthesis ◽  
Induced Apoptosis

Background:Aberrant expression of eukaryotic translation initiation factor 4E (eIF4E) is common in many types of cancer including acute myeloid leukaemia (AML). Phosphorylation of eIF4E by MAPK-interacting kinases (Mnks) is essential for the eIF4E-mediated oncogenic activity. As such, the pharmacological inhibition of Mnks can be an effective strategy for the treatment of cancer.Methods:A series of N-phenyl-4-(1H-pyrrol-3-yl)pyrimidin-2-amine derivatives was designed and synthesised. The Mnk inhibitory activity of these derivatives as well as their anti-proliferative activity against MV4-11 AML cells was determined.Results:These compounds were identified as potent Mnk2 inhibitors. Most of them demonstrated potent anti-proliferative activity against MV4-11 AML cells. The cellular mechanistic studies of the representative inhibitors revealed that they reduced the level of phosphorylated eIF4E and induced apoptosis by down-regulating the anti-apoptotic protein myeloid cell leukaemia 1 (Mcl-1) and by cleaving poly(ADP-ribose)polymerase (PARP). The lead compound 7k possessed desirable pharmacokinetic properties and oral bioavailability.Conclusion:This work proposes that exploration of the structural diversity in the context of Nphenyl- 4-(1H-pyrrol-3-yl)pyrimidin-2-amine would offer potent and selective Mnk inhibitors.

miR-25 promotes glioma cell proliferation by targeting CDKN1C

2015 ◽  
Vol 71 ◽  
pp. 7-14 ◽  
Author(s):  
Jihong Zhang ◽  
Xuhai Gong ◽  
Kaiyu Tian ◽  
Dongkai Chen ◽  
Jiahang Sun ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Glioma Cell ◽  
Glioma Cell Proliferation

Enhancement of temozolomide-induced apoptosis by valproic acid in human glioma cell lines through redox regulation

2011 ◽  
Vol 89 (3) ◽  
pp. 303-315 ◽  
Author(s):  
Ching-Hsein Chen ◽  
Yu-Jia Chang ◽  
Maurice S. B. Ku ◽  
King-Thom Chung ◽  
Jen-Tsung Yang
Keyword(s):  
Valproic Acid ◽  
Cell Lines ◽  
Glioma Cell ◽  
Redox Regulation ◽  
Human Glioma ◽  
Human Glioma Cell ◽  
Glioma Cell Lines ◽  
Induced Apoptosis

scholarly journals NOTCH3 Is a Prognostic Factor That Promotes Glioma Cell Proliferation, Migration and Invasion via Activation of CCND1 and EGFR

PLoS ONE ◽  
2013 ◽  
Vol 8 (10) ◽  
pp. e77299 ◽  
Author(s):  
Mohammad A. Y. Alqudah ◽  
Supreet Agarwal ◽  
Maha S. Al-Keilani ◽  
Zita A. Sibenaller ◽  
Timothy C. Ryken ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Prognostic Factor ◽  
Glioma Cell ◽  
Migration And Invasion ◽  
Glioma Cell Proliferation

scholarly journals prICE: a downstream target for ceramide-induced apoptosis and for the inhibitory action of Bcl-2

1996 ◽  
Vol 316 (1) ◽  
pp. 25-28 ◽  
Author(s):  
Miriam J. SMYTH ◽  
David K. PERRY ◽  
Jiandi ZHANG ◽  
Guy G. POIRIER ◽  
Yusuf A. HANNUN ◽  
...  
Keyword(s):  
Cell Death ◽  
Inhibitory Action ◽  
Second Messenger ◽  
The Novel ◽  
Over Expression ◽  
Downstream Target ◽  
Induced Apoptosis ◽  
Insight Into

The novel lipid second messenger, ceramide, specifically induced poly(ADP-ribose) polymerase cleavage through activation of the protease prICE. Over-expression of Bcl-2 inhibited ceramide-induced poly(ADP-ribose) polymerase proteolysis and protected cells from ceramide-induced death. These data provide the first insight into the mechanism by which ceramide mediates apoptosis and suggest a mechanism by which Bcl-2 protects from cell death.

Age-related and photoperiodic variation of the DAZ gene family in the testis of the Syrian hamster (Mesocricetus auratus)

Zygote ◽  
2018 ◽  
Vol 26 (2) ◽  
pp. 127-134 ◽  
Author(s):  
Candela Rocío González ◽  
Luciana Moverer ◽  
Ricardo Saúl Calandra ◽  
Silvia Inés González-Calvar ◽  
Alfredo Daniel Vitullo
Keyword(s):  
Protein Expression ◽  
Gene Family ◽  
Syrian Hamster ◽  
Mesocricetus Auratus ◽  
Cell Number ◽  
The Novel ◽  
Age Related ◽  
Mrna And Protein Expression ◽  
Long Photoperiod ◽  
Daz Gene

SummaryThe Deleted in AZoospermia (DAZ) gene family regulates the development, maturation and maintenance of germ cells and spermatogenesis in mammals. The DAZ family consists of two autosomal genes, Boule and Dazl (Daz-like), and the Daz gene on chromosome Y. The aim of this study was to analyze the localization of DAZL and BOULE during testicular ontogeny of the seasonal-breeding Syrian hamster, Mesocricetus auratus. We also evaluated the testicular expression of DAZ family genes under short- or long-photoperiod conditions. In the pre-pubertal and adult testis, DAZL protein was found mainly in spermatogonia. BOULE was found in the spermatogonia from 20 days of age and during the pre-pubertal and adult period it was also detected in spermatocytes and round spermatids. DAZL and BOULE expression in spermatogonia was strictly nuclear only in 20-day-old hamsters. We also detected the novel mRNA and protein expression of BOULE in Leydig cells. In adult hamsters, Dazl expression was increased in regressed testis compared with non-regressed testis and DAZL protein expression was restricted to primary spermatocytes in regressed testis. These results show that DAZL and BOULE are expressed in spermatogonia at early stages in the Syrian hamster, then both proteins translocate to the cytoplasm when meiosis starts. In the adult regressed testis, the absence of DAZL in spermatogonia might be related to the decrease in germ cell number, suggesting that DAZ gene family expression is involved in changes in seminiferous epithelium during photoregression.

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