PHAP1 promotes glioma cell proliferation by regulating the Akt/p27/stathmin pathway

Xie, Manyi; Ji, Zhe; Bao, Yaxing; Zhu, Y.; Xu, Yang; Wang, Lei; Gao, Shangfeng; Liu, Zhiyi; Tian, Zilu; Meng, Qingming; Shi, Hengliang

doi:10.1111/jcmm.13639

Cited by 22 publications

(21 citation statements)

References 43 publications

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“… 36 In addition, a correlation of STMN1 and chemoresistance in cancer has been reported 38 and glioma cell proliferation is known to be promoted by regulating the Akt/p27/stathmin pathway. 39 , 40 For the STMN1/ERBB4 complex, several inhibitors exist, including afatinib. In a case study of a recurrent GBM patient, treatment with afatinib and TMZ resulted in a significant regression of the disease.…”

Section: Discussionmentioning

confidence: 99%

Multiomics profiling of paired primary and recurrent glioblastoma patient tissues

Dekker

Kannegieter²,

Haerkens³

et al. 2020

Neuro-Oncology Advances

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Abstract Background Despite maximal therapy with surgery, chemotherapy and radiotherapy, glioblastoma (GBM) patients have a median survival of only 15 months. Almost all patients inevitably experience symptomatic tumor recurrence. A hallmark of this tumor type is the large heterogeneity between patients and within tumors itself which relate to failure of standardized tumor treatment. In this study, tissue samples of paired primary and recurrent GBM tumors were investigated to identify individual factors related to tumor progression. Methods Paired primary and recurrent GBM tumor tissues from 8 patients were investigated with a multi-omics approach using transcriptomics, proteomics and phosphoproteomics. Results In the studied patient cohort, large variations between and within patients are observed for all omics analyses. A few pathways affected at the different omics levels partly overlapped if patients are analyzed at the individual level, such as synaptogenesis (containing the SNARE complex) and cholesterol metabolism. Phosphoproteomics revealed increased STMN1(S38) phosphorylation as part of ERBB4 signaling. A pathway tool has been developed to visualize and compare different omics datasets per patient and showed potential therapeutic drugs, such as abobotulinumtoxina (synaptogenesis) and afatinib (ERBB4 signalling). Afatinib is currently in clinical trials for GBM. Conclusions Large variation on all omics levels exist between and within GBM patients. Therefore, it will be rather unlikely to find a drug treatment that would fit all patients. Instead, a multi-omics approach offers potential to identify affected pathways on the individual patient level and select treatment options.

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Section: Discussionmentioning

confidence: 99%

Multiomics profiling of paired primary and recurrent glioblastoma patient tissues

Dekker

Kannegieter²,

Haerkens³

et al. 2020

Neuro-Oncology Advances

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“…In the study by Xie et al . focusing on assessment of Putative HLA‐DR‐associated protein 1 (PHAP1) in glioma, immuno‐based assays ( n = 30 human glioma tissues and n = 12 specimens of nontumor brain tissues) revealed significant increase of PHAP1 abundance in tumoral versus nontumoral tissue.…”

Section: Discovery Of Potential Drug Targetsmentioning

confidence: 99%

Proteomics in Drug Development: The Dawn of a New Era?

Frantzi

Latosinska

Mischak

2019

Proteomics Clinical Apps

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Mass spectrometry offers the potential of acquiring high resolution data depicting the functional status of a group of healthy or diseased individuals, according to different conditions. As most of the drugs are currently targeting proteins, proteomics has a dual value, both in the discovery of new molecules as therapeutic targets, but also as a methodology to perform high throughput drug profiling. As there is an evident need for drugs to be improved in terms of efficacy, a mechanistic insight for downstream effectors can be valuable in order to predict side effects and resistance mechanisms. Recently developed assays, like thermal proteome profiling enables comprehensive drug target profiling and is, therefore, of high value in drug discovery. In this review, a systematic literature search is conducted and the most prominent proteomics studies as implicated in assisting drug discovery and development is presented. Focus is placed on investigations that are closer to implementation, therefore particular emphasis is given in studies conducted in human diseased population and further verified in vitro or in vivo.

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“…The most common histologic subtypes of glioma are astrocytoma and oligodendroglioma [2]. Despite multimodal therapeutic strategy, such as chemotherapy, radiotherapy and other adjuvant therapy have been combined to combat glioma over the last decade, the prognosis of glioma patients remains unoptimistic [3,4]. Lack of efficient and novel molecular target in clinical treatment is a vital reason for the unsatisfactory outcome [5].…”

Section: Introductionmentioning

confidence: 99%

EIF3J-AS1 promotes glioma cell growth via up-regulating ANXA11 through sponging miR-1343-3p

Jing

Wang²,

Zhao

et al. 2020

Cancer Cell Int

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Background: Glioma is one prevalent malignant tumor originates from the central nervous system. Dysregulation of long non-coding RNAs (lncRNAs) has been found to be a molecular signature behind the pathology of a variety of cancers, including glioma. EIF3J antisense RNA 1 (EIF3J-AS1) is a novel lncRNA, whose performance in carcinogenesis has been unfolded. Nevertheless, the role of EIF3J-AS1 has never been investigated in glioma. Methods: qRT-PCR analysis was adopted to evaluate the relative levels of RNAs. In vitro functional assays, including colony formation, EdU, TUNEL and caspase-3/8/9 activity assays were conducted to study the impacts of EIF3J-AS1 on glioma. Dual-luciferase activity assays, RNA pull down assay and RIP assay were performed to elucidate molecular interplay among genes. Results: EIF3J-AS1 was overexpressed in glioma cell lines. Knockdown of EIF3J-AS1 hampered glioma malignant phenotypes. MiR-1343-3p could bind to EIF3J-AS1. Moreover, miR-1343-3p targeted Annexin A11 (ANXA11) in its 3′UTR region. Mechanistically, EIF3J-AS1 relieved ANXA11 from miR-1343-3p silencing in the EIF3J-AS1/miR-1343-3p/ ANXA11 RNA induced silencing complex (RISC), thus eliciting promoting effects on glioma progression. MiR-1343-3p inhibitor and ANXA11 overexpression offset the inhibitory impacts of EIF3J-AS1 silencing on glioma development. Conclusion: EIF3J-AS1/miR-1343-3p/ANXA11 axis significantly affected biological behaviors in glioma, suggesting new therapeutic target for glioma treatment.

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PHAP1 promotes glioma cell proliferation by regulating the Akt/p27/stathmin pathway

Cited by 22 publications

References 43 publications

Multiomics profiling of paired primary and recurrent glioblastoma patient tissues

Multiomics profiling of paired primary and recurrent glioblastoma patient tissues

Proteomics in Drug Development: The Dawn of a New Era?

EIF3J-AS1 promotes glioma cell growth via up-regulating ANXA11 through sponging miR-1343-3p

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