Evading apoptosis in cancer

Fernald, Kaleigh; Kurokawa, Manabu

doi:10.1016/j.tcb.2013.07.006

Cited by 457 publications

(388 citation statements)

References 199 publications

(140 reference statements)

Supporting

Mentioning

376

Contrasting

Unclassified

Order By: Relevance

“…Cancer cells adopt various strategies to override apoptosis, including the upregulation of anti-apoptotic machinery, the down regulation of pro-apoptotic factors or a combination of these strategies (37). A number ofcancer-associated lncRNAs have been identified that affect apoptosis via various pathways (10,38,39).…”

Section: Discussionmentioning

confidence: 99%

Downregulated long non‑coding RNA TCONS_00068220 upregulates apoptosis in gastric cancer cells

et al. 2017

View full text Add to dashboard Cite

Abstract. Long non-coding RNAs (lncRNAs) are emerging as a fundamental class of biological effect or molecules that perform pivotal functions in the regulation of the genome. With advances in bioinformatics and genomics, extensive identification and characterization of lncRNAs is now possible. They regulate cellular growth, differentiation and apoptosis. Dysregulation of lncRNAs has been associated with numerous types of human cancer. In the present study, the expression profile of differentially expressed genes (DEGs) and lncRNAs in gastric cancer (GC) samples and normal tissue samples was evaluated with bioinformatics. The biological functions of the predicted lncRNA TCONS_00068220 were focused on; the DEGs co-expressed with TCONS_00068220 were enriched in cancer-associated pathways. TCONS_00068220 was demonstrated to be upregulated in GC tissues and cell lines compared with normal controls. In addition, an increased rate of apoptosis was observed in NCI-N87 cells following transfection with small interfering RNA against TCONS_00068220. These data suggest that TCONS_00068220 may be associated with the pathogenesis of GC, and it may serve as a potential therapeutic target.

show abstract

Section: Discussionmentioning

confidence: 99%

Downregulated long non‑coding RNA TCONS_00068220 upregulates apoptosis in gastric cancer cells

et al. 2017

View full text Add to dashboard Cite

show abstract

“…In addition to unlimited proliferation and elevated clonogenic capacity, evading apoptosis is also essential for tumour initiation and development (20,21). As eIF3c knockdown led to a reduction in cell number (Fig.…”

Section: Eif3c Knockdown Impairs the Ability Of U-87 Mg Cells To Formmentioning

confidence: 99%

Eukaryotic translation initiation factor 3, subunit C is overexpressed and promotes cell proliferation in human glioma U-87 MG cells

2015

View full text Add to dashboard Cite

Abstract. Disrupted protein translation is prevalent in tumours. Eukaryotic translation initiation factors (eIFs) were found to play an important role in various tumours. However, the involvement of eIFs in glioma remains to be elucidated. The present study explored the expression and the role of eIF 3, subunit C (eIF3c) in human glioma. The expression of eIF3c in glioma tissues was evaluated by immunohistochemistry. The impact of eIF3c inhibition on U-87 MG was explored in vitro and in vivo by lentivirus-mediated siRNA targeting eIF3c. The results revealed that overexpression of eIF3c was present in glioma tissues. Knockdown of eIF3c significantly impaired cell proliferation and colony formation, further induced cell cycle arrest and apoptosis in the U-87 MG cell line. Furthermore, tumoursphere formation in the U-87 MG glioma xenograft model was blocked by eIF3c knockdown. The involvement of eIF3c in the tumorigenesis of glioma was confirmed, suggesting eIF3c may be a promising therapy target in human glioma.

show abstract

“…Within the body, apoptosis occurs continuously under physiologic conditions. Almost every step during apoptosis is finely orchestrated; it is a "clean" kind of death as the remnants (apoptotic bodies) are engulfed and recycled by neighboring cells, and generally it does not trigger inflammation (12,13). In contrast, in cell cultures, apoptotic bodies are frequently identifiable for days after the challenge.…”

Section: Cell Death Mechanismsmentioning

confidence: 99%

“(Not) All (Dead) Things Share the Same Breath”: Identification of Cell Death Mechanisms in Anticancer Therapy

et al. 2015

View full text Add to dashboard Cite

During the last decades, the knowledge of cell death mechanisms involved in anticancer therapy has grown exponentially. However, in many studies, cell death is still described in an incomplete manner. The frequent use of indirect proliferation assays, unspecific probes, or bulk analyses leads too often to misunderstandings regarding cell death events. There is a trend to focus on molecular or genetic regulations of cell demise without a proper characterization of the phenotype that is the object of this study. Sometimes, cancer researchers can feel overwhelmed or confused when faced with such a corpus of detailed insights, nomenclature rules, and debates about the accuracy of a particular probe or assay. On the basis of the information available, we propose a simple guide to distinguish forms of cell death in experimental settings using cancer cell lines. Cancer Res; 75(6); 913-7.Ó2015 AACR.

show abstract

Evading apoptosis in cancer

Cited by 457 publications

References 199 publications

Downregulated long non‑coding RNA TCONS_00068220 upregulates apoptosis in gastric cancer cells

Downregulated long non‑coding RNA TCONS_00068220 upregulates apoptosis in gastric cancer cells

Eukaryotic translation initiation factor 3, subunit C is overexpressed and promotes cell proliferation in human glioma U-87 MG cells

“(Not) All (Dead) Things Share the Same Breath”: Identification of Cell Death Mechanisms in Anticancer Therapy

Contact Info

Product

Resources

About