Novel Anti-Apoptotic MicroRNAs 582-5p and 363 Promote Human Glioblastoma Stem Cell Survival via Direct Inhibition of Caspase 3, Caspase 9, and Bim

Floyd, Desiree H.; Zhang, Ying; Dey, Bijan K.; Kefas, Benjamin; Breit, Hannah; Marks, Kaitlyn; Dutta, Anindya; Herold‐Mende, Christel; Synowitz, Michael; Glaß, Rainer; Abounader, Roger; Purow, Benjamin

doi:10.1371/journal.pone.0096239

Cited by 87 publications

(69 citation statements)

References 73 publications

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“…miR-106b-25 was shown to be upregulated in human prostate cancer and functions by partly inhibiting of caspase-7 expression [182]. Floyd et al (2014) [183] demonstrated that miR-582-5p and miR-363 inhibit apoptosis by directly targeting caspase-3 and caspase-9 in glioblastoma. Caspase-3 has been shown to be a target of miR let7a in human squamous carcinoma cells and hepatocellular carcinoma cells [184].…”

Section: Micrornas In Extrinsic and Intrinsic Apoptotic Pathwaysmentioning

confidence: 99%

Major apoptotic mechanisms and genes involved in apoptosis

et al. 2016

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As much as the cellular viability is important for the living organisms, the elimination of unnecessary or damaged cells has the opposite necessity for the maintenance of homeostasis in tissues, organs and the whole organism. Apoptosis, a type of cell death mechanism, is controlled by the interactions between several molecules and responsible for the elimination of unwanted cells from the body. Apoptosis can be triggered by intrinsically or extrinsically through death signals from the outside of the cell. Any abnormality in apoptosis process can cause various types of diseases from cancer to auto-immune diseases. Different gene families such as caspases, inhibitor of apoptosis proteins, B cell lymphoma (Bcl)-2 family of genes, tumor necrosis factor (TNF) receptor gene superfamily, or p53 gene are involved and/or collaborate in the process of apoptosis. In this review, we discuss the basic features of apoptosis and have focused on the gene families playing critical roles, activation/inactivation mechanisms, upstream/downstream effectors, and signaling pathways in apoptosis on the basis of cancer studies. In addition, novel apoptotic players such as miRNAs and sphingolipid family members in various kind of cancer are discussed.

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Section: Micrornas In Extrinsic and Intrinsic Apoptotic Pathwaysmentioning

confidence: 99%

Major apoptotic mechanisms and genes involved in apoptosis

et al. 2016

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“…37–39 Briefly, single GBM157 clones were treated with different doses of TMZ (Supplementary Figure 4) and anti-miR363 (i.e., two pulses versus five pulses) on the 3D NEP setup (Figure 3a,b). Cell viability was then monitored for up to 96 h post-treatment via live- and dead-cell staining and fluorescence microscopy (Figure 3c,d).…”

Section: On-chip Therapy Efficacy Studies Revealing Of the Existence mentioning

confidence: 99%

On-Chip Clonal Analysis of Glioma-Stem-Cell Motility and Therapy Resistance

et al. 2016

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Enhanced glioma-stem-cell (GSC) motility and therapy resistance are considered to play key roles in tumor cell dissemination and recurrence. As such, a better understanding of the mechanisms by which these cells disseminate and withstand therapy could lead to more efficacious treatments. Here, we introduce a novel micro-/nanotechnology-enabled chip platform for performing live-cell interrogation of patient-derived GSCs with single-clone resolution. On-chip analysis revealed marked intertumoral differences (>10-fold) in single-clone motility profiles between two populations of GSCs, which correlated well with results from tumor-xenograft experiments and gene-expression analyses. Further chip-based examination of the more-aggressive GSC population revealed pronounced interclonal variations in motility capabilities (up to ∼4-fold) as well as gene-expression profiles at the single-cell level. Chip-supported therapy resistance studies with a chemotherapeutic agent (i.e., temozolomide) and an oligo RNA (anti-miR363) revealed a subpopulation of CD44-high GSCs with strong antiapoptotic behavior as well as enhanced motility capabilities. The living-cell-interrogation chip platform described herein enables thorough and large-scale live monitoring of heterogeneous cancer-cell populations with single-cell resolution, which is not achievable by any other existing technology and thus has the potential to provide new insights into the cellular and molecular mechanisms modulating glioma-stem-cell dissemination and therapy resistance.

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“…Additionally, caspase family members have major roles in cell apoptosis (40). The caspase cleavage cascade begins with initiator caspase being activated by intrinsic or extrinsic pathways.…”

Section: Discussionmentioning

confidence: 99%

TT‑1, an analog of melittin, triggers apoptosis in human thyroid cancer TT cells via regulating caspase, Bcl‑2 and Bax

Wan

Zhang

et al. 2017

Oncol Lett

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Abstract. Melittin is a 26 amino acid residue antimicrobial peptide with known antitumor activity. In the present study, a novel peptide TT-1, derived from melittin and contained only 11 amino acids, was designed, and its antitumor effect was investigated. The present study is aimed to elucidate the effects and relative mechanisms of TT-1 on a human thyroid cancer cell line (TT) in vitro and in vivo. Cell viability assays, Annexin V/propidium iodide assays, western blotting and quantitative reverse transcription polymerase chain reaction were performed. Furthermore, a tumor-xenograft model was established to investigate the apoptotic mechanisms of TT-1 on TT cells. The results obtained indicated that TT-1 was able to suppress the proliferation of TT cells and exhibited low cytotoxicity to normal thyroid cells in vitro. The apoptotic rates of TT cells were also increased following TT-1 treatment. Additionally, TT-1 stimulated caspase-3, caspase-9 and Bax, and inhibited B-cell lymphoma 2 mRNA and protein expression. Finally, it was also demonstrated that TT-1 is able to markedly suppress tumor growth in a TT-bearing nude mouse model. In summary, TT-1 may inhibit the proliferation of TT cells by inducing apoptosis in vitro and in vivo, indicating that TT-1 may be a potential candidate for the treatment of thyroid cancer.

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Novel Anti-Apoptotic MicroRNAs 582-5p and 363 Promote Human Glioblastoma Stem Cell Survival via Direct Inhibition of Caspase 3, Caspase 9, and Bim

Cited by 87 publications

References 73 publications

Major apoptotic mechanisms and genes involved in apoptosis

Major apoptotic mechanisms and genes involved in apoptosis

On-Chip Clonal Analysis of Glioma-Stem-Cell Motility and Therapy Resistance

TT‑1, an analog of melittin, triggers apoptosis in human thyroid cancer TT cells via regulating caspase, Bcl‑2 and Bax

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