Silencing of Histone Deacetylase 6 Decreases Cellular Malignancy and Contributes to Primary Cilium Restoration, Epithelial-to-Mesenchymal Transition Reversion, and Autophagy Inhibition in Glioblastoma Cell Lines

Urdiciain, Alejandro; Erausquin, Elena; Zelaya, María Victoria; Zazpe, Idoya; Lanciego, José L.; Meléndez, Bárbara; Rey, Juan A.; Idoate, Miguel A.; Galdo, Natalia A. Riobo-Del; Castresana, Javier S.

doi:10.3390/biology10060467

Cited by 8 publications

(12 citation statements)

References 72 publications

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“…In line with these studies, aberrant expression of tubulin deacetylase HDAC6 has been reported in several cancer cell lines and tumor models [70,71]. In addition, upregulation of HDAC6 increases cell motility in breast cancer cells, thus contributing to cancer metastasis [72], whereas in glioblastoma cells genetic silencing of HDAC6 decreases cellular malignancy and reverses the mesenchymal phenotype [73,74]. High level Lung Treatment response to paclitaxel [64] On the other hand, the role of tubulin deacetylase SIRT2 in cancer is controversial, as SIRT2 exerts either tumor-suppressive or oncogenic properties.…”

Section: The Tubulin Code and Its Associated Enzymes In Cancermentioning

confidence: 72%

Section: The Tubulin Code and Its Associated Enzymes In Cancermentioning

confidence: 99%

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The Tubulin Code and Tubulin-Modifying Enzymes in Autophagy and Cancer

Trisciuoglio

Degrassi

2021

Cancers

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Microtubules are tubulin polymers that constitute the structure of eukaryotic cells. They control different cell functions that are often deregulated in cancer, such as cell shape, cell motility and the intracellular movement of organelles. Here, we focus on the crucial role of tubulin modifications in determining different cancer characteristics, including metastatic cell migration and therapy resistance. We also discuss the influence of microtubule modifications on the autophagic process—the cellular degradation pathway that influences cancer growth. We discuss findings showing that inducing microtubule modifications can be used as a means to kill cancer cells by inhibiting autophagy.

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Section: The Tubulin Code and Its Associated Enzymes In Cancermentioning

confidence: 72%

Section: The Tubulin Code and Its Associated Enzymes In Cancermentioning

confidence: 99%

The Tubulin Code and Tubulin-Modifying Enzymes in Autophagy and Cancer

Trisciuoglio

Degrassi

2021

Cancers

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“…Glioblastoma is associated with high levels of the mesenchymal markers Snail, Slug, and N-cadherin. Glioblastoma cell lines show high levels of autophagic flux and activation of the sonic hedgehog (Shh) pathway [ 9 ]. HDAC6 is the most overexpressed isoform in glioblastoma [ 9 ].…”

Section: Role Of Hdac6 In Cancer Cell Proliferationmentioning

confidence: 99%

Targeting HDAC6 to Overcome Autophagy-Promoted Anti-Cancer Drug Resistance

Shim

Jeoung

2022

IJMS

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Histone deacetylases (HDACs) regulate gene expression through the epigenetic modification of chromatin structure. HDAC6, unlike many other HDACs, is present in the cytoplasm. Its deacetylates non-histone proteins and plays diverse roles in cancer cell initiation, proliferation, autophagy, and anti-cancer drug resistance. The development of HDAC6-specific inhibitors has been relatively successful. Mechanisms of HDAC6-promoted anti-cancer drug resistance, cancer cell proliferation, and autophagy are discussed. The relationship between autophagy and anti-cancer drug resistance is discussed. The effects of combination therapy, which includes HDAC6 inhibitors, on the sensitivity of cancer cells to chemotherapeutics and immune checkpoint blockade are presented. A summary of clinical trials involving HDAC6-specific inhibitors is also presented. This review presents HDAC6 as a valuable target for developing anti-cancer drugs.

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“…The three mixed phosphorylated polypeptides derived from GLI2 significantly increased the level of GLI2 phosphorylation and decreased the transcriptional activation of GLI2, and the radiation sensitization of GBM cells was significantly higher than that in the control group ( 128 ). HDAC6 was upregulated in GSCs and inhibited HDAC6 down-regulated glioma-associated oncogene GLI1 and PTCH1/2 receptors, as well as SHH signaling components, expression and activity, thereby inhibiting GSC proliferation, inducing differentiation and increasing the apoptosis rate through the SHH/GLI1 signaling pathway ( 109 , 129 ). Inhibition of HDAC6 by Tubasatin A enhanced the radiosensitivity of GBM tumor cells.…”

Section: Targeting the Hh Signaling Pathway In Gbmmentioning

confidence: 99%

Hedgehog signaling regulates the development and treatment of glioblastoma (Review)

et al. 2022

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Glioblastoma (GBM) is the most common and fatal malignant tumor type of the central nervous system. GBM affects public health and it is important to identify biomarkers to improve diagnosis, reduce drug resistance and improve prognosis (e.g., personalized targeted therapies). Hedgehog (HH) signaling has an important role in embryonic development, tissue regeneration and stem cell renewal. A large amount of evidence indicates that both normative and non-normative HH signals have an important role in GBM. The present study reviewed the role of the HH signaling pathway in the occurrence and progression of GBM. Furthermore, the effectiveness of drugs that target different components of the HH pathway was also examined. The HH pathway has an important role in reversing drug resistance after GBM conventional treatment. The present review highlighted the relevance of HH signaling in GBM and outlined that this pathway has a key role in the occurrence, development and treatment of GBM. Contents 1. Introduction 2. Overview of GBM 3. The HH signaling pathway 4. Molecular mechanisms of the HH signaling pathway in GBM 5. Targeting the HH signaling pathway in GBM 6. HH pathway and immunotherapy 7. Discussion 8. Conclusion

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Silencing of Histone Deacetylase 6 Decreases Cellular Malignancy and Contributes to Primary Cilium Restoration, Epithelial-to-Mesenchymal Transition Reversion, and Autophagy Inhibition in Glioblastoma Cell Lines

Cited by 8 publications

References 72 publications

The Tubulin Code and Tubulin-Modifying Enzymes in Autophagy and Cancer

The Tubulin Code and Tubulin-Modifying Enzymes in Autophagy and Cancer

Targeting HDAC6 to Overcome Autophagy-Promoted Anti-Cancer Drug Resistance

Hedgehog signaling regulates the development and treatment of glioblastoma (Review)

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