ALDH1 – A new immunohistochemical diagnostic marker for Schwann cell-derived tumors

Liesche, Friederike; Griessmair, Michael; Barz, Melanie; Gempt, Jens; Schlegel, Jürgen

doi:10.5414/np301190

Cited by 5 publications

(2 citation statements)

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“…Recent work showed expression of ALDH1 in human schwannoma tissue, but the mechanism of ALDH1 upregulation and its potential function is unclear. 47 …”

Section: Resultsmentioning

confidence: 99%

Inhibition of YAP/TAZ-driven TEAD activity prevents growth of NF2-null schwannoma and meningioma

Laraba

Guibert

Hewitt

et al. 2022

Brain

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Schwannoma tumours typically arise on the 8th cranial nerve and are mostly caused by loss of the tumour suppressor Merlin (NF2). There are no approved chemotherapies for these tumours and the surgical removal of the tumour carries a high risk of damage to the 8th or other close cranial nerve tissue. New treatments for schwannoma and other NF2-null tumours such as meningioma are urgently required. Using a combination of human primary tumour cells and mouse models of schwannoma, we have examined the role of the Hippo signalling pathway in driving tumour cell growth. Using both genetic ablation of the Hippo effectors YAP and TAZ as well as novel TEAD palmitoylation inhibitors, we show that Hippo signalling may be successfully targeted in vitro and in vivo to both block and, remarkably, regress schwannoma tumour growth. In particular, successful use of TEAD palmitoylation inhibitors in a pre-clinical mouse model of schwannoma points to their potential future clinical use. We also identify the cancer stem cell marker aldehyde dehydrogenase 1A1 (ALDH1A1) as a Hippo signalling target, driven by the TAZ protein in human and mouse NF2-null schwannoma cells, as well as in NF2-null meningioma cells, and examine the potential future role of this new target in halting schwannoma and meningioma tumour growth.

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“…Recent work showed expression of ALDH1 in human schwannoma tissue, but the mechanism of ALDH1 upregulation and its potential function is unclear. 47 …”

Section: Resultsmentioning

confidence: 99%

Inhibition of YAP/TAZ-driven TEAD activity prevents growth of NF2-null schwannoma and meningioma

Laraba

Guibert

Hewitt

et al. 2022

Brain

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“…The stem cell-like property of tumor cells is an important factor in drug resistance of tumor [44,45]. We found that knockdown of BCAR4 in HCT116 and HT29 cells suppressed the expression of ALDH1, an indicator related to stem cell-like properties and tumor sphere formation [46,47], indicating that BCAR4 promotes stem cell properties and therefore contributes to tumor growth.…”

Section: Discussionmentioning

confidence: 84%

Long Non-Coding RNA BCAR4 Promotes Oxaliplatin Resistance in Colorectal Cancer by Modulating miR-484-3p/RAB5C Expression

Chen

et al. 2023

Chemotherapy

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Background Oxaliplatin based chemotherapy resistance is a major cause of recurrence in patients with colorectal cancer (CRC). Increasing evidence indicates that LncRNA BCAR4 is involved in the occurrence and development of various cancers. However, the effect of BCAR4 on CRC chemotherapy resistance remains unclear. Methods Real-time quantitative PCR and western blotting were used to detect the expression levels of gene and protein, respectively. The role of BCAR4 in drug resistance was evaluated by cell viability and apoptosis experiments. Luciferase reporter assay and western blot analysis confirmed the relationship between BCAR4, miR-483-3p and RAB5C. Results Luciferase reporter assay and western blotting analysis confirmed the relationship among BCAR4, miR-483-3p and RAB5C. The results showed that the expression levels of BCAR4 and RAB5C were increased in CRC tumor tissue. The expression levels of BCAR4 were increased in patients with chemotherapy resistance. Functional analysis showed that knockdown of BCAR4 reduced the expression levels of proteins related to stemness, decreased the activity of cells and promoted apoptosis of CRC cells, while overexpression of RAB5C reversed these effects. Moreover, the results showed that BCAR4 promoted oxaliplatin resistance by inhibiting cell apoptosis. Mechanistically, BCAR4 sponged miR-483-3p and promoted the expression of RAB5C. Knockdown of BCAR4 reduced tumor size and enhanced cell sensitivity to oxaliplatin in vivo. Conclusion The results suggested that BCAR4/miR-483-3p/RAB5C axis has the potential to be explored as a novel therapeutic target for CRC treatment.

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The Role of Pi, Glutamine and the Essential Amino Acids in Modulating the Metabolism in Diabetes and Cancer

Vadlakonda¹,

Indracanti

Kalangi

et al. 2020

J Diabetes Metab Disord

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ALDH1 – A new immunohistochemical diagnostic marker for Schwann cell-derived tumors

Cited by 5 publications

References 0 publications

Inhibition of YAP/TAZ-driven TEAD activity prevents growth of NF2-null schwannoma and meningioma

Inhibition of YAP/TAZ-driven TEAD activity prevents growth of NF2-null schwannoma and meningioma

Long Non-Coding RNA BCAR4 Promotes Oxaliplatin Resistance in Colorectal Cancer by Modulating miR-484-3p/RAB5C Expression

The Role of Pi, Glutamine and the Essential Amino Acids in Modulating the Metabolism in Diabetes and Cancer

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