HDAC6 interacts with PTPN1 to enhance melanoma cells progression

Liu, Jiaqi; Luan, Wenjie; Zhang, Yong; Gu, Jiande; Shi, Yuedong; Yang, Yanwen; Qi, Fazhi

doi:10.1016/j.bbrc.2017.12.145

Cited by 24 publications

(19 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…PTP1B has long been known to regulate insulin and leptin receptor signaling negatively. Recently, it was reported to be aberrantly expressed in cancer cells and to function as an important oncogene [22]. Several studies have reported that PTPN1 promoted proliferation, colony formation, and migration while decreased apoptosis of cancer cell lines [22,23].…”

Section: Introductionmentioning

confidence: 99%

“…Recently, it was reported to be aberrantly expressed in cancer cells and to function as an important oncogene [22]. Several studies have reported that PTPN1 promoted proliferation, colony formation, and migration while decreased apoptosis of cancer cell lines [22,23]. Nonetheless, the anticancer effects of pristimerin and specific mechanisms of PTPN1 in diffuse glioma deserve investigation.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Pristimerin inhibits glioma progression by targeting AGO2 and PTPN1 expression via miR-542-5p

et al. 2019

Bioscience Reports

View full text Add to dashboard Cite

Glioblastoma multiform is the most common and malignant primary tumor of the central nervous system in adults, the high recurrence rate and poor prognosis are critical priorities. Pristimerin is a naturally occurring quinone methide triterpenoid isolated from the Celastraceae and Hippocrateaceae families. Its anticancer effects have garnered considerable attention; nonetheless, the mechanisms of action remain unknown. To predict the hub genes of pristimerin, PharmMapper and the Coremine database were used to identify 13 potential protein targets; protein–protein interaction, for which functional enrichment analyses were performed. Compound-target, target-pathway, and compound-target-pathway networks were constructed using Cytoscape. Biological process analysis first revealed that enrichment of these target genes correlated with negative regulation of symbiont growth in the host, and regulation of chronic inflammatory response to antigenic stimulus. Survival analysis in cBioPortal showed that protein tyrosine phosphatase, non-receptor type 1 (PTPN1) and Argonaute 2 (AGO2) might be involved in the carcinogenesis, invasion, or recurrence of diffuse glioma. In addition, we observed that low-dose pristimerin inhibited the viability of glioma cells, while miR-542-5p in vitro; and reduced PTPN1 expression. Notably, high-dose pristimerin induced apoptosis. Furthermore, miR-542-5p silence with siRNA in glioma cells lead to the elevation in AGO2, and decreased PTPN1 level. The effect was obviously post pristimerin treatment and miR-542-5p suppression. In conclusion, pristimerin inhibited glioma progression through AGO2 and PTPN1 expression via a canonical miRNA-mediated mechanism.

show abstract

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Pristimerin inhibits glioma progression by targeting AGO2 and PTPN1 expression via miR-542-5p

et al. 2019

Bioscience Reports

View full text Add to dashboard Cite

show abstract

“…Additionally, when combined to paclitaxel, pristimerin induced cell autophagy through inhibition of ERK1/2/p90RSK signaling-involved in cancer cell proliferation, differentiation, and migration [347,360]. Pristimerin-induced glioma overgrowth was dependent on AGO2 upregulation (a critical protein for tumorigenesis) and PTPN1 downregulation (a metabolism regulator oncogene reported to be aberrantly expressed in cancer cells) [361][362][363]. Furthermore, pristimerin induced glioma cell necrosis by promoting mitochondrial dysfunction, c-Jun activation, and consequently ROS overproduction [364].…”

Section: Pristimerinmentioning

confidence: 99%

Terpenoids, Cannabimimetic Ligands, beyond the Cannabis Plant

et al. 2020

View full text Add to dashboard Cite

Medicinal use of Cannabis sativa L. has an extensive history and it was essential in the discovery of phytocannabinoids, including the Cannabis major psychoactive compound—Δ9-tetrahydrocannabinol (Δ9-THC)—as well as the G-protein-coupled cannabinoid receptors (CBR), named cannabinoid receptor type-1 (CB1R) and cannabinoid receptor type-2 (CB2R), both part of the now known endocannabinoid system (ECS). Cannabinoids is a vast term that defines several compounds that have been characterized in three categories: (i) endogenous, (ii) synthetic, and (iii) phytocannabinoids, and are able to modulate the CBR and ECS. Particularly, phytocannabinoids are natural terpenoids or phenolic compounds derived from Cannabis sativa. However, these terpenoids and phenolic compounds can also be derived from other plants (non-cannabinoids) and still induce cannabinoid-like properties. Cannabimimetic ligands, beyond the Cannabis plant, can act as CBR agonists or antagonists, or ECS enzyme inhibitors, besides being able of playing a role in immune-mediated inflammatory and infectious diseases, neuroinflammatory, neurological, and neurodegenerative diseases, as well as in cancer, and autoimmunity by itself. In this review, we summarize and critically highlight past, present, and future progress on the understanding of the role of cannabinoid-like molecules, mainly terpenes, as prospective therapeutics for different pathological conditions.

show abstract

“…HDAC6 deacetylates Lys-72 of extracellular signal-regulated kinase 1 (ERK1) and promotes ERK1 activity (Wu et al, 2018). HDAC6 binds to Tyrosine-protein phosphatase non-receptor type 1 (PTPN1), activates extracellular signal-regulated kinase 1/2 (ERK1/2), inhibits apoptosis, and promotes melanoma cell proliferation (Liu et al, 2018). HDAC7 regulates the level of acetyl-H3K27 and is necessary for maintaining cancer stem cells (Caslini et al, 2019).…”

Section: The Roles Of Hdacs In Melanoma Growth and Anti-cancer Drug Rmentioning

confidence: 99%

Histone Deacetylase Inhibitors to Overcome Resistance to Targeted and Immuno Therapy in Metastatic Melanoma

Yeon

Kim

Jung

et al. 2020

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

Therapies that target oncogenes and immune checkpoint molecules constitute a major group of treatments for metastatic melanoma. A mutation in BRAF (BRAF V600E) affects various signaling pathways, including mitogen activated protein kinase (MAPK) and PI3K/AKT/mammalian target of rapamycin (mTOR) in melanoma. Target-specific agents, such as MAPK inhibitors improve progression-free survival. However, BRAF V600E mutant melanomas treated with BRAF kinase inhibitors develop resistance. Immune checkpoint molecules, such as programmed death-1 (PD-1) and programmed death ligand-1(PD-L1), induce immune evasion of cancer cells. MAPK inhibitor resistance results from the increased expression of PD-L1. Immune checkpoint inhibitors, such as anti-PD-L1 or anti-PD-1, are main players in immune therapies designed to target metastatic melanoma. However, melanoma patients show low response rate and resistance to these inhibitors develops within 6-8 months of treatment. Epigenetic reprogramming, such as DNA methylaion and histone modification, regulates the expression of genes involved in cellular proliferation, immune checkpoints and the response to anti-cancer drugs. Histone deacetylases (HDACs) remove acetyl groups from histone and nonhistone proteins and act as transcriptional repressors. HDACs are often dysregulated in melanomas, and regulate MAPK signaling, cancer progression, and responses to various anti-cancer drugs. HDACs have been shown to regulate the expression of PD-1/PD-L1 and genes involved in immune evasion. These reports make HDACs ideal targets for the development of anti-melanoma therapeutics. We review the mechanisms of resistance to anti-melanoma therapies, including MAPK inhibitors and immune checkpoint inhibitors. We address the effects of HDAC inhibitors on the response to MAPK inhibitors and immune checkpoint inhibitors in melanoma. In addition, we discuss current progress in anti-melanoma therapies involving a combination of HDAC inhibitors, immune checkpoint inhibitors, and MAPK inhibitors.

show abstract

HDAC6 interacts with PTPN1 to enhance melanoma cells progression

Cited by 24 publications

References 34 publications

Pristimerin inhibits glioma progression by targeting AGO2 and PTPN1 expression via miR-542-5p

Pristimerin inhibits glioma progression by targeting AGO2 and PTPN1 expression via miR-542-5p

Terpenoids, Cannabimimetic Ligands, beyond the Cannabis Plant

Histone Deacetylase Inhibitors to Overcome Resistance to Targeted and Immuno Therapy in Metastatic Melanoma

Contact Info

Product

Resources

About