scholarly journals LncRNA DCST1-AS1 downregulates miR-29b through methylation in glioblastoma (GBM) to promote cancer cell proliferation

2020 ◽  
Author(s):  
Sheng Hu ◽  
Yiqun Yao ◽  
Xiao Hu ◽  
Yongjian Zhu
Keyword(s):  
Cell Proliferation ◽  
Mortality Rate ◽  
Cancer Cell ◽  
Reverse Transcription ◽  
Brain Cancer ◽  
Methylation Level ◽  
Cancer Cell Proliferation ◽  
Inhibitory Effects ◽  
Poor Survival

Abstract Background: Glioblastoma (GBM) is the most malignant form of brain cancer, owing to the high mortality rate. We in this study analyzed the role of DCST1-AS1 in glioblastoma (GBM).Methods: QuantiTect Reverse Transcription Kit (QIAGEN) was used, with RNA samples as template to synthesize cDNA. Results: It is observed that upregulation of DCST1-AS1 in GBM predicted poor survival. MiR-29b was downregulated in GBM and inversely correlated with the expression of DCST1-AS1. In GBM cells, DCST1-AS1 overexpression led to the downregulation of miR-29b and the increased methylation level of miR-29b gene. Cell proliferation analysis showed that DCST1-AS1 overexpression led to increased cell proliferation rate. Moreover, DCST1-AS1 overexpression significantly reversed the inhibitory effects of miR-29b on cancer cell proliferation. Conclusions: DCST1-AS1 may downregulate miR-29b through methylation in GBM to promote cancer cell proliferation.

scholarly journals LINC 01436 is Overexpressed in Colorectal Cancer and Promotes Cancer Cell Proliferation by Suppressing the Maturation of Tumor Suppressive miR-466

2021 ◽  
Author(s):  
Hong Li ◽  
Wei Dong ◽  
Jie Hou ◽  
De He
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
Precursor Cell ◽  
Cancer Cell Proliferation ◽  
Poor Survival ◽  
Follow Up Study ◽  
Prognostic Analysis

Abstract LINC 01436 (lncRNA) promotes lung and gastric two types of cancers. However, it is unclear that whether this lncRNA also participate in colorectal cancer (CRC). This study was therefore carried out to analyze the role of LINC 01436 in CRC. Expression of LINC 01436 in CRC patient tissues was analyzed by RT-qPCR and follow-up study was performed for prognostic analysis. Correlation between LINC 01436 and mature miR-466 or miR-466 precursor was analyzed by linear regression. Mature miR-466 and miR-466 precursor expression in CRC cells with the overexpression of LINC 01436 was studied by performing RT-qPCR. The proliferation of CRC cells was subjected to CCK-8 assay analysis. LINC 01436 was upregulated in CRC and predicted poor survival. LINC 01436 and mature miR-466 were inversely correlated, but LINC 01436 and miR-466 precursor were not correlated. In CRC cells, LINC 01436 mediated the downregulation of mature miR-466, but not miR-466 precursor. Cell proliferation analysis showed that LINC 01436 overexpression rescued cell proliferation reduced by miR-466. LINC 01436 is overexpressed in CRC and it may promote cancer cell proliferation by suppressing the maturation of miR-466.

scholarly journals Downregulation of MANCR inhibits cancer cell proliferation in mantle cell lymphoma possibly by interacting with RUNX2

2019 ◽  
Author(s):  
Shujuan Wen ◽  
Min Zeng ◽  
Yan Li ◽  
Xin Hu ◽  
Shan Li ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Mantle Cell Lymphoma ◽  
Cancer Cell ◽  
Cell Lymphoma ◽  
Migration And Invasion ◽  
Cancer Cell Proliferation ◽  
Inhibitory Effects ◽  
Mantle Cell ◽  
Related Transcription Factor

Abstract The mitotically associated lncRNA (MANCR) participates in breast cancer cell proliferation, while its involvement in other cancers is still unknown. In this study, we therefore studied the role of MANCR in mantle cell lymphoma (MCL). We found that serum MANCR and Runt-related transcription factor 2 (RUNX2) were upregulated in MCL patients when compared with those in healthy controls. A positive correlation between serum MANCR and RUNX2 was found in MCL patients but not in controls. Upregulation of serum MANCR distinguished MCL patients from controls. MANCR overexpression promoted RUNX2 expression in MCL cells, while RUNX2 overexpression failed to significantly change the expression levels of MANCR. MANCR overexpression promoted the proliferation of MCL cells, while MANCR silencing inhibited the proliferation of MCL cells. In addition, RUNX2 overexpression attenuated the inhibitory effects of MANCR silencing on cell proliferation. However, MANCR overexpression and silencing had no significant effects on cell migration and invasion. Further bioinformatics analysis showed that MANCR may sponge miR-218 to upregulate RUNX2. Therefore, we conclude that downregulation of MANCR may inhibit cancer cell proliferation in MCL possibly by interacting with RUNX2.

scholarly journals PAMAM Dendrimers Augment Inhibitory Effects of Curcumin on Cancer Cell Proliferation: Possible Inhibition of Telomerase

2013 ◽  
Vol 14 (11) ◽  
pp. 6925-6928 ◽  
Author(s):  
Mahdie Mollazade ◽  
Kazem Nejati-Koshki ◽  
Abolfazl Akbarzadeh ◽  
Nosratollah Zarghami ◽  
Marzieh Nasiri ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cancer Cell ◽  
Pamam Dendrimers ◽  
Cancer Cell Proliferation ◽  
Inhibitory Effects

scholarly journals FZD10 Carried by Exosomes Sustains Cancer Cell Proliferation

Cells ◽  
2019 ◽  
Vol 8 (8) ◽  
pp. 777 ◽  
Author(s):  
Scavo ◽  
Depalo ◽  
Rizzi ◽  
Ingrosso ◽  
Fanizza ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cancer Cell ◽  
Culture Medium ◽  
Mrna Level ◽  
Substantial Reduction ◽  
Wnt Signaling Pathway ◽  
Active Role ◽  
Cancer Cell Proliferation ◽  
Long Distance

Extracellular vesicles (EVs) are involved in intercellular communication during carcinogenesis, and cancer cells are able to secrete EVs, in particular exosomes containing molecules, that can be transferred to recipient cells to induce pathological processes and significant modifications, as metastasis, increase of proliferation, and carcinogenesis evolution. FZD proteins, a family of receptors comprised in the Wnt signaling pathway, play an important role in carcinogenesis of the gastroenteric tract. Here, a still unknown role of Frizzled 10 (FZD10) protein was identified. In particular, the presence of FZD10 and FZD10-mRNA in exosomes extracted from culture medium of the untreated colorectal, gastric, hepatic, and cholangio cancer cell lines, was detected. A substantial reduction in the FZD10 and FZD10-mRNA level was achieved in FZD10-mRNA silenced cells and in their corresponding exosomes. Concomitantly, a significant decrease in viability of the silenced cells compared to their respective controls was observed. Notably, the incubation of silenced cells with the exosomes extracted from culture medium of the same untreated cells promoted the restoration of the cell viability and, also, of the FZD10 and FZD10-mRNA level, thus indicating that the FZD10 and FZD10-mRNA delivering exosomes may be potential messengers of cancer reactivation and play an active role in long-distance metastatization.

scholarly journals Exploiting GRK2 Inhibition as a Therapeutic Option in Experimental Cancer Treatment: Role of p53-Induced Mitochondrial Apoptosis

Cancers ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 3530
Author(s):  
Jessica Gambardella ◽  
Antonella Fiordelisi ◽  
Gaetano Santulli ◽  
Michele Ciccarelli ◽  
Federica Andrea Cerasuolo ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cancer Cell ◽  
Nude Mice ◽  
Specific Inhibitor ◽  
Cancer Cell Proliferation ◽  
In Vivo Models ◽  
P53 Expression

The involvement of GRK2 in cancer cell proliferation and its counter-regulation of p53 have been suggested in breast cancer even if the underlying mechanism has not yet been elucidated. Furthermore, the possibility to pharmacologically inhibit GRK2 to delay cancer cell proliferation has never been explored. We investigated this possibility by setting up a study that combined in vitro and in vivo models to underpin the crosstalk between GRK2 and p53. To reach this aim, we took advantage of the different expression of p53 in cell lines of thyroid cancer (BHT 101 expressing p53 and FRO cells, which are p53-null) in which we overexpressed or silenced GRK2. The pharmacological inhibition of GRK2 was achieved using the specific inhibitor KRX-C7. The in vivo study was performed in Balb/c nude mice, where we treated BHT-101 or FRO-derived tumors with KRX-C7. In our in vitro model, FRO cells were unaffected by GRK2 expression levels, whereas BHT-101 cells were sensitive, thus suggesting a role for p53. The regulation of p53 by GRK2 is due to phosphorylative events in Thr-55, which induce the degradation of p53. In BHT-101 cells, the pharmacologic inhibition of GRK2 by KRX-C7 increased p53 levels and activated apoptosis through the mitochondrial release of cytochrome c. These KRX-C7-mediated events were also confirmed in cancer allograft models in nude mice. In conclusion, our data showed that GRK2 counter-regulates p53 expression in cancer cells through a kinase-dependent activity. Our results further corroborate the anti-proliferative role of GRK2 inhibitors in p53-sensitive tumors and propose GRK2 as a therapeutic target in selected cancers.

The role of histone deacetylase 7 (HDAC7) in cancer cell proliferation: regulation on c-Myc

2010 ◽  
Vol 89 (3) ◽  
pp. 279-289 ◽  
Author(s):  
Caihua Zhu ◽  
Qin Chen ◽  
Zuoquan Xie ◽  
Jing Ai ◽  
Linjiang Tong ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Histone Deacetylase ◽  
Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Proliferation Regulation

Development of a novel method for the bioanalysis of benfotiamine and sulbutiamine in cancer cells

2016 ◽  
Vol 8 (28) ◽  
pp. 5596-5603 ◽  
Author(s):  
Jaeah Kim ◽  
Christopher P. Hopper ◽  
Kelsey H. Connell ◽  
Parisa Darkhal ◽  
Jason A. Zastre ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Biological Samples ◽  
Cancer Cell Proliferation ◽  
Essential Step ◽  
Novel Method

Quantification of benfotiamine and sulbutiamine, synthetic thiamine analogs, in biological samples is an essential step toward understanding the role of these thiamine analogs on cancer cell proliferation.

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