MiR-301a is activated by the Wnt/β-catenin pathway and promotes glioma cell invasion by suppressing SEPT7

Xiao, Yue; Cao, De-Chen; Lan, Fengming; Pan, Qiang; Xia, Tao; Yu, Huan

doi:10.1093/neuonc/now044

Cited by 42 publications

(39 citation statements)

References 29 publications

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“…Another possible pathway promoting cell growth upon GOLPH3 overexpression is the GOLPH3-Wls-Wnt axis [67]. As said above, GOLPH3 interacts with the VPS35 retromer protein [9] and Wnt/β-catenin [68,69], and consequently, Wntless (Wls, the chaperone protein of Wnt secretion) [70] are important in glioma etiology. Lu and collaborators [67] have recently demonstrated that GOLPH3 affects Wls recycling, and consequently Wnt secretion and function, promoting tumorigenesis [3].…”

Section: Golph3 Deregulation and Brain Tumorsmentioning

confidence: 97%

Oncogenic Roles of GOLPH3 in the Physiopathology of Cancer

Sechi

Frappaolo

Karimpour-Ghahnavieh

et al. 2020

IJMS

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Golgi phosphoprotein 3 (GOLPH3), a Phosphatidylinositol 4-Phosphate [PI(4)P] effector at the Golgi, is required for Golgi ribbon structure maintenance, vesicle trafficking and Golgi glycosylation. GOLPH3 has been validated as an oncoprotein through combining integrative genomics with clinopathological and functional analyses. It is frequently amplified in several solid tumor types including melanoma, lung cancer, breast cancer, glioma, and colorectal cancer. Overexpression of GOLPH3 correlates with poor prognosis in multiple tumor types including 52% of breast cancers and 41% to 53% of glioblastoma. Roles of GOLPH3 in tumorigenesis may correlate with several cellular activities including: (i) regulating Golgi-to-plasma membrane trafficking and contributing to malignant secretory phenotypes; (ii) controlling the internalization and recycling of key signaling molecules or increasing the glycosylation of cancer relevant glycoproteins; and (iii) influencing the DNA damage response and maintenance of genomic stability. Here we summarize current knowledge on the oncogenic pathways involving GOLPH3 in human cancer, GOLPH3 influence on tumor metabolism and surrounding stroma, and its possible role in tumor metastasis formation.

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Section: Golph3 Deregulation and Brain Tumorsmentioning

confidence: 97%

Oncogenic Roles of GOLPH3 in the Physiopathology of Cancer

Sechi

Frappaolo

Karimpour-Ghahnavieh

et al. 2020

IJMS

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“…Wang, Wang, Han, et al, 2013;Z. Wang, Dai, et al, 2015;Yue et al, 2016). Recently, Fang, Li, Xu, Hui, and Li (2018)…”

Section: Suppressive Roles Of Wnt/ β-Catenin Pathway In Glioma Devementioning

confidence: 99%

Wnt/β‐catenin signaling cascade: A promising target for glioma therapy

Zhou

Zeng

et al. 2018

Journal Cellular Physiology

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Glioma is one of the most treatment‐refractory intracranial tumors, and the aberrant expressed Wnt/β‐catenin pathway is closely associated with glioma malignancy. In this regard, Wnt/β‐catenin signaling has been reported to play an essential role in cellular proliferation, migration, invasion, and angiogenesis, therefore contributing to glioma progression. However, the underlying mechanisms of Wnt/β‐catenin signaling involvement in gliomagenesis remain unknown. Here, we present an overview of the Wnt components and then go on to summarize the current knowledge describing the multitude of roles of Wnt/β‐catenin in glioma, which are mediated by transcription factors, microRNAs, long noncoding RNAs, and so on. In the latter portion of the review, we elaborate the increasing apparent crosstalk of Wnt/β‐catenin pathway with PI3K/AKT signaling involved in these processes. Ultimately, compounds targeting the Wnt/β‐catenin are described in glioma. As better understanding of the regulatory mechanisms to glioma malignancies increases, Wnt/β‐catenin cascade may represent an area of developmental glioma therapeutics focus.

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“…They also observed that the serum exosomal miR-301a levels were lower after surgical resection of the tumour, but were increased during GBM recurrence, indicating that serum exosomal miR-301a could be a potential biomarker for diagnosis/prognosis for GBM patients. 127,128 Ebrahimkhani et al 129 used a panel of seven exosomal miRNAs-miR-182-5p, miR-328-3p, miR-339-5p, miR-340-5p, miR-485-3p, miR-486-5p and miR-543-to differentiate GBM patients from healthy controls with an accuracy rate of 91.7%. In addition, Santangelo et al 91 analysed a miRNA signature in exosomes from the serum of glioma patients in an attempt to differentiate tumour grading and gliomas from brain metastases.…”

Section: Microvesicles In Glioblastomamentioning

confidence: 99%

Circulating biomarkers in patients with glioblastoma

et al. 2019

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Gliomas are the most common tumours of the central nervous system and the most aggressive form is glioblastoma (GBM). Despite advances in treatment, patient survival remains low. GBM diagnosis typically relies on imaging techniques and postoperative pathological diagnosis; however, both procedures have their inherent limitations. Imaging modalities cannot differentiate tumour progression from treatment-related changes that mimic progression, known as pseudoprogression, which might lead to misinterpretation of therapy response and delay clinical interventions. In addition to imaging limitations, tissue biopsies are invasive and most of the time cannot be performed over the course of treatment to evaluate 'real-time' tumour dynamics. In an attempt to address these limitations, liquid biopsies have been proposed in the field. Blood sampling is a minimally invasive procedure for a patient to endure and could provide tumoural information to guide therapy. Tumours shed tumoural content, such as circulating tumour cells, cell-free nucleic acids, proteins and extracellular vesicles, into the circulation, and these biomarkers are reported to cross the blood-brain barrier. The use of liquid biopsies is emerging in the field of GBM. In this review, we aim to summarise the current literature on circulating biomarkers, namely circulating tumour cells, circulating tumour DNA and extracellular vesicles as potential non-invasively sampled biomarkers to manage the treatment of patients with GBM.

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MiR-301a is activated by the Wnt/β-catenin pathway and promotes glioma cell invasion by suppressing SEPT7

Abstract: Our findings revealed the mechanism of action for miR-301a in tumor cell invasion. Moreover, the Wnt/miR-301a/SEPT7 signaling axis might be a novel target in treating glioma.

Cited by 42 publications

References 29 publications

Oncogenic Roles of GOLPH3 in the Physiopathology of Cancer

Oncogenic Roles of GOLPH3 in the Physiopathology of Cancer

Wnt/β‐catenin signaling cascade: A promising target for glioma therapy

Circulating biomarkers in patients with glioblastoma

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